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Diabetes > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Metformin MOA

A
  • Activates AMP-kinase
    • Decreased HGP & intestinal glc absorption
    • Increased insulin action
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2
Q

Advantages of Metformin

A
  • No wt gain / assoc wt loss
  • No hypoglycemia
  • Reduction in CV events and mortality (UKPDS f/u)
    • Decreases LDL, TGs
  • Improves ovulatory function in insulin resistant women w/PCOS (make sure they know they can get pregnant!)
  • Low cost
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3
Q

Disadvantages Metformin

A
  • GI SEs
  • Lactic acidosis (rare)
  • VB12 deficiency
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4
Q

Contraindications / cautions to metformin

A
  • Reduced Kidney function (1.4 Cr for women, 1.5 Cr for men) (risk lactic acidosis)
  • Avoid in CHF, COPD, liver dz, FVD, alcoholism, metabolic acidosis
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5
Q

Efficacy of Biguanides

A
  • Decrease FPG 60-70 mg/dL
  • Reduce A1c 1-2%
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6
Q

How to titrate metformin

A
  • Start 500mg, titrate up weekly as tolerated to 2000mg daily
  • If needed, 500mg, 850mg, 1000mg tabs available.
  • 2-3 divided doses daily
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7
Q

How is basal bolus ratio determined?

A
  • Basal 50%, bolus 50%
  • Calculate mealtime bolus w/ IC and total grams carbs
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8
Q

Need to know when starting T1D on basal bolus regimen

A

Basal dose, bolus dose (IC), correction ratio, SBGM (4-6x/day)

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9
Q

A1c targets for children

A

<7.0% for most adults/adolescents and children (ADA) - notes

New 2015 ADA recs say <7.5%

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10
Q

ADA recommendation for protein restriction

A
  • No evidence of CKD – individualize protein intake
  • No evidence that restriction improves outcomes in diabetes + CKD.
  • = Diabetics do not need to restrict below RDA of 0.8g/kg/day
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11
Q

Causes for nighttime hypo/hyperglycemia

A
  • Basal too high or too low
  • Exercise, etoh – can lead to nighttime lows
  • not eating / not bolusing for meals / etc
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12
Q

Recommendations for wt loss iin DM

A
  • 1000-2000kcal/day for loss or maintenance
  • Optimal body weight BMI between 18.5 and 24.9
  • Sustained wt loss 5-10% can have lasting beneficial impact – not necessary to reach “ideal body weight”
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13
Q

Diagnostic criteria for T1D and T2D

A
  • Non-pregnant Adults
    • Casual glucose ≥ 200 plus symptoms (polyuria, polydipsia, polyphagia).
    • Fasting Glucose ≥126
    • OGTT (Oral Glucose Tolerance Test) 2 hour post prandial >200mg/dl
    • A1C ≥ 6.5%
  • Children
    • Same criteria as above
    • OGTT is contraindicated in infants and young children

needs to be repeated in absence of unequivocal hyperglycemia

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14
Q

Screening criteria for T1DM

A
  • No indication
  • Diagnostic testing only w/signs T1D (polyuria, polydipsia, wt loss, polyphagia, blurred vision, etc)
  • If have T1D, consider screening for: celiac, B12, thyroid, etc as appropriate/symptomatic
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15
Q

Screening criteria for T2D

A
  • Every 3 years in
    • Adults 45+
  • More frequently if:
    • Family Hx (parents, siblings, children)
    • Physically inactive
    • High risk ethnicity/race (NA, af am, latino, Asian, pacific islander)
    • Pre-diabetes
    • GDM or delivered baby >9lbs
    • HTN
    • HDL <35 and/or Trig >250
    • PCOS
    • Acanthosis nigricans
    • Severe obesity
    • CV dz
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16
Q

Screening criteria for GDM

A
  • Assess risk at first prenatal visit
    • Obesity
    • Previous GDM or delivery of 9lb baby or larger
    • Glycosuria
    • Diabetes in 1st degree relative
    • PCOS
  • OGTT weeks 24-28
  • Low risk = 1 step screening method
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17
Q

