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Endocrine II - Exam 2 > Complications of DM (Pales)- SRS > Flashcards

Complications of DM (Pales)- SRS Flashcards

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1
Q

Describe the likely findings in DKA for each of the following levels.

  1. Blood glucose
  2. Blood pH
  3. Serum Bicarbonate
  4. Ketones
A
  1. Blood glucose > 250 mg/dL
  2. Blood pH < 7.3
  3. Serum Bicarbonate < 15 mEq/L
  4. Ketones positive
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2
Q

Contrast DKA in type one and two DM.

A

Type I DM

  • Usually initial presentation
  • Insulin non-compliance
  • Increase in anti-insulin hormones (cortisol etc) during stress (infection, surgery etc.)

Type II DM

  • Late stages of Beta-Cells failure
  • During stress
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3
Q

DKA presents clinically with an onset of 1-2 days, polyuria and polydipsia, weakness, decreased appetite, nausea, vague abdominal pain.

Mental statuse changes also accompany this, what are they?

What is the mortality rate from DKA?

A

Mental status changes

  • Confusion
  • Lethargy
  • Coma/convulsions

5 - 20% mortality rate

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4
Q

The physical exam of a DKA patient will vary greatly depending on the severity of the episode. You will find signs that fall into two distinct categories.

  1. Signs of acidosis
  2. Signs of dehydration

What are the signs of acidosis you would expect to see? 4

A
  1. Confusion
  2. Lethargy
  3. Kussmal Respiration
  4. Fruity breath odor (acetone)
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5
Q

The physical exam of a DKA patient will vary greatly depending on the severity of the episode. You will find signs that fall into two distinct categories.

Signs of acidosis

Signs of dehydration

What are the signs of dehydration you would expect to see? 3

A
  1. Oral membranes dry/cracked
  2. Turgor of skin
  3. Hypotension/tachycardia
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6
Q

As we discussed earlier a patient in DKA will have high blood glucose (350-900), Low CO2/bicarb/pH, high ketones/acetone/ketoacids.

What will the following labs look like in a DKA patient?

  1. BUN
  2. Creatinine
  3. Serum K+
  4. Total K+
  5. Na+
  6. Phosphorous
A

High

  1. BUN
  2. Creatinine
  3. Serum K+
  4. Phosphorus

Low

  1. Na+
  2. Total K+
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7
Q

Describe the four main components of the treatment of the DKA patient.

A
  1. I.V. Insulin
  2. I.V. Fluids (typically 100 ml/kg water deficit)
  3. Electrolytes replacements
  4. Ventilatory support in severe cases
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8
Q

Once the DKA episode has resolved, you should switch from IV insulin to subq injections. How do you know that the DKA episode is over?

A

Normalization of anion gap is the most important indicator of resolution of DKA (as bicarb may remain low due to non-gap anion gap acidosis)

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9
Q

You have a patient with the following lab values…

  • Hyperglycemia > 600 mg/dL.
  • Serum osmolality > 310 mosm/kg.
  • No acidosis; blood pH above 7.3.
  • Serum bicarbonate > 15 mEq/L.
  • Normal anion gap (< 14 mEq/L).

What does this patient have?

A

Hyperosmolar hyperglycemic non-ketotic state, and type II DM

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10
Q

Describe the cycle of the hyperosmolar hyperglycemic non-ketotic state.

A

Hyperglycemia –> osmotic diuresis –> dehydration –> increased osmolality, decrease in free fluid –> hyperglycemia (solute concentration)

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11
Q

What are the possible consequences of a hyperosmolar hyperglycemic non-ketotic state?

A

Hypovolemic shock

End organ damage

  • Coma
  • Renal Failure
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12
Q

What patients are at risk for a hyperosmolar hyperglycemic non-ketotic state?

What does it arise d/t? 3

A

Type II diabetics only, typically older patients with poor care and dementia.

Due to:

  1. non-compliance with medications
  2. Acute infection/stress
  3. Inability to increase oral intake in response to increase urinary output
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13
Q

A Hyperosmolar Hyperglycemic Non-ketotic state presents with insidious onset, lethargy, very high glucose, no acidosis (unless lactic acidosis develops), low K+, Na+ high or low, and an elevated BUN/CR.

