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Med 411 > Week 11 Diabetes > Flashcards

Week 11 Diabetes Flashcards

1
Q

What are normal blood glucose levels?

A

80-90mg/100ml
4-6 mmol.

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2
Q

What is the major endocrine organ responsible for glucose homeostasis?

A

Pancreas (Islets of Langerhans)

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3
Q

What two hormones does the pancreas produce and what is their function?

A

Insulin: promotes glucose uptake form the blood and storage in tissues.
Glucagon: promotes glucose metabolism from tissues to increase blood glucose levels.

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4
Q

What are the clinical manifestations of hypoglycemia?

A

Early:
Palpitations
Tachycardia
Diaphoresis
Anxiety
Weakness, hunger, nausea

Prolonged:
Hypothermia
Confusion, hallucinations, seizures
Coma

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5
Q

What are the clinical manifestations of hyperglycemia?

A

Early:
Polydipsia
Polyuria
Altered vision
Weight loss, mild dehydration

Prolonged:
Cardiac arrythmias
Coma

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6
Q

How much of the pancreas is exocrine?/endocrine?

A

Exocrine: 97-99 by weight%
Endocrine: 1-3 by weight%

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7
Q

What are the Islet endocrine cell types?

A

a-cells (15-20%): secrete glucagon.
B-cell (65-80%): secrete insulin and Islet Amyloid PolyPeptide (IAPP/amylin)
d-cell (3-10%): secrete somatostatin
PP cell (3-5%): secrete pancreatic polypeptide
The amounts of each cell type varies from person to person.

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8
Q

What is the function of IAPP/amylin?

A

Decreases gastric emptying, suppresses glucagon secretion, stimulates satiety center.
Controls blood gluces in an insulin sparing fashion.

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9
Q

What is the function of pancreatic polypeptide (PP)?

A

Delays gastric emptying and reduces acute food intake.
Reduces appetite and food intake.

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10
Q

Discuss Islet blood flow

A

Rich vascular supply to Islets.
B, a, and d cells are aligned along blood vessels.
This allows communication for constant blood glucose regulation. “Very good neighbourhood to be in”

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11
Q

Discuss Islet innervation

A

Richly innervated by ANS.
PNS: Vagus nerve (CNX), Ach stimulates insulin secretion.

SNS: Post-ganglionic fibers originate in celiac ganglion. Norepi inhibits insulin secretion. Epi also plays a part.

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12
Q

Discuss proinsulin synthesis

A

A&B chains and a C peptide
Synthesized in the RER, transits through GA, packaged into secretory vesicles and can be stored in granules for hours or days.
In the mature secretory granule insulin forms a dense crystal with zinc in center, C-peptide in granule halo.
Glucose stimulates proinsulin synthesis.

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13
Q

Discuss proinsulin processing

A

Processed in granules by prohormone convertase enzymes PC1/3 and PC2.
Cleavage by PC1/3 and PC2 followed by removal of basic residues by carboxypeptidase E.
This results in equimolar amounts of Insulin and C-peptide.
C-peptide has no established biological action and is excreted in urine. Can be used to assess a person’s insulin secretory capability.
Proinsulin cleavage is efficient, only 2-5% of total insulin is secreted as proinsulin in normal folks.

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14
Q

What is the major stimulus for insulin secretion?

A

Glucose.
GLUCOSE-DEPENDENT: protects against inappropriate secretion of insulin.

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15
Q

Discuss neural regulation of insulin secretion

A

PNS: Vagus nerve, Ach: Simulates islets
SNS: Norepi/epi: Inhibit islets
GLUCOSE-DEPENDENT

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16
Q

Discuss hormonal regulation of insulin secretion

A

STIMULATORY HORMONES:
Incretins (GIP, GLP-1) enhance glucose stimulated insulin secretion.
Released in intestines after a meal.
GLP-1 suppresses glucagon release, delays gastric emptying, inhibits food intake

INHIBITORY HORMONES:
Somatostatin from gut inhibits adenylyl cyclase and PKA: inhibits both insulin and glucagon secretion.

GLUCOSE-DEPENDENT

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17
Q

What other nutrients play a stimulatory role other than glucose?

A

Arg, Lys: potentiate the GLUCOSE stimulus for insulin secretion.
GLUCOSE-DEPENDENT

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18
Q

List the stimulatory and inhibitory mechanisms of insulin secretion.

A

STIMULATORY:
GIP, GLP-1 (incretins)
Glucagon - yes glucagon (thats all you need to know right now)
Ach (PNS CN X)
Glucose
Arg, Lys
Free fatty acid exposure

INHIBITORY:
Somatostatin (Gut and d-cells)
Norepi/epi (SNS post ganglionic fibers from celiac ganglion)

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19
Q

What does prolonged exposure to glucose or free fatty acids lead to?

A

Glucotoxicity and lipotoxicity
Apoptosis of B-cells

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20
Q

Discuss the simplified mechanism of glucose-induced insulin secretion

A
  1. Glucose enters B-cell via GLUT-2 transporter.
  2. Glucokinase phosphorylates Glucose to G6P.
  3. Glycolysis produces ATP.
  4. ATP sensitive K channels (with sulfonylurea receptors) close.
  5. B-cell depolarizes.
  6. Voltage gated Ca channels open and Ca enters cell.
  7. Exocytosis of insulin secretory granules.
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21
Q

What is the rate limiting step of glucose induced insulin secretion?

A

Glucokinase phosporylation.
Considered the GLUCOSE SENSOR of the B-cell.

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22
Q

What is the general mechanism of sulfonylurea treatment?

A

Sulfonylurea receptor is part of ATP sensitive K channels.
Binding of sulfonylureas could lead to closure of K channel and stimulate insulin secretion by a glucose-INdependent mechanism.

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23
Q

What are the major target tissues of insulin?