One vs Two step methods for GDM

A
  • One step 75gm GTT, + if _>_1 abnormal
    • FBG ≥ 92
    • 1h ≥ 180
    • 2h ≥ 153
  • Two step method for GDM
    • Non-fasting 50gm screening GTT
      • Normal ≤ 130
      • Abnormal >130
    • 100gm GTT ≥ 2 abnormal (Fasting)
      • FBG ≥ 95
      • 1h ≥ 180
      • 2h ≥ 155
      • 3h ≥ 140
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18
Q

Definition of T2D according to Kibbey

A

Resistance to action of insulin and relative inability of pancreas to produce adequate insulin

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19
Q

Diagnostic criteria for prediabetes

A
  • Impaired fasting glucose (IFG): ≥ 100mg./dl and <126mg/dl
  • Impaired Glucose tolerance test (IGT):
    • Based on 75g OGTT
    • 2hr ≥ 140
    • 2hr <200
  • A1C: 5.7-6.4%
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20
Q

How often test for A1c?

A
  • Healthy: Q6mo
  • Not controlled: Q3mo
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21
Q

Disadvantages of HbA1c

A
  • Can have false highs and lows in certain disorders
    • Hemoglobinopathies (thalassemia)
    • Hemolytic anemias
    • Chronic Kidney Disease (Yields lower A1C value) – especially those requiring epogen
    • Iron deficiency (High A1C) due to LOW cell turn over.
  • Studies show HgA1C identifies fewer patients with DM than traditional testing (FPG/OGTT)
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22
Q

Individualizing A1c goals

A
  • <7 for most adults/adolescents and children (ADA)
  • 6-6.5 (AACE)
  • 7.5-8 or slightly higher for high risk pts (ADA)
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23
Q

ADA dietary recs for fat and carbs

A
  • ADA recs for carbs
    • If T1D, offer intensive insulin T using carb counting, meal planning
    • Consistent carb intake if fixed daily dose
    • Simple meal planning approach if low health literacy
  • ADA recs for fat intake
    • Individualized!
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24
Q

Definition T1D (Kibbey)?

A
  • Absolute inability of pancreas to produce insulin
  • Kids, teens, young adults. Lean. Rapid onset islet destruction. Insulin dependent.
  • Typically presents w/ketoacidosis
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25
Q

Children BP Goals in DM:

A
  • based on percentiles. <130/80 or <90th percentile, choose the lower.
  • If not reached 3-6 mo, initiate pharm tx.
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26
Q

Pregnant women DM w/chronic HTN BP goals

A
  • <140/90
  • individualize – try to keep near baseline if usually lower
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27
Q

adults w/DM BP goals

A
  • ADA target <140/90
  • Initiate lifestyle if >120/80
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28
Q

LDL goals: DM pts

A
  • Calculated ascvd risk … but:
  • No overt CVD: <100 mg/dL
  • W/overt CVD: <70 mg/dL + high intensity statin is option
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29
Q

When to Rx asa as primary prevention

A
  • Consider 75-162mg/day
    • Primary prevention strategy if T1 or T2D w/increased 10 year CV risk
    • Includes men >50, women >60 with: FHx CVD, HTN, smoking, HLD, albuminuria
  • NOT for low CVD risk: <5% in men <50 and women <60 w/no other major CVD risk factors
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30
Q

When to Rx asa as secondary prevention

A

Prescribe!