What is a significant PE finding you will see in these patients?

A

Severe state of dehydration with around 15% ECF loss.

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14
Q

What are the four main components of the treatment of a Hyperosmolar Hyperglycemic Non-ketotic state?

A
  1. I.V. fluids (most critical)
  2. Some iv insulin
  3. Electrolyte replacement
  4. Ventilatory support needed at times
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15
Q

Hypoglycemic coma can present with initial symptoms at what blood glucose level?

A

Blood glucose less than 80… unless the patient has had high glucose for a long time, in which case they have a “new normal”, and a return to actual normal glucose levels represents a hypoglycemic state for that patient.

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16
Q

So, the symptoms of hypoglycemic coma arise around a blood glucose of ~80 normally. When does the Coma/passing out stage hit?

A

Coma/passing out only if blood glucose is less than 50.

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17
Q

What patients are a high risk for hypoglycemic coma?

Why?

A

ÒLong term diabetics or patients on beta blockers may not have any initial symptoms until they pass out (hypoglycemia unawareness)

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18
Q

What are the key signs of hypoglycemic coma?

10

A
  1. Shaking
  2. Sweating
  3. anxious
  4. dizziness
  5. hunger
  6. fast heartbeat
  7. impaired vision
  8. weakness, fatigue
  9. headache
  10. irritable
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19
Q

What should be done to treat a patient in a hypoglycemic coma?

A
  1. Sugar orally if able or iv D50
  2. Glucagon SQ injection
  3. Review the causes
  • Too much medication
  • Skipped meal
  • Exercises
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20
Q

What is a card prompt I wonder…

What two main categories do the chronic complications of DM fall under?

A

Macrovascular

Microvascular

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21
Q

What are the 3 main categories of microvascular complications of DM?

A
  1. Neuropathy
  2. Nephropathy
  3. Retinopathy
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22
Q

The major macrovascular complication of DM is atherosclerosis of large arteries. What are the main problems we see arise in these patients as a result of this?

looking for 5, but there are tons you could hit

A
  1. Coronary—->MI
  2. Cerebral/Carotid—> Stroke
  3. LE—>LE amputation
  4. Renal—> HTN—> MI/Stroke
  5. Mesenteric à Bowell ischemia
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23
Q

Neuropathy is a common microvascular complication of DM, and hits what components of the nervous system?

A

Peripheral

Autonomic

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24
Q

Ocular complications of diabetes develop 15 -30 years after diagnosis typically. Diabetic retinopathy is the leading cause of adult onset blindness in the US. What are the two types of retinopathy seen in these patients?