A

Muscle
Fat
Liver
**Promotes energy storage = Anabolic

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24
Q

What effects does insulin have on carbohydrate metabolism?

A

Overall: increased glucose storage and utilization

Myocytes & adipocytes:
Stimulates glucose uptake by upregulating GLUT4 on cell surface.
In mm glucose is used as energy or stored as glycogen.
In fat glucose is stored at G3P+FFAs = triglycerides.

Liver:
Activation of glycogen synthase = increased glucose storage.
Activation of glucokinase, phosphofructokinase and pyruvateK = increased glucose utilization.
Inhibits glycogenolysis via inactivation of liver glycogen phosphorylase.
Inhibits gluconeogenesis via inhibition of pyruvate carboxylase, PEPCK and fructose 1,6 diphsphatase.

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25
Q

What effects does insulin have on fat metabolism?

A

Overall: Increased fat storage in adipose tissue.

Increased FA and Triglyceride synthesis by stimulation of lipoprotein lipase = breaks down lipoproteins to FFAs so they can enter adipocytes.
Simulates FA synthesis from glucose.
Inhibits lipolysis in adipocytes.

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26
Q

What effects does insulin have on protein and aa metabolism?

A

Overall: Increased protein synthesis.

MM: stimulates aa uptake
LIVER and MM: increased rate of protein synthesis, inhibits protein catabolism. Inhibition of gluconeogenesis.

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27
Q

What are the chronic metabolic effects of insulin?

A

Changes the expression of many metabolic enzymes:
Increased expression of anabolic enzymes, decreased catabolic enzymes.

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28
Q

What are the effects of insulin on cell growth?

A

Stimulates cell growth and DNA synthesis (mitogen - links to cancer).

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29
Q

What type of receptor is the insulin receptor?

A

Tyrosine Kinase enzyme.

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30
Q

What is the precursor to glucagon and where is it made?

A

Proglucagon (LARGE precursor)
a-cells in pancreas
L-cells in intestine
Processing of proglucagon ends up giving Glucagon (a-cells), GLP-1 and GLP-2 (intestinal)

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31
Q

What is the major site of glucagon action?

A

Liver.
Increases liver glucose release to increase blood glucose levels.
Increased glycogenolysis (Glycogen phosphorylase)
Increase gluconeogenesis (Increase uptake of glycogenic aa’s).

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32
Q

Discuss regulation of glucagon secretion

A

STIMULATION:
Neural: PNS (CNX Ach) & SNS (epi/norepi)
Hormonal: GIP, CCK (also stimulates gallbladder contraction and pancreatic enzyme secretion, slows gastric emptying)
Nutrients: Low glucose, aa (ala, arginine)

INHIBITION:
Hormonal: GLP-1, somatostatin, insulin
Nutrients: High glucose.

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33
Q

Discuss somatostatin

A

The major form in islet cells is SS-14, but found in many tissues.
Release from d-cells is stimulated by glucose, sulfonylureas, aa’s, CCK, cAMP.
Release from d-cells is inhibited by cholinergic stimulation.
d-cells provide (-) feedback by inhibiting both insulin and glucagon. This ensures islet endocrine output is reset when blood glucose gets back to set point.
Ensures timely reduction of insulin secretion.

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34
Q

Discuss IAPP/amylin

A

Cosecreted with insulin from B-cells.
Slows gastric emptying.
Slows glucagon secretion.
Regulates blood glucose in an INSULIN SPARING fashion.

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35
Q

Discuss pancreatic polypeptide (PP)

A

Secreted postprandially.
Delays gastric emptying.
Reduces acute food intake.

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36
Q

Discuss ghrelin

A

Expressed in islet during development.
Secreted by endocrine cells in gastric fundus.
Stimulates growth hormone from pituitary (GH inhibits insulin action).
Important in appetite regulation, increases appetite.

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37
Q

What is the major clearance site for glucagon?

A

Renal capillary bed.

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38
Q

Discuss the role of glucocorticoids (cortisol) in carbohydrate metabolism.

A

Counter-regulatory to insulin action.
Important for blood glucose during fasting.
Increases liver gluconeogenesis.

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39
Q

At what mM levels do the following mechanisms take action:
1. Insulin release
2. Glucagon release
3. Epinephrin release
4. Growth hormone release
5. Cortisol release

A
  1. 4.6
  2. 3.8
  3. 3.8
  4. 3.7
  5. 3.2 (dangerous level)
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40
Q

What type of dysfunction is central to both T1D and T2D?

A

Islet dysfunction.
T1D: Beta-cell-specific AUTOIMMUNITY, involves both genes and environmment.
T2D: Diabetogenic environment (obesity/insulin resistance) - B cell stressors

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41
Q

What can be used to predict T1D in an individual?

A

Autoantibodies that are markers of immune response.

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42
Q

What type of disease is T1D classified as?

A

Autoimmune.
Associated with other autoimmune diseases.
Strong genetic association with HLA loci.
Islet cell antibodies (ICAs) to B cell granule proteins (insulin, GAD)
Specific T lymphocyte attack on B cells.

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43
Q

Disease concordance for T1D in identical twins

A

> 50% (suggests environmental component is necessary)
Polygenetic.

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44
Q

Discuss the environmental component of T1D

A

Disease SUSCEPTIBILITY is inherited, disease is not.
Environmental triggers:
*Viruses (enteroviruses-coxsackie)
Diet/nutrition (Vit D deficiency)
Stress (B cell stress, insulin resistance)

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45
Q

Diabetes Mellitus definition

A

A chronic incurable disease characterized by elevated blood glucose, resulting from defective insulin production and/or action.
***need B cell dysfunction

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46
Q

Discuss the epidemiology of T1D

A

Most common in children, but also found in adults.
Incidence: 1:400
Increasing at 3%/year
Approximately 300,000 Canadians

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47
Q

Therapeutic interventions for T1D

A

Replace B cells via stem cell or donor islet transplantation.
Replace insulin with pumps.