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31
Q

What to Rx if allergy to asa

A

clopidogrel

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32
Q

When to check fasting lipid panel, lipids adults

A
  • At least annually in most adults
  • If low risk (LDL <100, HDL >50, TGs <150) may do Q2 years
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33
Q

When to check fasting lipid panel, lipids kids

A
  • Family hx HLD or DV event before 55y, or unknown FH – at diagnosis if >2yo before puberty
  • If no risk factors, or diagnosed after puberty, first screening at puberty (~10yo)
  • If lipid abnl – annually
  • If lipids nl (<100)– Q5years
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34
Q

Etoh and T1D

A
  • Etoh is oxidized by the liver → may impair gluconeogenesis → hypogylcemia.
  • **Because both etoh and insulin can inhibit gluconeogenesis, T1D who use insulin and drink etoh w/o eating are at risk for severe hypoglycemia**
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35
Q

Goals of MNT

A
  • Achieve and maintain blood glucose levels, lipid levels, and blood pressure
  • To prevent, or at least slow, the rate of development of the chronic complications of diabetes by modifying nutrient intake and lifestyle
  • To address individual nutrition needs, taking into account personal and cultural preferences and willingness to change
  • To maintain the pleasure of eating by only limiting food choices when indicated by scientific evidence
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36
Q

Major studies on lifestyle

A

Da Quin, Finnish DPP, DPP – lifestyle is good!

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37
Q

Major studies on medications

A

DPP (metformin), Stop NIDDM (acarbose), ACT NOW (pioglitazone)

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38
Q

Nurses Health Study: risk factors vs protective factors

A
  • Risk: low ses, underweight, malnourished, stress (cortisol)
  • Protective: Moderate etoh, moderate caffeine, chocolate, brown rice
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39
Q

What is FINDRISK?

A

Gold standard DM screening tool that came out of Finnish DPP

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40
Q

DPP: metformin vs lifestyle

A
  • Lifestyle and metformin better than placebo at delaying/preventing T2D
  • Lifestyle better than metformin at delaying/preventing T2D
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41
Q

Look AHEAD study: findings

A
  • Intensive lifestyle intervention results in
    • Avg 8.6% wt reduction
    • Significant decrease in A1c
    • Reduction in CVD RFs – though had to stop early d/t not enough
  • Benefits sustained at 4 years
  • = intervene early!! Once at DM, almost too late
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42
Q

How to calculate carb ratio

A
  • 500 rule: 500/TDD = I/C ratio
    • if TDD is 40: 500/40 = 12.5
    • = I/C ration is 1u for every 12.5 carbs
  • designed for meal bolus, to bring BG back to where it started
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43
Q

How to calculate meal bolus

A
  • Total # carbs / I/C ratio
  • E.g.
    • Total carbs 96
    • I/C 1 unit per 12 g
    • 96/12 = 8 units
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44
Q

How to calculate a correction bolus

A
  • Based on correction factor/insulin sensitivity factor, target BG, actural BG
  • First calculate ISF: 1800 rule à 1800/TDD = ISF
  • Calculation: (Actual BG – Target BG) / CF
    • CF: 1 unit per 125
    • Target: 100
    • Actual: 295
    • 295-100 = 195/125 = 1.6u
  • Do not give more than Q 2 hours!!
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45
Q

NPH: OPD

A
  • Onset: 2-4 hours
  • Peak: 6-8 hours (officially labeled 4-14hrs)
  • Duration: 10-12 hours (officially labeled 12-24hrs)
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46
Q

Lantus: OPD

A
  • Onset: 2-3hr
  • Peak: None
  • Duration: ~ 24 hours
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47
Q

Levemir: OPD

A
  • Onset: 1hr
  • Peak: None
  • Duration: ~ 12-24 hours
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48
Q

Novolog/humalog/apidra: OPD

A
  • Onset: 10-15 minutes
  • Peak: 1.5-2 hours
  • Duration: 2-4 hours
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49
Q

Regular: OPD

A
  • 0.5 – 1hr
  • 2-4hr
  • 4-8hr
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50
Q

Novolin 70/30 vs Novolog mix 70/30

A

Novolin should be BID

Novolog mix should be dosed AC

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51
Q

Humulin R U-500 – when to use

A
  • If marked insulin resistance
  • Cannot mix w/other insulins
  • Careful of error!
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52
Q

Options for insulin regimens, T1D lecture

A
  • 2+ injections
  • 3+ injections
  • 4+ injections/day or Insulin Pump
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53
Q

How does BID insulin work / cautions?

