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FS HN 461 > Diabetes Diagnostics and Insulin > Flashcards

Diabetes Diagnostics and Insulin Flashcards

1
Q

What malfunctions of organs can result in hyperglycemia?

A

Pancreas: decrease insulin secretion
Liver: increased hepatic glc production, decreased hepatic glc uptake
Muscles: decreased glc uptake if person is insulin deficient = glc levels increase in blood

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2
Q

What is a Certified Diabetes Educator?

A

An RD or nurse can specialize once have 5 years of practice then test every 5 yrs

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3
Q

Who is a part of the diabeties health care team?

A

Pt, physician, RD, CDE, NP, nurse, PA, PharmD, mental health

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4
Q

What is the function of insulin, how does this relate to CHO, protein, and fat?

A
  • secreted from beta cells of the islets of Langerhans in the pancreas to decrease blood glc and increase cellular uptake
  • Anabolic hormone (storage/formation)
  • CHO: uptake of glc, glycogenesis
  • protein: uptake of AAs to create new protein/body mass
  • fat: lipogenesis, insulin takes up glc into adipocytes to store as fat, activates lipoprotein lipase which breaks down TG (cleaves off FA so adipocyte can uptake)
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5
Q

What hormone opposes the action of insulin? How does this hormone affect CHO, protein, fat?

A

Glucagon- raises blood glc
CHO: glycogenolysis
Protein: gluconeogenesis, proteolysis
Fat: lipolysis, glucagon stimulates hormone sensitive lipase to get TG back into bloodstream

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6
Q

How does insulin serve as an anticatabolic hormone?

A

insulin can inhibit the actions of glucagon,

this is also true for glucagon (can act as antianabolic role by inhibiting actions of insulin)

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7
Q

What is the correct nomenclature for Type 1 Diabetes Mellitus and Type 2 Diabetes Mellitus?

A

(1) T1DM or DM1 (real #, not RN)
NOT: Type 1, juvenille-onset, insulin-dependent diabetes mellitus
(2) T2DM or DM2
NOT: Type II, adult onset, non-insulin dependent

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8
Q

Describe T1DM:

  • prevalence
  • cause
  • symptoms
A
  • 5-10% of diabetic population
  • pancreas produces little or no insulin (nothing to do with whether the insulin works well or not)
  • exogenous insulin needed for survival (ketosis leads to death)
  • can occur at any age but ~75% develop before 30
  • ***Key difference: Autoimmune disease, rapid onset
  • genetic predisposition but cannot be tracked through family as T2DM (only 30-50% identical twins develop)
  • trigger for autoimmune attack unknown but viral is suspected
  • Symptoms: unexplained wt loss, polyuria, polyphagia (eating), polydipsia (thirst)
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9
Q

Describe T2DM:

  • prevalence
  • cause
  • symptoms
  • prone to ketosis?
A
  • 90-95% of diabetic population
  • insulin resistance
    • pancreas produces sufficient insulin- may not require exogenous insulin
    • decreased tissue sensitivity/responsiveness to insulin so glc cannot enter cell
  • genetic predisposition
    • strong association of family hx
    • Native, African, and Asian Americans and Hispanics
  • Asymptomatic, but 80% are obese at dx and older age
  • physical inactivity
  • not prone to ketosis
    - hyperosmolar hyperglycemia nonketotic syndrome (HHNKS) still getting glc, not ketotic build up, acidic
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10
Q

What are the conversions for glucose?

A
  • mmol/L = 0.0555 x mg/dL
  • mg/dL = mmol/L / 0.0555
    • when writing mg/dL use whole numbers
    • when writing mmol/L use tenths
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11
Q 
What are the diagnostic criteria for:
- A1C
- FPG
-CPG
- two hour plasma glc tolerance test
How many abnormal tests are needed for diagnosis?
A
  • AIC > or = 6.5%
  • FPG (no kcal for 8 hr): >126 mg/dL confirmed with repeat test
    • this test is easy to administer, convenient, acceptable to pt, low cost
  • CPG: >200 mg/dL plus classic symptoms
  • two hour plasma glucose tolerance test (75 g glc load given)
    • > 200 mg/dL

*** need to have two abnormal tests in order to diagnose, and ideally two different tests

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12
Q

What is the diagnostic criteria for DM and PreDM?

A

Diabetes: >126 mg/dL

Pre-diabetes: (79 million Americans, rf for CVD and DM)

  • impaired glc tolerance (140-199 mg/dL on OGTT)
  • impaired fasting glc (100-125 mg/dL)
  • A1C 5.7-6.4%
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13
Q

What criteria is used for testing for DM in adults that are asymptomatic?