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48
Q

Other potential sources for islet transplant

A

Human organ donors
Xenotransplant (pigs)
Embryonic stem cells (genetic engineering for better B cells)

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48
Q

Immunotherapy in T1D prevention and recent-onset T1D

A

Has alot of promise:
Peptide antigen therapy (insulin)
Abatacept
Ustekinemab
Golimumab
Teplizumab - $200k/yr, only delays disease by 2 years.

Target different parts of immune pathway.
Carry risk.
Delay but do not prevent.

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49
Q

T2D epidemiology

A

Usually occurs in >45 years but now seen in children.
90% of all diabetes.
6.4% prevalence worldwide
12-14% prevalence US
>90% concordance in identical twins
Frequent in certain ethnic groups.
Associated with sedentary lifestyle and western diet.

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50
Q

Progression of T2D

A

Early:
Impaired glucose tolerance (IGT)
Normal fasting glucose w/abnormal
Treated w/diet and exercise.

Overt but mild:
Moderate fasting hyperglycemia (7mM)
Insulin resistance present
Insufficient insulin secretion
Treated with diet/exercise, oral agents.

Advanced:
Severe fasting hyperglycemia (>9mM)
Insulin secretion greatly impaired or absent
Often requires insulin for treatment.

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51
Q

Characteristics of insulin secretion in T2D

A

Impaired glucose-induced insulin secretion.
Impaired proinsulin processing (hyperproinsulinemia).
Inability to adapt to increasing insulin resistance.
Progressive decline in insulin secretion.

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52
Q

Causes of loss of insulin secretion in T2D

A
  1. Glucolipotoxicity: prolonged exposure to high glucose and FFAs is toxic to B cells.
  2. Pro-inflammatory cytokines: increased # of islet macrophages making pro-inflammatory cytokines.
  3. Islet amyloid deposits: toxic amyloid deposits composed of IAPP/amylin

**Includes both B cell dysfunction and death. B cell exhaustion/stress/failure.

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53
Q

Discuss insulin resistance in T2D

A

Involved genetic and/or acquired post-receptor defects in insulin action.
Associated w/obesity, *Visceral obesity. BMI:insulin resistance.
Can arise with other syndromes (polycystic ovaries) or rare gene mutations.
Associated with inflammation in adipose tissue.

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54
Q

What is the best prevention for T2D?

A

Lifestyle (58% risk reduction).

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55
Q

Genes associated with T2D

A

Most are related to B cell function
HHEX/IDE
Zinc transporter
TCF7L2
PAM
Usually confer risk of disease: disease is POLYGENIC.

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56
Q

Monogenic forms of diabetes

A

MODY Mature Onset Diabetes of the Young
Usually occurs before age 30.
Not associated with obesity.
Familial.
14 different types of genetic mutations.

Neonatal Diabetes Mellitus
Rare.
Sulfonylurea receptor mutation.

Gestational Diabetes Mellitus
Appears during pregnancy and resolves after birth.
Risk for infant: increased size, difficult birth.
>50% later develop T2D.
Pregnancy may unmask genetic impairments in B cell function.
Insulin resistance d/t protective factor that makes sure baby gets the nutrients preferentially.

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57
Q

How is diabetes classified?

A

By the pathogenic process leading to hyperglycemia.
1. T1D
2. T2D
3. GDM
4. MODY
5. Secondary diabetes: medication/drug related, exocrine pancreas related, endocrinopathy (Cushings), infection, other.

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58
Q

Etiology of T1D

A

Autoimmune or non-autoimmune-mediated destruction of B cells.

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59
Q

What lab investigations can be used to help diagnose T1D?

A

C-peptide
anti-GAD Ab
anti-ICA Ab

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60
Q

Type 1a vs Type 1b

A

Type 1a: immune-mediated B cell destruction (95%)
Type 1b: idiopathic B cell destruction (5%)

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61
Q

T2D etiology

A

Insulin resistance due to obesity, abnormal insulin receptors, adipokines, inflammation, B cell defects, and metabolic syndrome.

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62
Q

Risk factors for T2D

A

Genetic!!
Family hx
Ethnicity
Obesity
Diet
Sedentary lifestyle
Smoking

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63
Q

What lab investigations can be used to help diagnose T2D?

A

Cr/eGFR
UACR
Lipid panel
Diabetic eye exam

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64
Q

What are the 4 ways BG is monitored?

A
  1. A1c
  2. CBG: capillary blood glucose
  3. isCGM: intermittently-scanned continuous glucose monitoring
  4. trCGM: real-time continous glucose monitoring
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65
Q

List the benefits and limitations of the 4 ways of BC monitoring.

A
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66
Q

Discuss a structured educational program to facilitate behaviour change results in patients.

A

Teach patients:
How and when to perform CBG
How to record the results
Meaning of various BG levels
How behaviour and actions affect BG results

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67
Q

Discuss frequency of CBG monitoring with:
Dietary/Lifestyle or Oral medication
Basal insulin once daily
Twice daily insulin
Basal bolus insulin QID or insulin pump

A

Dietary/Lifestyle or Oral Medication:
Glucose in target - test 1-2 times/week.
Glucose not in target - before and 2 hours after a different meal each day OR 7/day for 1 day/week AND before and after exercise.

Basal insulin 1/day:
Glucose in target - test before breakfast daily.
Glucose not in target - test before breakfast daily and alternate before supper/hs daily.

Twice daily insulin:
Glucose in target - test before breakfast and before supper.
Glucose not in target - test QID acmeals and hs until in target.

Basal bolus insulin QID or insulin pump:
Glucose is stable/in target - test QID acmeals and hs
Glucose not in target - test 7 times/day.

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68
Q

What is important to remember about CGM?

A

Monitors BG in interstitium ea 1-5 minutes.
5-15 minute lag = may not helpful for hypoglycemic events.
BG should be confirmed with CBG before changing treatment.
Alarms can be programmed for highs/lows.