A
  • Humalog 75/25, novolog 70/30, Humalog 50/50
  • 2/3 in a.m. 1/3 in afternoon or evening
  • Difficult to maintain adequate coverage (especially in T1D)
  • Used in patients who won’t take more injections
  • T2D may have late morning or nocturnal hypoglycemia d/t excessive insulin
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54
Q

How does 3+ doses of insulin/day work - cautions?

A
  • Initial doses based on TDD of 1u/kg/day
  • 2/3 in a.m., 1/3 at dinner (image)
  • Often used in our newly diagnosed patients
  • Limited success after honeymoon period
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55
Q

How to Tx obesity

A
  • Intensive lifestyle intervention
  • Insulin sensitizer
  • Dual drug therapy
  • Bariatric procedure
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56
Q

When to get microalbumin

A
  • Yearly
  • Nl <30
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57
Q

How to treat HTN in DMs

A

Lifestyle + Ace or arb!!

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58
Q

Smoking in DMs

A

No good!

Assess, advise, assist, arrange

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59
Q

Insulin: normal stimulation vs T2DM

A

Normal: beta cells sense rise in glc levels in bloodstream, send enough insulin to lower sugar into normal range (70-105mg/dL)

T2DM: lack of adequate stimulation to lower BG to normal range

60
Q

Insulin in liver: normal vs T2DM

A
  • Normal: insulin allows glc to be stored as glycogen to be later released during fasting states; promotes conversion of liver glc into fatty acids/inhibits lipolysis
  • T2DM: lack of insulin or sensitivity means body thinks it’s in a fasting state when it’s not and releases glc from glycogen and FAs = high BG and free fatty acids
61
Q

Insulin in skeletal muscle: normal vs T2DM

A

normal: insulin stimulates storage of glc as muscle glycogen to be used for energy by muscle cell

T2DM: glycogen released b/c body believes it’s in fasting state, but can’t get into cells since glc transporters on cell depend on insulin

62
Q

TZDs: advantages

A
  • No hypoglycemia
  • Durability
  • decreased TGs, ­increased HDL-C
  • ? decreased CVD (pio)
63
Q

TZDs disadvantages

A
  • Gastrointestinal
  • Dosing frequency
  • Modest decrease in A1c
64
Q

a-GIs: MOA

A
  • Inhibits a-glucosidase
  • Slows carbohydrate absorption
65
Q

a-GIs: Advantages

A
  • No hypoglycemia
  • Nonsystemic
  • decreased Post-prandial glucose
  • ? decreasedCVD events
66
Q

DPP-4 Inhibitors: MOA

A
  • Inhibits DPP4 activity, prolongs survival of endogenously released incretin hormones
    • Increased insulin, decreased glucagon
67
Q

DPP-4 inhibitors: Advantages

A
  • No hypoglycemia
  • Well tolerated
68
Q

DPP-4 Inhibitors: disadvantages

A
  • Modest decrease A1c
  • ? Pancreatitis
  • Urticaria
69
Q

DPP-4 Inhibitors: cost

A

high

70
Q

GLP-1 receptor agonists: MOA

A
  • Activates GLP-1 R
  • increased Insulin, decreased glucagon
  • decreased gastric emptying
  • increased ­ satiety
71
Q

GLP-1 receptor agonists: Advantages

A
  • Weight loss
  • No hypoglycemia
  • ? Beta cell mass
  • ? CV protection
72
Q

GLP-1 receptor agonists: Disadvantages

A
  • GI
  • ? Pancreatitis
  • Medullary ca
  • Injectable
73
Q

SGLT2 Inhibitors: MOA

A
  • ­increased urinary excretion of glucose
  • decreased reabsorption of glucose prox. segment of the convoluted tubule

sodium / glc cotransporter 2

74
Q

SGLT2 Inhibitors: Advantages

A
  • Weight loss
  • No hypoglycemia
75
Q

SGLT2 Inhibitors: Disadvantages

A
  • UTIs
  • Genital infections
  • no change in serum Cr/electrolytes!! (advantage)
76
Q

How / when should initial retinopathy screenings be done?