A
  • All pts >45 yo, q3yrs if normal
  • younger or more often if overwt (>25 kg/m2) and additional RF:
    • physical inactivity
    • first degree relative with DM
    • high risk group (African American, Latino, Nam, Asian-Am, Pacific Islander)
    • Dx of gestational DM or delivered >9# baby
    • HTN (>140/90 mmHg or HTN meds)
    • HDL 250 mg/dL
    • PCOS
    • A1C >5.7%, IGT or IFG on previous tests
    • other conditions associated with insulin resistance (severe obesity)
    • CVD hx
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14
Q

What is a non-insulin dependent tissue and what tissues meet this criteria?

A
  • glc can freely cross membrane w/o insulin, damaged if hyperglycemia present (excessive glc in blood = excessive amts of glycosylated Hb (A1C levels)
  • kidneys, eye, nerves, RBC
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15
Q

How does hyperglycemia affect the non-insulin dependent organs (Eye, Kidneys, Nerves)?

A

Eye –> retinopathy, cataract, glaucoma –> blindness
kidney –> nephropathy: micro or gross alnuminuria –> kidney failure
Nerves –> neuropathy: peripheral, autonomic –> amputation

Biology:

  • kidney develops holes, albumin released, shows up in urine
  • amputation most often caused by infection
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16
Q

What does A1C value mean? What are the normal levels?

A

A1C reflects BG control over past 3-4 months (glycosylated Hb)

Normal 6-7%
Acceptable 8-9%
Poor Control >10%

  • <6% improved risk reduction for microvascular complications
  • can have good A1C despite poor control
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17
Q

At what level must BG be at in order for glc or ketones to show up in urine?

A

Glc in urine when BG >180 mg/dL
Ketones in urine when BG consistently >250 mg/dL
- test for ketones with infection, illness, stress

18
Q

How is serum Na affected by BG?

A
  • osmotically active glc draws H20 from cells, so:

Serum Na decreases 1.6 mEq/L for each 100 mg/dL glc above normal

19
Q

How will electrolytes and HCO3 levels be affected?

A
  • osmotic diuresis will result in loss of free water, K, lytes
  • HCO3 used to buffer acidic ketones, so the concentration will decrease
20
Q

What is the mechanism through which glc is brought into a cell?

A
  1. pancreas produces insulin in response to increase glc in blood
  2. insulin binds to membrane bound receptor
  3. binding of insulin to receptor signals glc transporters to move from cytoplasm to cell membrane (GLUT4)
  4. Glucose transporters enable glc to move into cell
21
Q

What are the different glc transporters and on what tissues are they found?

A

GLUT 1: ubiquitously distributed
GLUT 2: present in gut (energy dependent transport), liver, pancreatic islets
GLUT 3: CNS and brain
GLUT 4: insulin responsive tissues (skeletal muscle, adipose, heart)

22
Q

What affects does insulin have on cellular processes?

A
  • increased glycogenesis in liver and muscle cells
  • increased FA synthesis through stimulus to LPL
  • increased esterification of FA- resynthesis of TG from glycerol and FA
  • increased AA uptake (protein synthesis)
  • increased K uptake- forces cells to absorb serum potassium, lack of insulin inhibits absorption
  • increase in HCl secretion by parietal cells in stomach
23
Q

What are the anti-catabolic roles of insulin?

A
  • inhibits proteolysis
  • inhibits lipolysis
  • inhibits gluconeogenesis- primarily in the liver
24
Q

What are the macrovascular complications of DM?

A
  • cardiovascular: low to normal LDL and high TG
  • stroke
  • HTN
  • diabetics have a 2-3 fold increase risk of CVD, risk of MI is same as someone who already had an MI
25
Q

What is Diabetic Ketoacidosis?

A
  • life threatening but reversible complications
  • result of inadequate insulin
  • rely on fat for energy (ketones)
  • symptoms: polyuria, polydipsia, hyperventilation, dehydration, fruity breath
  • if left untreated –> coma and death
26
Q

What is Hyperosmolar hyperglycemic non-ketotic syndrome?

A
  • occurs in DM2- still getting glc, ketones do not build up
  • life threatening with high mortality rate
  • severely elevated BG (600-2000 mg/dL) and dehydration
  • loss of consciousness, altered mental state
  • Trt = hydration and insulin
  • elderly, undertreated/undx DM2
27
Q

What is hypoglycemia and how would you decrease risk?