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69
Q

What is advantage of an ambulatory glucose profile?

A

Makes it easier to visualize glycemic patterns by taking 14 days and superimposing them over a 24 hour pattern.
Shows median, quartiles and 10/90th percentiles.

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70
Q

What glucose metric is becoming the Gold standard.

A

Time In Range (TIR)
% of values between 3.9-10.0mM/L
70% TIR equates to approx A1c of 7.0% with each 10% of TIR equating to about 0.5% change in A1c.

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71
Q

Glucose Management Indicator (GMI)

A

Glucose metric that shows approximate A1c based on avg CGM readings for 14+ days.
May differ from measured A1c because it is from 14ish days, not 8-12 weeks.

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72
Q

What questions help with interpretation of AGP graphics?

A
  1. Are there patterns of hypoglycemia?
  2. Are the readings within the target range?
  3. What is the shape of the median curve?
  4. What is the degree of variability?
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73
Q

What are shown benefits of CGM for those on basal-bolus insulin therapy?

A

Reduce A1c (~0.5%)
Increase TIR
Reduce hypoglycemic events
Improve QOL and hypoglycemic distress

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74
Q

Diabetes Canada guidelines for BG monitoring

A

A1c ea 3 months

T2D not on insulin: CBG individualized depending on meds, A1c level, and risk of hypoglycemia.

Increased testing at QID and/or overnight when A1c not in target or episodes of hypoglycemia.

T1D w/basal bolus or CSII: rtCGM

T2D w/basal-bolus and not in A1c target: rtCGM or isCGM

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75
Q

Discuss the basal/bolus concept of insulin secretion

A

Bolus: Facilitates glucose uptake after meals.
Basal: Suppresses glucose production between meals and overnight.

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76
Q

Discuss insulin pumps

A

AKA CSII Continuous Subcutaneous Insulin Infusion
Contains rapid acting analogue insulin
Delivers basal rate through the day, rates can be adjusted for different times.
Bolus released prior to meals, adjusted for carb intake and current BG.
Insertion site changed ea 2-3 days.

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77
Q

Advantages of insulin pumps

A

More precise dosing
Multiple basal rates
More reliable insulin absorption
Improved BG control and A1c w/out hypoglycemia
Flexibility in lifestyle
Stabilizes BG
Improved QOL/satisfaction

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78
Q

Disadvantages of insulin pumps

A

Mechanical failure more likely (educate patients on trouble shooting)
DKA may develop more rapidly if pump fails
Skin probs/infections
Expensive
Complex
Psychological factors/body image
Must be supervised by specialist/experienced team.

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79
Q

Indications for insulin pumps

A

Insulin treated diabetes
Need to normalize glucose
Need for flexibility
Hectic lifestyle (shift work/excercise)
Motivated, responsible, and considers safety (carries emergency supply)

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80
Q

Discuss establishing basal and bolus pump doses.

A

Start by calculating 80% of prepump total daily dose.
Of this amount 50% is basal and 50% is allocated to bolus.
Divide basal by 24 hours for hourly basal dose.
Calculate average daily carb intake and divide by total bolus amount (eg 1:10 means 1 unit insulin for ea 10 g carbs) OR 500/TDI = carb ratio

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81
Q

Discuss Insulin Sensitivity or Correction Factor

A

How much do we think 1 unit of insulin will lower BG.
100/TDD of insulin.
eg TDD = 40 U
100/40 = 2.5; 1 unit of insulin will lower BG by 2.5 mM/L

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82
Q

Closed-Loop syher stems

A

CGM connected to pump
Allows for automated insulin delivery (AID).
Still need to tell the pump when and how much you are eating.
Improve A1c and TIR more than other systems.
Free downloadable software algorithms available:
Loop, iAPS, AndroidAPS

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83
Q

Smart insulin pens

A

Reusable insulin pen that connects via bluetooth.
Records and tracks doses.
Helps calculate dose for a meal.

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84
Q

Online resources for insulin dosing.

A

Boluscalc.
mySugr
MyFitnessPal
CalorieKing

85
Q

What is the main risk factor for complications in chronic DM?

A

Hyperglycemia.
Genetics, BP, lipids, and epigenetic factors also important.

86
Q

Which cells are most predisposed to hyperglycemic change?

A

Retina
Glomerular mesangial cells
Schwann cells
They are less able to deal with intracellular hyperglycemia.

87
Q

What are the 3 classic types of microvascular complications of chronic DM?

A
  1. Diabetic nephropathy
  2. Diabetic retinopathy
  3. Diabetic neuropathy
88
Q

What is the #1 cause of end-stage renal disease (ESRD) (aka kidney failure) worldwide?

A

Diabetic nephropathy.
Often correlates with diabetic retinopathy.

89
Q

Discuss the pathophysiology of diabetic nephropathy.

A

Podocyte loss through detachment and apoptosis leads to hypertrophy, reduction in slit diaphragms, and basement membrane thickening.
Albumin leaks out of blood into glomerulus, leading to glomerluar HTN.
Increased pressure forces larger molecules into urine.
Tubular cells have to work harder leading to hypertrophy, scarring, and decreased reabsorption capacity.
Mesangial cells undergo hypertrophy and proliferation.

90
Q

What is used to assess diabetic nephropathy?

A

GFR (eGFR from creatinine measurement)
Albumin in the urine (Urine ACR will be high in diabetic nephropathy)

91
Q

What are the stages of diabetic nephropathy?