A
  1. Nonproliferative (“background”) retinopathy
  2. Proliferative retinopathy
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25
Nonproliferative ("background") retinopathy is the most common cause of visual impairment in patients with type 2 DM, and presents with three characteristic changes in microvasculature. What are they?
1. Microaneurisms 2. Dot hemorrhages 3. Retinal edema.
26
Proliferative retinopathy involves the growth of new capillaries and fibrous tissue within the retina due to ischemic retinal infarcts (cotton wool spots), and is more common in type 1 diabetics. What can this lead to in severe cases? 2
1. Vitreous hemorrhage 2. Retinal detachment
27
What do you see in this fundoscopic exam? What does it indicate?
Dot hemorrhages - Point to nonproliferative (background) retinopathy
28
What is this fundoscopic finding? What does this say about the patients diabetes?
Proliferative retinopathy Much more common in Type 1 DM.
29
What is shown in the attached fundoscopic exam? Type of retinopathy?
Cotton wool spots - seen in proliferative (background) retinopathy
30
What are two other ocular complications that are seen in diabetic patients beyond the retinopathy?
1. Lens Swelling 2. Diabetic cataracts
31
What causes the glomerular damage in diabetic nephropathy?
The high pressure system created by increased vascular pressure leading to increased GFR and renal hyperfunction causes the damage. Not the nonenzymatic glycosylation.
32
What is often the fist complication that develops in diabetic patients?
Peripheral neuropathy
33
Diabetic neuropathy primarily affects the sensory nerves, especially the long nerves of the lower extremities, leading to distal symmetric polyneuropathy with a stocking/glove pattern. What are the positive and negative symptoms?
**_Positive (things they have that they shouldn't):_** 1. Burning pain 2. parasthesia **_Negative (things they don't have that they should):_** 1. hyposthesia 2. decreased temp sensation 3. decreased vibratory sensation 4. loss of achilles reflex
34
Does DM neuropathy hit motor neurons?
Yes, but less commonly and only in advanced cases typically.
35
The DM peripheral neuropathy presents as either a mononeuropathy or mononeuropathy multiplex, with isolated nerve(s) affected. What is most likely the etiology of this complication?
Likely ischemic in nature
36
What are the specific nerves that tend to be affected in DM peripheral neuropathy? What is the duration that each are afflicted?
**_Cranial nerves - usually resolves in 2-3 months_** 1. III 2. IV 3. VI **_Femoral nerve - lasts months to years, pain on front thigh and Quads weakness_**
37
What is a test we can use for identifying diabetic neuropathy?
Monofilament test
38
What is this and how did it happen?
Charcot foot d/t diabetic neuropathy
39
What are the four conditions of Charcot foot formation?
1. Loss of sensation 2. Initial trauma 3. Repetitive traumas 4. Good blood flow to feet.
40
Alright smarty pants, what conditions lead to this?
Charcots foot again... 1. Loss of sensation 2. Initial trauma 3. Repetitive traumas 4. Good blood flow to feet.
41
What are ways that autonomic neuropathy from DM can hit a patient?
1. Postural hypotension 2. Diabetic gastroparesis 3. diarrhea/constipation 4. impotence 5. Neurogenic bladder 6. Profuse sweating/temperature dysregulation
42
Diabetic gastroparesis is accompanied by nausea/vomiting, abdominal pain, weight loss/malnutrition. How is this diagnosed?
Gastric emptying study - normally should take 1-2 hours to empty, in an afflicted diabetic can take up to a day.
43
What are the six main suspects for the cause of the accelerated atherosclerosis seen in DM?
1. Hyperglycemia 2. Hyperlipidemia 3. Abnormalities of platelet adhesiveness 4. Hypertension 5. Oxidative stress 6. Inflammation
44
To what degree do adults with DM have an increased risk of heart disease or stroke?
2 - 4 times more likely
45
The ÒIncidence of stroke increases up to 4 fold in patients with diabetes and in particular what three things are seen?
1. Large artery thrombosis 2. Embolic and lacunar infarcts
46
What are the peripheral vascular complications of DM?
1. Intermittent claudication 2. Ischemic changes/ulcers/gangrenes
47
What is the big metabolic complication of DM that Pales mentioned?
**_Dyslipidemia_** 1. High LDL cholesterol 2. High triglycerides 3. Low HDL cholesterol
48
What are four common dermatological complications of DM?
1. Chronic pyogenic infections 2. Yeast infections 3. Acanthosis Nigricans 4. Necrobiosis Lipidoica Diabetorum
49
What is the "snapshot" measure of glycemic control? When is it typically performed?
**_Blood sugar/finger stick_** * Fasting/before meals * 2 hours after meals
50
