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Clin 3 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Explain the glucose metabolism. (Where glucose is produced and where glucose is used + hormones involved)

A

Produced in liver & kidneys -> with glucagon

Used in muscle and adipocytes + brain, retina, kidneys, erythrocytes, leukocytes -> with insulin

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2
Q

What are the processes involved with the regulation of blood glucose related to glucagon and insulin separately ?

A

Glucagon:

  • glycogenolysis
  • gluconeogenesis

Insulin:

  • glycogenesis
  • glycolysis
  • glucose oxisation
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3
Q

Describe the glucose flow during the fasting and postprandial states.

A

Fasting:
Glucose is produced 90% from liver and 10% from kidneys. Goes to circulation. 64% brain, 18% muscle/fat, 10% kidneys, 8% liver

Postprandial:
100% of the glucose comes from the gut. 33% brain, 33% muscle/fat, 34% liver

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4
Q

Describe the difference between a healthy and diabetic person in terms of glucose, insulin and glucagon levels in the blood after a meal.

A

Healthy:
Glucose goes up. A lot of insulin is secreted to store the glucose. Low glucagon.

Diabetic:
Glucose is very high. Not so much insulin is secreted, which allows for glucose to remain high. Glucagon is very elevated, which increases the glucose levels.

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5
Q

What are the actions of insulin on glucose metabolism?

A

ANABOLIC:

  • glucose transport
  • glycolysis (energy)
  • glycogenesis

ANTI-CATABOLIC:

  • gluconeogenesis
  • glycogenolysis
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6
Q

What are the actions of insulin on lipid metabolism?

A

ANABOLIC:

  • lipogenesis (make TG and FFA)
  • LPL activity

ANTI-CATABOLIC:

  • lipolysis
  • LPL
  • ketogenesis
  • FA oxidation
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7
Q

What are the actions of insulin on protein/electrolytes metabolism?

A

ANABOLIC:

  • makes proteins (stimulates uptake of aa by muscles)
  • promotes electrolyte balance (more K enters cells)

ANTI-CATABOLIC:
- protein catabolism

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8
Q

Describe the insulin production/release.

A

glucose enters beta cells through GLUT2. calcium also enters the cells. Insulin is then produced, and released through exocytosis.
Insulin is released along with C-peptide

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9
Q

What is first and second phase insulin?

A

FIRST PHASE insulin is the initial burst of insulin (5-10min after beta cells are exposed to rapid increase in glucose)
Decreased hepatic glucose production and lipolysis

SECOND PHASE is when insulin secretion rises more gradually and is directly related to the degree and duration of the stimulus

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10
Q

What are the main 4 symptoms of diabetes and what are the 3 tests that can be done?

A

Increased:

  • thirst (polydipsia)
  • hunger (polyphagia)
  • urination (polyuria)
  • weight loss (T1) or obesity (T2)

TESTS:

  • OGTT
  • Glucosuria
  • Hyperglycemia
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11
Q

Describe the catabolic state of diabetes (what happens in the absence of insulin).

A 
gluconeogenesis
muscle/fat use ketones and FA
glycolytic enzyme activity lowers
hypoglycemia
liver increases VLDL production
adipose tissue release FFA
hexokinase increases
cardiac and skeletal muscles rely on ketone bodies
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12
Q

What is the importance of incretins? What are the 2 main incretins?

A

when glucose is given through IV, there is no release of insulin. When glucose is given orally, glucose stimulates the release of incretins, which stimulates the release of insulin

Glucose -> incretins -> insulin

Main: GLP-1 and GIP

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13
Q

What factors determine the plasma concentration of glucose?

A 
carb composition of food
rate of gastric emptying
rate of glucose absorption
concurrent state of glucose disposal
acute illness
emotional stress
alcohol intake
diurnal change in insulin sensitivity
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14
Q

What is the main clinical presentation of T1DM?

A

DKA
Complication of severe insulin deficiency leading to hyperglycemia, causing glucosuria, dehydration and ketogenesis to the eventual acidosis

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15
Q

What are the symptoms of T1DM?

A
  • vomiting
  • abdominal pain
  • hyperventilation
  • lethargy
  • confusion
  • dehydration
  • severe fatigue
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16
Q

What are the 2 factors that affect b-cells in T2DM?

A

decreased mass AND function

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17
Q

What are the 5 pathogenic features of hyperglycemia?

A
  • decreased incretin effect
  • increased hepatic glucose production
  • decreased glucose uptake (increased lipolysis)
  • increased glucose reabsorption
  • increased glucagon secretion
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18
Q

Who secretes the most insulin?

A

Obese, non-diabetic, insulin resistant

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19
Q

What are the 3 things that happen in insulin resistance (decreased…)?

A

Decreased:

  • ability of insulin to suppress endogenous glucose production in the liver
  • uptake of glucose in tissues with insulin-dependent glucose transporters (skeletal muscles)
  • inhibition of lipolysis
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20
Q

What 4 people are insulin sensitive?

A
  • children with T1DM
  • lean ppl with T1DM
  • conditioned athletes
  • newly diagnosed with T1DM
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21
Q

What are the 4 factors used to diagnose diabetes?

A

FPG: >7mmol/L
A1C: >6.5%
2hPG: >11.1mmol/L
Random PG: >11.1mmol/L

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22
Q

What is the macronutrient distribution for a diabetic person?

A

CHO: 45-60%
Pro: 15-20%
Fat: 20-35%

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23
Q

What is covered in the basic carb counting?

A
  • introduces the concept

- encourages inclusion of consistent amounts of CHO at meals and snacks

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24
Q

What is covered in the advanced carb counting (on inuslin)?

A
  • teaches patients who use MDI or insulin pump how to match short acting insulin to CHO using ratios
  • match the amount of insulin to take with the amount of carb you want to eat
  • still need to control intake in order to prevent weight gain
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25
Q

Where are the hidden carbs?