A
  • Initial dilated and comprehensive eye examination by an ophthalmologist or optometrist
    • Adults and children aged 10 years or older
      with type 1 diabetes
      • Within 5 years after diabetes onset
    • Patients with type 2 diabetes
      • Shortly after diagnosis of diabetes
  • Women with preexisting diabetes/pregnancy: every trimester

kids going through puberty

77
Q

Eye exams in women with preexisting diabetes who are pregnant or planning to get pregnant - when and how?

A
  • Comprehensive eye examination
  • Counseled on risk of development and/or progression of diabetic retinopathy
  • Eye examination should occur in the first trimester (B)
  • Close follow-up throughout pregnancy
  • For 1 year postpartum
78
Q

How should nephropathy be screened for in DM?

A
  • Assess urine albumin excretion annually
    • In type 1 diabetic patients with diabetes duration of ≥5 years
    • In all type 2 diabetic patients at diagnosis
  • Measure serum creatinine at least annually
    • In all adults with diabetes regardless of degree of urine albumin excretion
    • Serum creatinine should be used to estimate GFR and stage level of chronic kidney disease, if present
79
Q

TZDs MOA

A

Activates nuclear transcription factor PPAR-gamma –> increased peripheral insulin sensitivity

80
Q

Important monitoring for thiazolidinediones

A

Monitor LFTs before and after tx

81
Q

Benefits of actos

A

Can reduce SBP & fatty liver

82
Q

BBW for thiazolidinediones

A
  • Avandia: increased risk of MI and heart related deaths
  • Actos: increased CHF requiring hospitalization, w/o assoc mortality risk
83
Q

Alpha glucosidase CIs

A

IBD, cirrhosis

84
Q

Exanatides and reduced GFR

A

Avoid if GFR <30

85
Q

DPP-4 and dose adjustments

A

All but linagliptin excreted renally, dose adjust

86
Q

DPP-4 Monitoring

A

Renal function

Risk of pancreatitis: d/c if abdominal pain, draw amylase, lipase, LFTs

87
Q

Stages of CKD

A
  • 1 – protein in urine, normal GFR >90
  • 2 – protein in urine GFR 60-89
  • 3a – GFR 45-59
  • 3b – GFR 30-44
  • 4 – GFR 15-29
  • 5 – FGR <15 (failure, dialysis or transplant needed)
88
Q

Nl GFR

A
  • >90-130.
  • >130 suggestive of hyperfiltration
89
Q

Needed to diagnose CKD

A

At least 2 specimens, preferable first morning voids, w/in 3-6mo apart

90
Q

Protein vs GFR in CKD

A

Protein used to diagnose CKD

GFR used to stage CKD

91
Q

Diabetic nephropathy vs CKD

A

CKD in setting of microalbuminuria: 30-300mg/Gm

CKD + Diabetic nephropathy when over macroalbumin: >300gm/GM/Cr

92
Q

Cr Clearance vs GFR in diagnosis of CKD

A

Cr clearance requires timed urine, exceeds GFR d/t includes Cr secreted by proximal tubule and filtered by glomerulus, frequently innacurate,

GFR: calculated based off of serum creatinine (MDRD)

93
Q

Role of pancreas in glc homeostasis

A
  • Islets of Langerhans: cells that house beta cells
  • Beta cells: “sense” elevations in BG, release right amt of insulin to lower sugar to nl range (70-100)
  • Insulin: signal to cells to take up glc
94
Q

Where does GLC come from?

