Final Exam Flashcards
(146 cards)
1
Q
Metformin MOA
A
- Activates AMP-kinase
- Decreased HGP & intestinal glc absorption
- Increased insulin action
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
3
Q
Disadvantages Metformin
A
- GI SEs
- Lactic acidosis (rare)
- VB12 deficiency
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
5
Q
Efficacy of Biguanides
A
- Decrease FPG 60-70 mg/dL
- Reduce A1c 1-2%
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
7
Q
How is basal bolus ratio determined?
A
- Basal 50%, bolus 50%
- Calculate mealtime bolus w/ IC and total grams carbs
8
Q
Need to know when starting T1D on basal bolus regimen
A
Basal dose, bolus dose (IC), correction ratio, SBGM (4-6x/day)
9
Q
A1c targets for children
A
<7.0% for most adults/adolescents and children (ADA) - notes
New 2015 ADA recs say <7.5%
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
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
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”
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
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
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
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
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
- Non-fasting 50gm screening GTT
18
Q
Definition of T2D according to Kibbey
A
Resistance to action of insulin and relative inability of pancreas to produce adequate insulin
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%
20
Q
How often test for A1c?
A
- Healthy: Q6mo
- Not controlled: Q3mo
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)
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)
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!
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
25
Children BP Goals in DM:
* based on percentiles. \<130/80 or \<90th percentile, choose the lower.
* If not reached 3-6 mo, initiate pharm tx.
26
Pregnant women DM w/chronic HTN BP goals
* \<140/90
* individualize – try to keep near baseline if usually lower
27
adults w/DM BP goals
* ADA target \<140/90
* Initiate lifestyle if \>120/80
28
LDL goals: DM pts
* Calculated ascvd risk … but:
* No overt CVD: \<100 mg/dL
* W/overt CVD: \<70 mg/dL + high intensity statin is option
29
When to Rx asa as primary prevention
* 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
30
When to Rx asa as secondary prevention
Prescribe!
31
What to Rx if allergy to asa
clopidogrel
32
When to check fasting lipid panel, lipids adults
* At least annually in most adults
* If low risk (LDL \<100, HDL \>50, TGs \<150) may do Q2 years
33
When to check fasting lipid panel, lipids kids
* 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
34
Etoh and T1D
* 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\*\*
35
Goals of MNT
* 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
36
Major studies on lifestyle
Da Quin, Finnish DPP, DPP – lifestyle is good!
37
Major studies on medications
DPP (metformin), Stop NIDDM (acarbose), ACT NOW (pioglitazone)
38
Nurses Health Study: risk factors vs protective factors
* Risk: low ses, underweight, malnourished, stress (cortisol)
* Protective: Moderate etoh, moderate caffeine, chocolate, brown rice
39
What is FINDRISK?
Gold standard DM screening tool that came out of Finnish DPP
40
DPP: metformin vs lifestyle
* Lifestyle and metformin better than placebo at delaying/preventing T2D
* Lifestyle better than metformin at delaying/preventing T2D
41
Look AHEAD study: findings
* 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
42
How to calculate carb ratio
* 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
43
How to calculate meal bolus
* Total # carbs / I/C ratio
* E.g.
* Total carbs 96
* I/C 1 unit per 12 g
* 96/12 = 8 units
44
How to calculate a correction bolus
* 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!!
45
NPH: OPD
* Onset: 2-4 hours
* Peak: 6-8 hours (officially labeled 4-14hrs)
* Duration: 10-12 hours (officially labeled 12-24hrs)
46
Lantus: OPD
* Onset: 2-3hr
* Peak: None
* Duration: ~ 24 hours
47
Levemir: OPD
* Onset: 1hr
* Peak: None
* Duration: ~ 12-24 hours
48
Novolog/humalog/apidra: OPD
* Onset: 10-15 minutes
* Peak: 1.5-2 hours
* Duration: 2-4 hours
49
Regular: OPD
* 0.5 – 1hr
* 2-4hr
* 4-8hr
50
Novolin 70/30 vs Novolog mix 70/30
Novolin should be BID
Novolog mix should be dosed AC
51
Humulin R U-500 – when to use
* If marked insulin resistance
* Cannot mix w/other insulins
* Careful of error!
52
Options for insulin regimens, T1D lecture
* 2+ injections
* 3+ injections
* 4+ injections/day or Insulin Pump
53
How does BID insulin work / cautions?
* 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
54
How does 3+ doses of insulin/day work - cautions?
* 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
55
How to Tx obesity
* Intensive lifestyle intervention
* Insulin sensitizer
* Dual drug therapy
* Bariatric procedure
56
When to get microalbumin
* Yearly
* Nl \<30
57
How to treat HTN in DMs
Lifestyle + Ace or arb!!
58
Smoking in DMs
No good!