A
  1. Hyperfiltration, increased GFR
  2. Silent, normal GFR
  3. Microalbuminuria - usually the first clinically apparent sign
  4. Macroalbuminuria - overt nephropathy, larger amounts of albumin in urine
  5. ESRD (Ends stage renal disease)

**Not all patients have this typical progression
**Not all patients have albuminuria

92
Q

Discuss screening for nephropathy in DM

A

Creatinine & eGFT at least 1/year and increased frequency if abnormal.
Spot urine ACR 1/year (lots of false positives from infection, dehydration)
Start screening at most 5 years after Dx of T1D
Start screening at Dx of T2D

93
Q

Discuss management of diabetic nephropathy

A

Overarching: Control BG, HTN, lipids

Secondary prevention in order:
1. ACE inhibitor or ARB
2. SGLT2 inhibitor
3. MRA (finerenone)
4. GLP1 agonist

94
Q

What is the leading cause of blindness in developed countries and what ethnic profiles are most affected?

A

Diabetic retinopathy
White then Hispanic then Black.

95
Q

What 2 processes are associated with diabetic eye disease?

A
  1. Diabetic retinopathy; non-proliferative, proliferative
  2. Diabetic macular edema

Can be 2 separate processes.

96
Q

Discuss the pathophysiology of diabetic eye disease.

A

High BG leads to pericyte loss, basement membrane thickening, retinal blood flow change.
This leads to microaneurysm formation which leads to vascular leakage (MAKULAR EDEMA w/moderate visual loss).
Microaneurysms progress to retinal hemorrhages (w/moderate visual loss)
MILD NON-PROLIFERATIVE DIABETIC RETINOPATHY
Eventually see increased vascular endothelial growth factors which leads to vascular leakage (MAKULAR EDEMA) and neovascularization
PROLIFERATIVE DIABETIC RETINOPATHY

97
Q

Diagnosis of retinopathy

A
  1. Fundoscopy: microaneurysms, exudates, cotton wool spots, neovascularization
  2. Optical Coherence Tomography for macular edema
  3. Fluorescein Angiography to evaluate blood flow and leakage (rarely done)
98
Q

Screening of retinopathy

A

Dilated retinal exam annually.
Start at MOST 5 years post Dx of T1D
Start at Dx of T2D

99
Q

Management of diabetic retinopathy

A
  1. Anti-VEGF antibodies (intravitreal injections):
    Can be used for macular edema or severe/proliferative retinopathy.
    Ranibizumab, Bevacizumab, Aflibercept
  2. Photocoagulation (laser):
    Pantretinal for severe/proliferative retinopathy.
    Focal for edema
  3. Vitrectomy (removal of vitreous humour) rare:
    Used for non-clearing vitreous hemorrhage, persistent neovascularization, vitreoretinal traction
100
Q

What are the challenges in diagnosing diabetic neuropathy?

A

Vastly underdiagnosed in clinical practice bc the tools used for diagnosis are not perfect and a full neuro exam is time consuming.

101
Q

List the types of diabetic neuropathy

A
  1. Distal symmetric polyneuropathy (stocking-glove distribution, 40-80% of DN)
  2. Radiculopathy plexopathy (nerve root or plexus distributions, <5% of DN)
  3. Mononeuropathy (single nerve distribution, 5-30% of DN)
  4. Autonomic neuropathy **Most worrisome (Heart, Stomach, Intestines, Bladder, 5-15% of DN)
102
Q

Discuss screening for diabetic neuropathy

A

HISTORY
(+) sx: paresthesia, burning, lancinating, allodynia
(-) sx: loss of pain, temp, vibration, proprio

CLINICAL EXAMINATION
Detail foot exam annually
10g monofilament testing
128 Hz tuning fork
Strength, reflexes

103
Q

Management of diabetic neuropathy

A

Gabapentinoids (gabapentin, pregabalin)
SNRI antidepressants (duloxetine, venlafaxine)
Tricyclic antidepressants (amitriptyline, nortritypline)

Improvement of 30-50% with single agent. Can use combos but risk of side effects.

104
Q

What are the macrovascular complications of DM?

A
  1. CV disease
  2. Cerebrovascular disease
  3. Peripheral vascular disease (claudication, arterial ulcer, acute limb ischemia)
104
Q

Multifactorial complications of DM

A
  1. Diabetic foot infections and ulcers
  2. Sexual dysfunction
105
Q

Diabetes Control & Complications Trial (DCCT)

A

Intensive control vs conventional therapy over 9 years
A1c w/intensive reduced (7.2 vs 9.1 in conventional)
Nephropathy reduction
Retinopathy reduction
Macrovascular complication reduction

106
Q

Epidemiology of Diabetes Interventions & Complications (EDIC) study

A

Followed sample populations from DCCT for 20+ years after intervention (still ongoing)
A1c from both groups averages around 8%
Reduction in macrovascular complications = METABOLIC MEMORY

107
Q

UK Prospective Diabetes Study (UKPDS)

A

Intensive vs conventional in newly diagnosed T2D
Original cohort followed for 10 years with longer updates (current)
Intensive:
Decrease CV complications

108
Q

Prevention of complications in DM (acronym)

A

A: A1c </=7%
B: Blood pressure <130/80
C: Cholesterol LDL < 2mM/L
D: Drugs; ACE inhibitors, ARBs, statins, ASA, SGLT2, GLP1
E: Exercise/Eating healthy
S: Smoking cessation, Stress mngmt, Screening

109
Q

How often should DM screening tests be done?

A
110
Q

What are the main methods of T2D prevention?

A

Lifestyle modifications
Pharmacologic agents
Surgical interventions

111
Q

Diagnostic criteria for diabetes

A

Fasting glucose >= 7
2hour glucose on OGTT >=11.1
Random glucose >= 11.1
A1c >=6.5

112
Q

Diagnostic criteria for prediabetes

A

Fasting glucose 6.1-6.9
2-hour glucose on OGTT 7.8-11
A1c 6-6.4

113
Q

Recommendations for those w/prediabetes

A

Moderate weight loss
150 min/week over 5 days of physical activity
May consider metformin

114
Q

Recommendations for those at risk of T2D

A

Mediterranean diet
DASH diet
exercise
weight loss

115
Q

What are the names of the most important studies regarding diet and exercise and diabetes risk?