A

Ingested, stored (glycogen), newly made (gluconeogenesis)

95
Q

Glycogenesis vs glycogenolysis vs gluconeogenesis

A
  • All are sources of endogenous glucose
  • Glycogenesis: formation of glycogen from glucose
  • Glycogenolysis: glycogen stored in liver and muscles released as glc via glucagon or epinephrine (can proceed to glycolysis for energy, or glc for cells)
  • Gluconeogenesis: formation of glucose from a non-carb source (lactic acid, some AAs, glycerol from fat)
96
Q

Glc homeostasis: what does a healthy body do in setting of hypoglycemia?

A
  • Insulin secretion turned off
  • Alpha-cells release glucagon
  • Adrenal glands release cortisol and epinephrine
  • Liver releases glucose (FAs and ketones)
  • Net effect: prevent glc uptake into non-essential tissues, keeping brain supplied
97
Q

DM: short term sequelae of high blood sugar

A
  • Dehydration (urine, thirst)
  • Weakness, fatigue
  • Blurred vision
  • Poor wound healing
  • Decreased ability to fight infectons
98
Q

DM: long term sequelae of high blood sugar

A

Retinopathy, nephropathy, neuropathy, CV dz (MI, CVA, gangrene, amputations)

99
Q

What are the major insulin dependent tissues?

A

Liver, muscle, adipose cells

100
Q

Role of the liver in glc homeostasis?

A
  • Hepatocytes (and muscle cells) store glucose as glycogen
  • **Hepatic TG content is associated w/insulin resistance (impaired insulin signaling
101
Q

Relationship between fat and high calories/glucose + hyperinsulinemia?

A
  • Glc –> FAs –> transported as lipoproteins to adipocytes for storage
  • FAs stored as TGs are most important depot of stored fuel in the body
    • Our ability to store glycogen is limited, whereas capacity for fat storage is virtually unlimited
  • TGs in liver and muscle –> insulin resistance d/t impaired signaling
102
Q

Hormones responsible for glc regulation

A
  • Elevate glc (“counter-regulatory hormones”)
    • Acutely: glucagon, catecholamines
    • Chronically: glucocorticoids, growth hormone
  • Lowers glc
    • Insulin
103
Q

Role of insulin in glc regulation?

A
  • Lowers BG
  • Increase liver and muscle glc uptake and storage
  • Decreases HGP
  • Stimulates FA synthesis
104
Q

T2D reason for fasting hyperglycemia

A

Increased HPG / gluconeogenesis by liver. Not totally understood why.

105
Q

T2D reason for postprandial hyperglycemia

A

Primarily muscle tissue resistance to insulin, inability to suppress HGP

106
Q

S/S of DKA

A
  • Polys, FVD, abdominal pain, vomiting, s/s poor perfusion, Confusion/lethargy, kussmaul respirations, coma
  • Risk of cerebral edema – 0.5-1% of all DKA episodes
  • Leading cause of M&M in kids w/T1D
  • More common <2yo, delayed Dx, lower SES
107
Q

Definition of DKA

A
  • BG >200 mg/dL
  • Ketosis (serum and urine)
  • Acidosis ph <7.3 or bicarb <15
    • Mild: pH <7.3, Bicarb < 15
    • Moderate: pH < 7.2, Bicarb < 10
    • Severe: pH < 7.1, Bicarb < 5
108
Q

T1D Abs

A
  • GAD65, Tyrosene phosphatase I-A2, I-A2β, autoantibody to insulin, islet cell autoantibodies
    • antibodies found in 80-90% of T1DM
109
Q

How much destruction of beta cells before symptoms in T1D?

A

80-90%

110
Q

Defects of each organ involved in T2D

A
  • The three core physiologic defects of T2D
    • insulin resistance, β-cell dysfunction, and increased liver glucose production
111
Q

What to suspect in a diabetic w/warm swollen foot, no open sore?

A

Charcot! Cellulitis, clot…

112
Q

Common sequelae of diabetic foot problems

A
  • Thick, striated, ingrown toenails
  • Toenail fungus
  • Charcot
  • Neuropathy
  • Ulcers
  • Hammer toes
  • etc
113
Q

Acanthosis nigricans: what is it / etiology

A

Diffuse dark, brownish black velvety thickening of skin folds, such as axillae, neck, groin, and hands. Etiology may be related to factors of heredity, endocrine disorders, obesity, drugs, and/or malignancy.