A 
BG < 50 mg/dL
Decrease risk:
- routine self monitoring
- observe/respond quickly to symptoms
- ingest appropriate quantities and choices of CHO pre-ex
- use consistent meal plan and pattern
28
Q

What is the Hypoglycemia treatment plan?

A

15/15 guidelines:

  • BG < 70 mg/dl eat 15g CHO
    - BG should increase 50 mg/dL in 15-30 min
  • retest in 15 min
  • if BG < 80 mg/dL eat additional 15 g CHO
  • if BG > 80 mg/dL eat 15 g if next meal is > 1 hr away
  • retest in 15 min if unsure rx is over
29
Q

What is 1st phase vs 2nd phase insulin?

A

First phase: “robust” release of insulin, begins w/in 2 min of nutrient ingestion and continues for 10-15 min, reflective of beta cell function (sensitivity/responsiveness)

Second phase: “functional” release of insulin” after 1st phase if BG not yet under 100 then another burst

**same insulin, just released at dift times

30
Q

What is Basal, Bolus, and Basal/bolus insulin?

A

Basal: “background”- between meals and through night

Bolus: “burst”, 1st and 2nd phase release, matches food consumed or elevated glc

Basal/bolus: term used by health care professionals to describe flexible (intensive) therapy

- 4 or more insulin injections to keep BG in target range
- insulin pump
31
Q

What are the BG goals recommended by the ADA?

A

Before meal: 70-130 mg/dL
2 hours after meal: < 7%

Target glc: single # that falls w/in BG goals

32
Q

What is peak action of insulin?

A

when insulin works hardest to lower BG

  • different for each individual, must determine to prepare for lowest BG
  • wide ranges are provided for peaks- varies greatly b/n individuals (can be frustrating)
33
Q

What are some reasons to use insulin?

A
  • T1DM
  • Pregnancy
  • surgery
  • critical illness
  • renal disease
  • decompensation
    - acute injury, stress, infection
    - uncontrolled wt loss
  • T2DM if significant hyperglycemia at presentation despite maximal dose of oral agents
  • T2DM that cannot use oral agents (allergy or serious rxn)
34
Q

For rapid action insulin:

  • examples
  • onset of action
  • peak action
  • duration
A

Examples: Humalog (lispro), Novolog, Apidra
Onset of action: 15 min
Peak action: 30-90 min
Duration: 3-5 hours

35
Q

For short acting insulin:

  • examples
  • onset of action
  • peak action
  • durations
A

Examples: Humulin R, Novolin R, “regular”
*trying to get people off of regular b/c it needs to be used 30 min before a meal
Onset of action: 30 min
peak action: 2-5 hrs regular, 2-3 hrs Velosulin
Duration: 5-8 hrs regular, 2-3 hrs Velosulin

36
Q

For intermediate acting insulin:

  • examples
  • onset of action
  • peak action
  • duration
A

Examples: NPH (N), Lente (L)
Onset of Action: N: 1-2 hrs, L: 1-2.5 hrs
Peak Action: N: 4-12 hrs, L: 3-10 hrs
Duration: 18-24 hours for both

37
Q

For long acting insulin describe:

  • examples
  • onset of action
  • peak action
  • duration
A

Ultralente:

  • onset of action: 30 min-3 hours
  • peak action: 10-20 hours
  • duration: 20-36 hours

Lantus (most common basal insulin)

  • onset of action: 1-1.5 hours
  • no peak action
  • duration: 20-24 hours
38
Q

What are the old and current insulin protocols?

A

Old: NPH + Regular

Current “gold standard”: Lantus (background)- long 20-24 hours +Humalog (bolus)- rapid 30-90 min

39
Q

What is rebound hyperglycemia?

A
  • Somogyi effect, posthypoglycemic hyperglycemia
  • pt was hypoglycemic (undetected)–> hyperglycemic
  • cause is too much insulin (exogenous)
  • secretion of counter regulatory hormones –> increased hepatic glucose production
  • does not have to be at night
40
Q

What is the dawn phenomenon?

A
  • abnormal early morning BS increase as counter regulatory hormones increase
  • hormonal increase occurs in everyone but can be exagerrated in in individuals with DM
    • key difference- not associated with nocturnal hypoglycemia
  • may need more insulin to cover early AM (4-8 AM vs 1-3 AM)
41
Q

What can be done to counteract Somogyi and Dawn Effect?

A

Somogyi
- have bedtime snack of protein
- decrease insulin dose (don’t modify until several nights)
Dawn Phenomenon
- use insulin that peaks later or increase dose (must see several nights)
- if using pump, alter amt of basal
- limit CHO at bedtime

FS HN 461 (6 decks)

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