A

Da Qing
DPS
DPP

116
Q

What do studies show regarding diet and exercise vs risk of T2D?

A

Overall 32% reduction in risk.

117
Q

Discuss DPP

A

Diabetes Prevention Program
Basis of international risk management recommendations.
Standard lifestyle vs intensive lifestyle vs metformin
Intensive lifestyle decreased risk 58%, 27% at follow up.
Metformin decreased risk 31%, 18% at follow up.

118
Q

Principles of nutrition therapy in managing T2D risk

A

Must be individualized and involve a dietician.
No specific macros are ideal.
Reduce overall carb consumption.
Low GI carbs.
Strongest evidence for low-carb & Mediterranean diets.

119
Q

What medications are used for risk management against T2D?

A

Metformin
GLP1 agonists
SGLT2 inhibitors

120
Q

What surgical interventions are used for risk management against T2D?

A

Bariatric surgery for those with BMI >=35 when healthy interventions are inadequate

121
Q

Exercise fuel paradox

A

Protect muscle glycogen but also protect blood glucose.

122
Q

Insulin’s effect on the liver

A

Promotes glycogen synthesis/inhibits glycogenolysis.
Promotes glycolysis/inhibits gluconeogenesis.
Promotes lipid synthesis and storage.
Promotes protein synthesis.

123
Q

Insulin’s effect on muscle

A

Promotes glucose uptake.
Promotes glycogen synthesis (glycogenesis)
Promotes protein synthesis.

124
Q

Insulin’s effect on adipose tissue

A

Promotes glucose uptake.
Promotes lipid synthesis and storage.

125
Q

Exercise effects on the liver and glucose

A

Promotes glycolysis (breakdown of glucose)

126
Q

Exercise effects on muscle and glucose

A

Promotes glucose uptake

127
Q

Epinephrine effects on liver

A

Promotes glycogenolysis
Promotes gluconeogenesis

128
Q

Epinephrine effects on muscle

A

Promotes glucose uptake.
Promotes glycogenolysis.
Promotes glycolysis.

129
Q

Epinephrine effects on adipose tissue

A

Promotes lipolysis

130
Q

Epinephrine effects on the pancreas

A

Inhibits insulin secretion.
Promote glucagon secretion.

131
Q

Glucagon effects on the liver.

A

Promotes glycogenolysis.
Promotes gluconeogenesis.
Inhibits glycogen synthesis.

132
Q

Glucagon effects on adipose tissue.

A

Promotes lipolysis.

133
Q

Discuss molecular signalling in contraction-induced GLUT4 translocation.

A

Contraction causes NO to act within the cell:
Contraction causes ATP to AMP to AMPK pathway:
Contraction causes Ca release:
All result in bringing the GLUT4 storage vesicle to the cell membrane.
Can induce a 100x increase in glucose uptake (intensity and duration dependent)

134
Q

How long can the effects of exercise last on GLUT4 receptors?

A

Up to 72 hours.

135
Q

How does muscle act as an endocrine organ?

A

Contraction causes production of MYOKINES (IL6)
IL6 activates:
Muscle - increased glucose uptake and fat oxidation
Liver - increase glucose production
Adipose - increased lipolysis
Blood vessels - growth/proliferation

136
Q

What are the factors that influence muscle glucose uptake during exercise?

A

Supply - perfusion/BG concentration
Transport - GLUT abundance, glucose gradient
Metabolism - Hexokinase activity, substrate flux
Myokine IL6 - Increased mm temp and mechanical effects.

137
Q

What types of factors show the impact of activity on T2D?

A

Incidence of T2D/expression of risk
BG levels
GLUT4 volume and activity
A1c values

138
Q

What were the findings of the Finnish Diabetes Prevention study?

A

A few years of lifestyle focussed prevention gives long-term protection.
Postpones T2D in those with high risk by years.
Legacy effect on BG control.

139
Q

2 weeks of HIT training had what effect on GLUT4 transporters?

A

370% increase.

140
Q

What type of activity showed an absolute decrease of .9 in A1c

A

Combined resistance and aerobic.

141
Q

Exercise prescription for T2D

A

Frequency: 24 hr guidelines: aerobic and resistance, no more than 2 days without exercise.
Intensity: moderate-vigorous
Type: combination
Timing: AM/PM, pre/post prandial.

142
Q

What are the 3 characteristics of DKA (aka DKA triad)?

A

Hyperglycemia
Presence of ketones
Acidosis

143
Q

Epidemiology of DKA

A

T1D: 66%
T2D: 33%
4.6-8 per 1000 person years.
5000-10000 hospitalizations
.2-2.5% mortality with recurrent DKA 30%

144
Q

DKA clinical features

A

Prodrome (1-2days)
Volume depletion
Kussmaul breathing
Acetone breath
Myalgia
Normal temp/hypothermia
Abdominal pain

145
Q

Precipitating conditions for DKA

A

Acute illness
New onset diabetes
Insulin under-dosing
Meds; corticosteroids, anti-psychotics, anticonvulsants, SGLT2 inhibitors, immune checkpoint inhibitors.
Drugs

146
Q

Mechanism of DKA

A

Absolute insulin deficiency.
Loss of suppression of glucagon leading to gluconeogenesis and FFAs.
B oxidation leads to acetoacetate production.
Acetoacetate in equilibrium w/B hydroxybutyrate and acetone.

147
Q

Discuss serum K in DKA

A

Can be high or low.
However, DKA is a K depleted state so need to monitor serum K hourly because they will need it at some point.

148
Q

Mechanisms of hypokalemia in DKA

A

Osmotic diuresis (mass effect) and Hyperaldosteronism lead to kaliuresis.
Anorexia
Loss d/t vomiting or diarrhea.