Assess, advise, assist, arrange
59
Insulin: normal stimulation vs T2DM
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
Insulin in liver: normal vs T2DM
* 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
Insulin in skeletal muscle: normal vs T2DM
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
TZDs: advantages
* No hypoglycemia
* Durability
* decreased TGs, increased HDL-C
* ? decreased CVD (pio)
63
TZDs disadvantages
* Gastrointestinal
* Dosing frequency
* Modest decrease in A1c
64
a-GIs: MOA
* Inhibits a-glucosidase
* Slows carbohydrate absorption
65
a-GIs: Advantages
* No hypoglycemia
* Nonsystemic
* decreased Post-prandial glucose
* ? decreasedCVD events
66
DPP-4 Inhibitors: MOA
* Inhibits DPP4 activity, prolongs survival of endogenously released incretin hormones
* Increased insulin, decreased glucagon
67
DPP-4 inhibitors: Advantages
* No hypoglycemia
* Well tolerated
68
DPP-4 Inhibitors: disadvantages
* Modest decrease A1c
* ? Pancreatitis
* Urticaria
69
DPP-4 Inhibitors: cost
high
70
GLP-1 receptor agonists: MOA
* Activates GLP-1 R
* increased Insulin, decreased glucagon
* decreased gastric emptying
* increased **** satiety
71
GLP-1 receptor agonists: Advantages
* Weight loss
* No hypoglycemia
* ? Beta cell mass
* ? CV protection
72
GLP-1 receptor agonists: Disadvantages
* GI
* ? Pancreatitis
* Medullary ca
* Injectable
73
SGLT2 Inhibitors: MOA
* ****increased urinary excretion of glucose
* decreased reabsorption of glucose prox. segment of the convoluted tubule
## Footnote
*sodium / glc cotransporter 2*
74
SGLT2 Inhibitors: Advantages
* Weight loss
* No hypoglycemia
75
SGLT2 Inhibitors: Disadvantages
* UTIs
* Genital infections
* no change in serum Cr/electrolytes!! (advantage)
76
How / when should initial retinopathy screenings be done?
* 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
Eye exams in women with preexisting diabetes who are pregnant or planning to get pregnant - when and how?
* 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
How should nephropathy be screened for in DM?
* 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
TZDs MOA
Activates nuclear transcription factor PPAR-gamma --\> increased peripheral insulin sensitivity
80
Important monitoring for thiazolidinediones
Monitor LFTs before and after tx
81
Benefits of actos
Can reduce SBP & fatty liver
82
BBW for thiazolidinediones
* Avandia: increased risk of MI and heart related deaths
* Actos: increased CHF requiring hospitalization, w/o assoc mortality risk
83
Alpha glucosidase CIs
IBD, cirrhosis
84
Exanatides and reduced GFR
Avoid if GFR \<30
85
DPP-4 and dose adjustments
All but linagliptin excreted renally, dose adjust
86
DPP-4 Monitoring
Renal function
## Footnote
Risk of pancreatitis: d/c if abdominal pain, draw amylase, lipase, LFTs
87
Stages of CKD
* 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
Nl GFR
* \>90-130.
* \>130 suggestive of hyperfiltration
89
Needed to diagnose CKD
At least 2 specimens, preferable first morning voids, w/in 3-6mo apart
90
Protein vs GFR in CKD
Protein used to diagnose CKD
GFR used to stage CKD
91
Diabetic nephropathy vs CKD
CKD in setting of microalbuminuria: 30-300mg/Gm
CKD + Diabetic nephropathy when over macroalbumin: \>300gm/GM/Cr
92
Cr Clearance vs GFR in diagnosis of CKD
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
Role of pancreas in glc homeostasis
* **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
Where does GLC come from?
Ingested, stored (glycogen), newly made (gluconeogenesis)
95
Glycogenesis vs glycogenolysis vs gluconeogenesis
* 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
Glc homeostasis: what does a healthy body do in setting of hypoglycemia?
* 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
DM: short term sequelae of high blood sugar
* Dehydration (urine, thirst)
* Weakness, fatigue
* Blurred vision
* Poor wound healing
* Decreased ability to fight infectons
98
DM: long term sequelae of high blood sugar
Retinopathy, nephropathy, neuropathy, CV dz (MI, CVA, gangrene, amputations)
99
What are the major insulin dependent tissues?
Liver, muscle, adipose cells
100
Role of the liver in glc homeostasis?
* Hepatocytes (and muscle cells) store glucose as glycogen
* \*\*Hepatic TG content is associated w/insulin resistance (impaired insulin signaling
101
Relationship between fat and high calories/glucose + hyperinsulinemia?
* 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
Hormones responsible for glc regulation
* Elevate glc (“counter-regulatory hormones”)
* Acutely: glucagon, catecholamines
* Chronically: glucocorticoids, growth hormone
* Lowers glc
* Insulin
103
Role of insulin in glc regulation?