114
Q

Balanoposthitis and balanitis

A
  • Balanoposthitis: Inflammation of the foreskin and glans in uncircumcised males. Can be bacterial or fungal.
  • Balanitis: inflammation of the glans penis
115
Q

Candida: what is it, how to prevent, mgmt.

A
  • Superficial fungal infection occurring on moist cutaneous sites, predisposing factors are increased moisture, diabetes, or alteration in systemic immunity
  • Prevention – keep area clean and dry
  • Management: Topical miconazole powder/cream.
116
Q

Carbuncle: what is it, mgmt.

A
  • Deep bacterial infection of the hair follicle resulting in an abcess. Appears as a very large inflammatory plaque studded with multiple pustules, surrounded by erythema and edema
  • Requires immediate medical attention
  • Management: Systemic antimicrobial therapy, heat application, and cleanliness.
117
Q

Cellulitis: what is it, mgmt.

A
  • Resulting from entry of bacteria into the skin
  • Presenting as a red, hot, tender, swelling
  • Management: IV or PO antibiotics, warm soaks, hygiene.
118
Q

Diabetic bullae: what is it, who gets it, mgmt.

A
  • Self-limiting non-inflammatory condition unique to diabetic patients.
  • Usually in long standing diabetics
  • Males >females
  • 0.5% of diabetics
  • No tx necessary – resolves in 2-6 weeks, can recurr.
  • Abx may be necessary if secondary infection occurs.
119
Q

Diabetic dermopathy: what is it, mgmt.

A
  • Most common skin disease in diabetics
  • Red or blistering spots can precede brown spots.
  • Due to small vessel changes in the skin
  • Self-limiting areas, no specific treatment
120
Q

Diabetic neuropathic ulcer: what is it, prevention, mgmt.

A
  • Occlusion of blood vessels to nerves, causing a burning, tingling, numbness sensation to feet
  • Decreased pain sensation with resulting skin/sores/ulcers due to trauma
  • Prevention with good foot care
  • Management: Surgical intervention often necessary
121
Q

Eruptive xanthomas: what is it, mgmt.

A
  • Discrete, inflammatory-type papules erupt suddenly and in showers, apearing typically on the buttox, elbows, knees, back, or anywhere
  • Results from high lipid levels in blood
  • Management: Low calorie and low-fat diet, lipid lowering agent
122
Q

Gangrenous toe: what is it, mgmt.

A
  • Severe occlusion of large blood vessels can lead to gangrenous changes in the toes as a result of tissue death
  • Management: surgical amputation and abx if necessary.
123
Q

Necrobiosis Lipoidica Diabeticorum: what is it, mgmt.

A
  • Rare complication due to small blood vessel disease of the skin
  • Appearing as a red brown raised firm order with a yellowish center. This skin disorder may precede the diagnosis of DM. Screening is necessary
  • Management: No well established rx, but topical steroids can be used.
124
Q

Scleredema Diabeticorum: what is it, who gets it, mgmt.

A
  • Localized thickening of the skin which usually occurs of the upper back. Overlying erythema w/ development of peau d’orange appearance centrally
  • Management: a 12 weeks course of psoralens plus ultraviolet A (PUVA) can be considered.
  • Hyperglycemia control does NOT improve sx
  • More common in middle aged males
  • AKA: Type 3 Scleredema
125
Q

Tinea: what is it, where is it, mgmt.

A
  • Tina Corporis/Tinea Pedis
  • Patients with DM at greater risk for contracting Tinea. (corporis or pedis)
  • Management: Topical antifungal agents and oral ketoconazole for refractory infections.
126
Q

Vitiligo: what is it, mgmt.