149
Q

Mechanisms of hyperkalemia in DKA

A

Shift of K from intra to extra cellular space (insulin deficiency and acidosis)
Decrease K excretion in kidney d/t volume depletion.

150
Q

Normal anion Gap vs Wide or High anion gap

A

Normal 10-14
High >16

151
Q

MUDPILES

A

Methanol
Uremia
DKA
Propylene glycol
Iron/Isoniazid
Lactic acidosis
Ethanol/ethylene glycol
Salicylates/ASA/Aspirin

152
Q

GOLDMARK

A

Glycols (ethylene & propylene)
Oxoproline
L-lactate
D-lactate
Methanol
Aspiring
Renal failure
Ketoacidosis

153
Q

Management of DKA

A
  1. Volume repletion - NS 4-6L, 1/2NS if Na elevated
  2. Insulin infusion - 6-10 unit bolus, then .1 units/kg/hr except is K is >3.3
  3. K repletion
  4. Reduce plasma glucose
  5. Treat precipitating condition
  6. Avoid complications - hypokalemia, CE
    ***MONITOR
154
Q

Discuss Cerebral Edema

A

Occurs in children usually within 4-24 hours after initiation of tx for DKA.
Occurs in 1.5% of cases.
Mortality rate as high as 24%.
D/t a combination of factors: secondary to acidosis, damage to cerebral vascular endothelium which increases blood brain barrier premeability.

155
Q

S&S of Cerebral Edema in pediatric DKA

A

Mental status - somnolence, irritability
Focal neurologic deficits
Age-inappropriate incontinence
Headache
***Cushings triad - HTN, brady cardia, irregular respiration
Hypoxemia - compression of respiratory center

156
Q

Management of CE

A

EMERGENCY - NEVER WAIT TO CONFIRM
Elevate head of bed
Reduce fluid IV 33%
Mannitol, repeat if no clinical response in 30-120 minutes
3% hypertonic saline
May require intubation/mech vent to manage respiratory depression

157
Q

Define Hyperglycemic Hyperosmolar State

A

Metabolic decompensation (usually T2D) resulting from relative insulin deficiency, severe hyperglycemia, leading to hyperosmolality and volume depletion.

158
Q

What are the 3 characteristics of HHS

A

SEVERE hyperglycemia
Hyperosmolality
SEVERE volume depletion

159
Q

HHS clinical features

A

Age - often >60
Prodome - early polydipsia/polyuria, late weakness, confusion, lethargy, decreased urine output.
TAKES WEEKS TO DEVELOP
Poor fluid intake, glucose containing fluid when they do.
Volume depletion
Lethargy, stupor, coma
Hypothermia d/t decreased peripheral perfusion.

160
Q

HHS precipitating conditions

A

Acute illness
Druges - CCBs, phenytoin, thiazides, steroids

161
Q

HHS clinical presentation

A

Volume depletion
Neurological - lethargy, coma, hemianopsia, hemiparesis, seizures.
BG>33.3

162
Q

How does the pathophysiology differ in HHS vs DKA

A

DKA has an increase in counter-regulatory hormones d/t lack of insulin.
HHA has no increase in counter-regulatory hormones bc there is only a relative insulin deficiency. This means not as many ketone bodies produced.

163
Q

Calculating plasma osmolality

A

2x[Na] + [glucose] + [urea]
normal 285-295
HHS >320

164
Q

HHS management

A
  1. Volume repletion - 1/2NS 5-10L
  2. Normalize glucose
  3. K repletion
  4. Treat precipitating condition
  5. MONITOR
165
Q

Counselling a patient upon discharge after DKA/HHS

A

Must be eating and drinking well.
Glucose controlled w SC insulin
Precipitating condition must be treated.
Instructions:
Increase insulin w/ illness
Increase fluid intake w/ illness
Monitor BG frequently
Treat infections early
Contact MD if no improvement within 24 hours.

166
Q

Clinical features of hypoglycemia

A

Autonomic (epi/norepi) - perspiration, tachycardia, tremor, hunger, anxiety, increased tem, nausea.
Neuroglycopenic - Dizzy, weak, blurred vision, drowsy, confusion, seizure/coma

167
Q

Pathophysiology of hypoglycemia in T1D

A

Increased exogenous insulin leads to
Decreased BG
BUT no glucagon/epinephrine (loss of ability to counter regulate can occur 10-15 years after diagnosis)
Reduced or absent hepatic glucose output means no increase in BG.

168
Q

Risk factors for hypoglycemia

A

Age
Cognitive dysfunction
Liver/kidney dysfunction
Adrenal insufficiency
Lack of diabetes education
Alcohol consumption
Exercise
Food insecurity
Missed/late meals
Meds
Long standing diabetes

169
Q

Progressive loss of hypoglycemic symptoms

A

The more you have hypoglycemic events, the less you experience the adrenergic symptoms and have to rely on the neuro symptoms.

170
Q

Prevention of hypoglycemia

A

Identify high risk patients and re-evaluate glycemic goals.
Frequent self-monitoring.
Teach support network to identify subtle symptoms.
Use multiple small insulin doses.
Frequent meals/snacks.

171
Q

Treatment of hypoglycemia

A

Home glucagon injection kits.
Strict hypoglycemic avoidance so that the symptoms can be recognized.
Rapid-acting glucose, repeat if no change in 10-15 mintues.

172
Q

Goals of treatment for diabetes

A

Reduce risk of macrovascular complications
Reduce risk of microvascular complications
Reduce risks associated with high A1c

173
Q

Why do we focus on A1c for diabetes management?

A

It is a validated measure of glycemic status.

174
Q

A1c target management

A

Should be individualized based on:
Risk of complications
Risks of severe hypoglycemia and hypoglycemia unawareness
Age
Functional status
Life expectancy

175
Q

A1c treatment targets if low risk for hypoglycemia but high risk for microvascular complications.