What is the "long exposure photography" measure of diabetic control? How long does it give control information for?
Hemoglobin A1c (glycohemoglobin) - offers insight into control over a three month period
51
Hemoglobin is one of the proteins that get glycosylated by glucose, and the higher glucose level in the blood, the higher percentage of protein molecules will be glycosylated. The HbA1C is well correlated with the rate of complications. What are the goal HbA1C ranges per the ADA and AACE?
1. ADA: 7.0 2. AACE: 6.5
52
Conditions that shorten the lifespan of erythrocytes will decrease HbA1C, why? What are three examples?
These cases will typically have younger RBCs that just haven't been around long enough to become glycosylated to the degree that the blood glucose levels would ultimately lead to. 1. Hemolytic anemia 2. Hypersplenism 3. Frequent transfusions
53
ÒDiseases in which lack of new reticulocytes entering the pool results in aged RBCs being in circulation will cause hemoglobin A1C to progressively rise. What is one example of a condition in which we would see this phenomenon?
Aplastic anemia
54
What is the "videotaping" method of blood glucose monitoring?
Continuous monitoring 72 hour period or in conjunction with an insulin pump.
55
What were the big trials that were instrumental in developing our current understanding of how to approach the care of a diabetic patient? 5
1. DCCT 2. UKPDS 3. ACCORD 4. ADVANCE 5. VADT
56
The Diabetes Control and Complication Trial (DCCT) was a ten-year study of 1,441 type 1 patients in 29 centers. What were the conclusions of this study?
Intesive therapy, bringing patients HbA1c to 7.2 vs. 9.0 with conventional therapy lead to the following reductions in complications: 1. Retinopathy decreased by up to 76 % 2. Nephropathy decreased by up to 56 % 3. Neuropathy decreased by up to 60 %
57
What were two of the major take-aways from the UKPDS trial?
1. Stringent control of HbA1c has significant effects on microvascular complications but not on macrovascular. 2. Blood pressure control in DM patients has an enourmous impact on prevention of the macrovascular complications.
58
One fear of using intensive therapy to keep HbA1c low was complications d/t hypoglycemia. What did the UKPDS study reveal about this?
Not a major risk. * Annual incidence of major hypoglycemic events in patients treated with insulin----- 2.3% patients/year * One death from hypoglycemia out of 27,000 patient-years of intensive therapy
59
The ACCORD trial focused on patients who either had CV disease or were at risk for it and broke patients into two groups, one where the HbA1c was maintained at 7.5 and one where it was targeting 6.0 (actually averaged 6.4). What happened in this study?
The patients in the group that were targeted at the HbA1c level of 6.0 started dying faster, with a relative increase in mortality of 22% and an absolute increase of 1.0% after a mean of 3.5 years.
60
The advance trial was a randomized trial of blood pressure lowering and intensive glucose control in 11,140 patients with type 2 diabetes. What was the outcome?
1. Confirmed that HbA1c levels were critical in managing microvascular complications but not highly beneficial for macrovascular complications. 2. Confirmed that macrovascular complications were best managed by blood pressure control.
61
The advance trial also looked at the safety of intesive therapy to an HbA1c of 6.5, what were the conclusions reached on this topic? 3
1. No excess mortality 2. No weight gain 3. No excess of serious sequelae from hypoglycemia
62
What were the five major conclusions of all these studies?
1. Intensive control of diabetes mellitus has a definite positive effect on the rate of microvascular complications 2. Intensive control of diabetes mellitus has a modest positive effect on the rate of macrovascular complications only in a newly diagnosed diabetics and those with no or early macrovascular complications 3. Effect of hypoglycemia (including occult hypoglycemia) is unclear 4. Goal of Hb A1c of 7 remains the goal for most patients 5. Multifaceted approach to prevention of complication including glucose, blood pressure and lipids control is more appropriate for this multifaceted disease
63
What is the best strategy for prevention of DM retinopathy? Frequency for check up?
1. Optimize glycemic and blood pressure control 2. Yearly retinal exam
64
What is the best way to prevent diabetic neuropathy? Frequency of exam?
* Optimize glycemic control * Annual foot exam (including monofilament) and visual inspection at every visit
65
What are the best ways to prevent DM nephropathy? 2