A
  • Associated with autoimmune type 1 DM. Loss of skin pigment accounts for the white color of lesion
  • Treatment consists of sunlight and vitamin D exposure.
127
Q

Types of autonomic neuropathy

A

CV, GI, GU, sudomotor

128
Q

S/S of CV autonomic neuropathy

A

Resting tachycardia, orthostasis, loss of beat-to-beat variation, cardiac denervation (silent mis), failure of hypoxia induced respiratory drive, systolic and diastolic dysfunction, increased risk sudden death

129
Q

S/S of GI autonomic neuropathy

A
  • Gastroparesis (bloating, nausea, early satiety), can affect post meal glc levels
  • Constipation, abdominal pain, cramping, sphincter function changes
  • Diarrhea – bacterial overtgrowth in bowel: change in fecal appearance, foul odor
130
Q

S/S of GU autonomic neuropathy

A

Urinary dysfunction-incontinence, bladder hypomotility, ED, vaginal dryness, diminished sexual response

131
Q

S/S of sudomotor autonomic dysfunction

A

Gustatory sweathing – upper body diaphoresis when eating, hyper or anhidrosis – promotes skin breakdown, pupilomotor dysfunction – issues w/night vision or diplopia

132
Q

Peripheral vs proximal neuropathy

A
  • Peripheral: pain/loss of feeling in toes, feet, legs, hands, arms
  • Proximal: pain in thighs, hips, buttocks leading to weakness in legs
133
Q

Focal neuropathy

A

Sudden weakness of one nerve, or a group of nerves, causing muscle weakness or pain

E.g., Bell’s palsy

134
Q

Distal symmetrical polyneuropathy

A
  • Most common type of diabetic neuropathy
  • Result of sensory nerve damage
  • Stocking and glove distribution common
135
Q

Pain assessment of diabetic neuropathy

A

Onset (acute vs chronic), location (unilateral vs bilateral), pain (constant, fluctuating?), aggravating factors, alleviating factors

136
Q

PE for neuropathy

A
  • Skin, peripheral pulses, sensorimotor, MS, gait, balance, foot structure (each visit), foot appearance (each visit), pulses each visit,
  • Annually: neurosensory: vibratory, monofilament, DTRs
137
Q

Diabetic Retinopathy: when to send

A
  • T1D: 5 years after diagnosis
  • T2D: see immediately
  • Special times:
    • puberty – retinopathy progresses for unclear reasons, possibly lack of adherence or hormones
    • pregnancy: even if mild, must see every trimester
138
Q

Home glc monitoring: goals, according to kibbey

A
  • FBG: 90-130
  • PP: <160-180
  • HS: 100-140
139
Q

Causes and risk factors for GDM

A

Insulin resistance d/t pregnancy

overweight and obesity

genetic predisposition

140
Q

Characteristics of GDM

A

Carb intolerance identified by screening those at risk during pregnancy

Usually asymptomatic

Strong risk factor for later development of T2D

141
Q

Components of GDM treatment

A

meal planning, exercise, weight management, medications

142
Q

Meal planning for GDM

A

provide adequate calories and carbs w/o hyperglycemia or ketonemia, often divided into meals and snacks to space carb intake

143
Q

Exercise in GDM

A

program that does not cause fetal distress, contractions, HTN

144
Q

Medications for GDM

A
  • Insulin: consider if unable to consistently maintain PG < 90 mg/dL fasting and <120 1-2 hrs post prandial
  • Lispro and aspart are the only insulin analogs currently classified as pregnancy risk category B, which is the same risk as regular insulin
  • Oral agents: glyburide, metformin sometimes used (NOT recommended by ADA)
145
Q

Should GDM patients monitor BG?

A

yes!

required to determine efficacy of tx and possible need for insulin. Glc should be checked fasting and 1-2h PP

146
Q

How does 4+ doses of insulin/day work?

A
  • Most closely resembles native beta cell function
  • Considered Intensive Insulin Management and the GOLD STANDARD
  • Basal/Bolus/Correction: 1-2 of basal, bolus w/meals, correction prn

Diabetes (1 decks)

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