A

> =6.5

176
Q

A1c treatment targets for most adults w/T1D or T2D

A

> =7

177
Q

A1c treatment targets for those with recurrent severe hypoglycemia or hypoglycemia unawareness, frail/elderly, dementia, limited life expectancy.

A

7.1-8.5

178
Q

9 classes of diabetes medications

A
  1. Biguanides
  2. Sulfonylureas
  3. SGLT2 inhibitors
  4. GLP-1 agonists
  5. DPP4 inhibitors
  6. Thizolidinediones
  7. Alpha-glucosidase inhibitors
  8. Meglitinides
  9. insulins
179
Q

Biguanide mechanism of action and give example of common medication.

A

Increases insulin mediated glucose uptake
Increases anaerobic glucose metabolism
Decreases gluconeogenesis
Decreases glycogenolysis
Decreases FA oxidation

Metformin

180
Q

Advantages of biguanides

A

Effective A1c lowering
No significant hypoglycemia
No associated weight gain

181
Q

Disadvantages of biguanides

A

GI side effects; pain, nausea, diarrhea
Metallic taste
Lactic acidosis (rare)

DN use if eGFR <30

182
Q

Sulfonylurea mechanism of action and give an example of common medication(s)

A

Close the ATP K channels in B cells. This depolarizes the cell and causes Ca mediated insulin release, independent of glucose.

Glyburide, Gliclazide

183
Q

Advantages of sulfonylureas

A

Effective A1c lowering
Inexpensive
Easy to administer

184
Q

Disadvantages if sulfonylureas

A

Risk of hypoglycemia
Weight gain
Unknown effects on the B cell over time.

DN use if eGFR <30

185
Q

SGLT2 inhibitor mechanism of action and give an example of common medication(s)

A

Blocks SGLT2 channels in the kidney, reducing glucose re-uptake and causing glucosuria

Canagliflozin, Dapagliflozin, Empagliflozin

186
Q

SGLT2 inhibitor advantages

A

Effective A1c lowering
Easy to administer
Promotes weight loss
Lower BP
Low risk of hypoglycemia
Cardio and renoprotective.

187
Q

SGLT2 inhibitor disadvantages

A

Polyuria
Volume depletion
UTI
Euglycemic DKA (rare)
Cana may increase amputation/fracture risk

DN use if eGFR <20

188
Q

GLP1 agonist mechanism of action and give example of common medication(s)

A

Increases endogenous insulin production and secretion
Increases somatostatin
Decreases glucagon secretion
Decreases appetite
Slows gastric emptying
Slows gall bladder secretions
Decreases blood pressure

Liraglutide, Dulaglutide, Semaglutide (Ozempic), Rybelsus

189
Q

GLP1 agonist advantages

A

Effective A1c lowering
Cardioprotective
Renoprotective
Significant weight loss

190
Q

GLP1 agonist disadvantages

A

Injections required
Nausea, vomiting, pancreatitis
Expensive

191
Q

DPP4 inhibitor mechanism of action and example of common medication(s)

A

Inhibits DPP4 which usually breaks down GLP-1

Linagliptin, Saxagliptin, Sitagliptin

192
Q

DPP4 advantages

A

Easy to administer
Linagliptin can be used even w/low eGFR/renal failure

193
Q

DPP4 disadvantages

A

Less effective A1c lowering
Pancreatitis, pemphigoid
Cost

194
Q

Thiazolidinediones mechanism of action and example of common medication

A

PPARgamma activator, increases transcription of genes involved in glucose and lipid metabolism.
Leads to decreased gluconeogenesis and fat content.
Increased glucose uptake in skmm
Increased glucose uptake in adipose, increase lipogenesis, increased FA uptake.

Pioglitazone

195
Q

Thiazolidinediones advantages

A

Effective A1c lowering
Easy to administer
Durable effect

196
Q

Thiazolidinediones disadvantages

A

Weight gain, edema
Worsening heart failure
Distal bone fractures
Bladder cancer
Expensive/not covered

197
Q

Alpha glucosidase inhibitor mechanism of action and name of common medication

A

Inhibits intestinal amylases and glucosidases.
Delays/decreases glucose absorption in the GI tract.

Arcarbose

198
Q

Alpha glucosidase inhibitor advantages

A

Not systematically absorbed
Targets post-prandial hyperglycemia

199
Q

Alpha glucosidase inhibitor disadvantages

A

Less effect A1c lowering
Bloating, GI pain, diarrhea, flatulence
Multiple daily dosing
Expensive

DN use if eGFR <30

200
Q

Meglitinides mechanism of action and name of common medication

A

Closes ATP K channels in B cells, depolarizing cell, leading to insulin release.
Dependent on glucose levels.

Repaglinide

201
Q

Meglitinide advantages

A

Effective A1c lowering
May be used if meals are irregular

202
Q

Meglitinide disadvantages

A

Hypoglycemia
Weight gain
Multiple daily dosing
Expensive

203
Q

Short-acting Insulins

A

Regular
Lispro
Aspart
Glulisine

204
Q

Long-acting insulins

A

NPH
Glargine
Detemir
Degludec

205
Q

Advance therapy for treatment of A1c or hyperglycemia

A

Add or substitute GLP1, SGLT2, or insulin

206
Q

Guidelines for treatment of diabetes

A

Goal - attain A1c target by 3 months
Lifestyle changes/no pharm
Metformin
Insulin +/- metformin if symptomatic or metabolic decomp.

If A1c not at target at 3 months
Start metformin
Adjust or advance therapy

Reassess A1c ea 3 months

207
Q

Advance therapy for treatment of ASCVD, CKD or HF age >60

A

Add or substitute GLP1 or SGLT2

208
Q

Discuss initiating insulin treatment

A

Fasting glucose or A1c not on target or metabolic decomp.
Start basal insulin and titrate to get to fasting glucose target.
Continue metformin.
Review/add/adjust other AHAs
Add bolus insulin.

Med 411 (4 decks)

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