1. Optimize glucose and blood pressure control 2. Limit protein intake to 0.8-1.0 g/kg in earlier stages, and 0.8 g/kg in later stages
66
How often should the diabetic get their kidney function checked?
Annual serum Creatinine/GFR calculation and microalbuminuria determination
67
What are the five major treatment methods for prevention of macrovascular disease in the diabetic?
1. Aspirin for patients over 40 or those with more than 1 risk factor 2. Smoking Cessation 3. Manage HTN and Hyperlipidemia 4. Assess for PVD with pedal pulses and ABI 5. ACEI/ARBS with HTN or without if over 55
68
Why do you need to be proactive with cardiac testing in the diabetic?
Silent ischemia can be a problem d/t the neuropathy
69
What are the components of the DM managment plan? 8
1. Statement of short- and long-term goals 2. Individualized nutrition recommendations and instructions, preferably by a registered dietitian 3. Recommendations for appropriate lifestyle changes 4. Medications 5. Regular lab workups. 6. Blood glucose monitoring instructions 7. Consultations for specialized services 8. Agreement on continuing support, follow up and return appointments
70
What are the types of oral diabetic meds? 4
1. Secretogogues 2. Decreased glucose absorption 3. Insulin sensitizers 4. Glucosuric SGLT-2 inhibitors
71
What are the main secretogogues? 3
1. Sulfanyl-ureas 2. Meglitinides 3. Incretins - DPP IV inhibitors
72
What are the two insulin sensitizers?
Biguanides TZDs
73
What is the MOA of sulfonylurea drugs?
Increase in insulin secretion by blocking K channels of b-cells of pancreas.
74
Sulfonylureas tend to become less effective with prolonged use. What is the efficacy at 5 years on average?
50% failure by 5 years
75
Contraindications to sulfonylurea?
1. Pregnancy/lactation 2. liver insufficiency 3. renal insufficiency 4. sulfa allergy
76
What are some common side effects of Sulfonylureas? 6
1. **Hypoglycemia** 2. GI upset 3. Urticaria 4. Jaundice (due to biliary stasis) 5. SIADH (ßNa, Ý BP) 6. Weight gain
77
In what patients in hypoglycemia d/t sulfonylureas a major concern?
Those who are... 1. Over age of 60 2. Impaired renal function 3. Poor nutrition 4. On multidrug therapy
78
Of the three sulfonyl ureas typically used, Glyburide, Glipizide and Glimepride, which would you want to use in a patient with chronic renal failure?
Glipizide/Glimepride - these have dual liver/renal elimination Don't use glyburide as it is solely renally eliminated.
79
Examples of meglitinides include Repaglinide and Nateglinide, these are short acting drugs (2-4 hours) and can be used as mono or combo therapy. What is their MOA? How should they be taken?
Act by closing ATP-dependent K channels of b-cells. Should be taken with meals and if patient skips a meal, he should skip a dose as well
80
What are some ADRs of meglitinides?
hypoglycemia weight gain
81
Incretins-related medications include GLP-1 and DPP-IV inbibitors. How are GLP-1 drugs administered? What are two examples?
Injection 1. Exenatide 2. Liraglutide
82
Incretins-related medications include GLP-1 and DPP-IV inbibitors. How are DPP-IV drugs administered? What are 5 examples?
Oral 1. Sitagliptine 2. Saxagliptine 3. Vildagliptin 4. Linagliptin 5. Alogliptin
83
DPP-IV inhibitors may be used in renal failure but should be dose adjusted. To what degree is the HbA1c adjusted with these agents? Discuss the extent of the hypoglycemia and weight gain ADRs associated with these drugs.
Modest HbA1c reduction (about 0.7) * Doesn’t cause hypoglycemia * No weight change
84
GLP-1 analogs are administered via SQ injections and have no risk of hypoglycemia when used alone or with metformin. What patients is this particularly good for and why? What are the major side effects? 2
Obese diabetics, typically lead to 7-12 lb average weight loss 1. Nausea 2. Pancreatitis
85
Metformin, which is a biguanide works by decreasing liver glucose production and increasing the sensitivity of insulin receptors. What are the other benefits this drug confers? 3
1. Improved lipid profile: decreased LDL, TC and TG 2. Promotes weight loss 3. Doesn't cause hypoglycemia
86
What are common side effects of metformin?
1. GI upset 2. **Lactic acidosis** 3. Decreased B12 and folate absorption
87
What are five contraindications for metformin?
1. Renal and liver insufficiency (Cr.\>1.5) 2. Chronic hypoxia 3. past Hx of lactic acidosis 4. alcoholism 5. Withhold if Pt. getting iodinated contrast
88
MOA for thiasolidinediones?
Increased sensitivity to insulin and decreased hepatic gluconeogenesis
89
What is a significant downside to Rosiglitazone and Pioglitazone?
Thiazolidinediones may cause significant weight gain.
90

Endocrine II - Exam 2 (16 decks)

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