* Lowers BG
* Increase liver and muscle glc uptake and storage
* Decreases HGP
* Stimulates FA synthesis
104
T2D reason for fasting hyperglycemia
Increased HPG / gluconeogenesis by liver. Not totally understood why.
105
T2D reason for postprandial hyperglycemia
Primarily muscle tissue resistance to insulin, inability to suppress HGP
106
S/S of DKA
* 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
Definition of DKA
* 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
T1D Abs
* GAD65, Tyrosene phosphatase I-A2, I-A2β, autoantibody to insulin, islet cell autoantibodies
* + antibodies found in 80-90% of T1DM
109
How much destruction of beta cells before symptoms in T1D?
80-90%
110
Defects of each organ involved in T2D
* The three core physiologic defects of T2D
* insulin resistance, β-cell dysfunction, and increased liver glucose production
111
What to suspect in a diabetic w/warm swollen foot, no open sore?
Charcot! Cellulitis, clot…
112
Common sequelae of diabetic foot problems
* Thick, striated, ingrown toenails
* Toenail fungus
* Charcot
* Neuropathy
* Ulcers
* Hammer toes
* etc
113
Acanthosis nigricans: what is it / etiology
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
Balanoposthitis and balanitis
* Balanoposthitis: Inflammation of the foreskin and glans in uncircumcised males. Can be bacterial or fungal.
* Balanitis: inflammation of the glans penis
115
Candida: what is it, how to prevent, mgmt.
* 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
Carbuncle: what is it, mgmt.
* 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
Cellulitis: what is it, mgmt.
* Resulting from entry of bacteria into the skin
* Presenting as a red, hot, tender, swelling
* Management: IV or PO antibiotics, warm soaks, hygiene.
118
Diabetic bullae: what is it, who gets it, mgmt.
* 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
Diabetic dermopathy: what is it, mgmt.
* 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
Diabetic neuropathic ulcer: what is it, prevention, mgmt.
* 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
Eruptive xanthomas: what is it, mgmt.
* 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
Gangrenous toe: what is it, mgmt.
* 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
Necrobiosis Lipoidica Diabeticorum: what is it, mgmt.
* 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
Scleredema Diabeticorum: what is it, who gets it, mgmt.
* 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
Tinea: what is it, where is it, mgmt.
* 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
Vitiligo: what is it, mgmt.
* 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
Types of autonomic neuropathy
CV, GI, GU, sudomotor
128
S/S of CV autonomic neuropathy
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
S/S of GI autonomic neuropathy
* 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
S/S of GU autonomic neuropathy
Urinary dysfunction-incontinence, bladder hypomotility, ED, vaginal dryness, diminished sexual response
131
S/S of sudomotor autonomic dysfunction
Gustatory sweathing – upper body diaphoresis when eating, hyper or anhidrosis – promotes skin breakdown, pupilomotor dysfunction – issues w/night vision or diplopia
132
Peripheral vs proximal neuropathy
* Peripheral: pain/loss of feeling in toes, feet, legs, hands, arms
* Proximal: pain in thighs, hips, buttocks leading to weakness in legs
133
Focal neuropathy
Sudden weakness of one nerve, or a group of nerves, causing muscle weakness or pain
E.g., Bell’s palsy
134
Distal symmetrical polyneuropathy
* Most common type of diabetic neuropathy
* Result of sensory nerve damage
* Stocking and glove distribution common
135
Pain assessment of diabetic neuropathy
Onset (acute vs chronic), location (unilateral vs bilateral), pain (constant, fluctuating?), aggravating factors, alleviating factors
136
PE for neuropathy
* **S**kin, peripheral pulses, sensorimotor, MS, gait, balance, foot structure (each visit), foot appearance (each visit), pulses each visit,
* Annually: neurosensory: vibratory, monofilament, DTRs
137
Diabetic Retinopathy: when to send
* 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
Home glc monitoring: goals, according to kibbey
* FBG: 90-130
* PP: \<160-180
* HS: 100-140
139
Causes and risk factors for GDM
Insulin resistance d/t pregnancy
overweight and obesity
genetic predisposition
140
Characteristics of GDM
Carb intolerance identified by screening those at risk during pregnancy
Usually asymptomatic
Strong risk factor for later development of T2D
141
Components of GDM treatment
meal planning, exercise, weight management, medications
142
Meal planning for GDM
provide adequate calories and carbs w/o hyperglycemia or ketonemia, often divided into meals and snacks to space carb intake
143
Exercise in GDM
program that does not cause fetal distress, contractions, HTN
144
Medications for GDM
* 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
Should GDM patients monitor BG?
yes!
required to determine efficacy of tx and possible need for insulin. Glc should be checked fasting and 1-2h PP
146
How does 4+ doses of insulin/day work?
* 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