A
  • breading on meat/poultry
  • meal components (ex: cornstarch)
  • pasta sauce
  • croutons in salads
  • large amount of salad dressing
  • ketchup
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26
Q

What are the 4 teaching resources in order of complexity?

A
  • just the basics
  • beyond the basics
  • glance at meal planning
  • meal planning quebec
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27
Q

What are the 5 LCS?

A
  • sucralose
  • saccharin
  • aspartame
  • rebaudioside A
  • acesulfame-k
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28
Q

What are the 4 proposed mechanisms for the fact that LCS are associated with weight gain?

A
  1. sweet-taste receptor mediated changes in gut hormones
  2. impaired predictive relationship between sweet taste and calories
  3. altered nutrient absorption via changing the gut microbiota
  4. change in taste preferences and dietary preferences
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29
Q

What are the 4 types of appropriate snacking?

A
  1. bedtime snack should include protein
  2. have a snack if gap of 5-6h between meals
  3. ppl that have low BG at a certain time of the day should have a snack at that time
  4. snack if starting a new exercise program or exercise longer than usual
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30
Q

What is A1C?

A

A series of stable minor hbg components formed slowly nonenzymatically from hgb and glucose
The rate of formation if proportional to the concentration of glucose
It provides a glycemic history of the previous 2-3months
It can also predict the risks of complications

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31
Q

What are 2 other types of glycated proteins?

A

GSA and GSP

They are used when A1C cannot be measured or during hemolytic anemia

32
Q

What are 3 ways to measure plasma glucose?

A
  1. blood glucose meter
  2. continuous glucose monitor
  3. flash glucose monitor
33
Q

What are the 6 classes of medications? Name one name for each and explain the mechanism.

A
  1. Biguanides
    Metformin - decreased hepatic glucose production
  2. alpha-glucosidase inhibitors
    acarbose - delay intestinal glucose absorption
  3. insulin secretagogues (meglitinide & sylfonylurea)
    repaglinide glyburide - stimulates insulin secretion
  4. Increatin mimetics (DPP-4 inhibitors & GLP-1 RA)
    sitagliptin exenatide - stimulates insulin and reduce glucagon secretion and delays gastric emptying
  5. TZDs
    pioglitazone - increase insulin sensitivity in peripheral tissues and liver
  6. SGLT2 inhibitors
    empaglifozin - decrease glucose reabsortion
34
Q 
Name which drugs act on the following organs:
pancreas
liver
GUT/GIT
Kidneys
muscles/fat?
A
  1. insulin secretagogues + incretin mimetics
  2. biguanides + TZDs
  3. Alpha-glucosidase inhibitors
  4. SGLT2 inhibitor
  5. TZDs
35
Q

What are the benefits and risks of biguanides?

A 
BENEFITS:
1-1.5% REDUCTION IN A1C
No weight gain
No hypoglycemia
improved CV outcomes in overweight people
RISKS:
GI side effects
Decreased kidney function
Lactic acidosis
B12 deficiency
36
Q

What are the benefits and risks of insulin secreatgogues?

A 
BENEFITS:
0.7-0.8% reduction in A1C
Rapid onset of response
meglitinides: greatly reduces postprandial glucose
lowers microvascular risks
RISKS:
hypoglycemia!!!
weight gain
MI
blood sugar control is lost earlier
37
Q

What are the benefits and risks of alpha-glucosidase inhibitors?

A 
BENEFITS:
0.6% reduction in A1C
no hypo
no weight gain
in people with IGT: prevention of T2DM and decreases CV events by 49%
RISKS:
GI side effects
TID dosing
Not recommended if A1C>8.5%
Contraindication: DKA and IBD
38
Q

What are the benefits and risks of TZDs?

A

BENEFITS:
0.8% reduction in A1C
no hypo
good lipid profile

RISKS:
weight gain
could induce edema or CHF
MI
takes 6-12 weeks for full glycemic effect
bladder cancer
fractures
contraindications: serious liver dysfunction, known heart failure
39
Q

What are the benefits and risks of DPP-4 inhibitors?

A 
BENEFITS:
0.7% reduction in A1C
no hypo
no weight gain
well tolerated

RISKS:
rare cases of pancreatitis
long-term safety
cardiac insufficiency

40
Q

What are the benefits and risks of GLP-1 RA?

A 
BENEFITS:
1% reduction in A1C
no hypo
significant weight loss
lowers BP, CV events and mortality
potential for improved beta cell mass/function
RISKS:
GI side effects
rare cases of pancreatitis
cell hyperplasia
long-term safety
contraindications: history of thyroid cancer
41
Q

What are the benefits and risks of SGLT2 inhibitor?

A 
BENEFITS:
0.7% reduction in A1C
no hypo
weight loss
lowers BP, CV events and mortality
RISKS:
mycotic genital infection
hypovolemia
increases LDL
ketoacidosis
long-term safety
42
Q

What are the 2 types of acute and chronic complications of diabetes?

A

ACUTE:

  1. hypoglycemia
  2. hyperglycemia (DKA, hyperosmolar)

CHORNIC:

  1. microvascular (retinopathy, nephropathy, neuropathy)
  2. macrovascular (stroke, CVD)
43
Q

What are the neurogenic (autonomic) and neuroglycopenic symptoms of hypoglycemia?

A

Neurogenic:

  • trembling
  • palpitations
  • sweating
  • anxiety
  • hunger
  • nausea

neuroglycopenic:

  • difficulty concentrating
  • confusion
  • weakness
  • drowsiness
  • vision changes
  • difficulty speaking
  • dizziness
44
Q

What is the cut off of BG for someone to be hypo?

A

<4mmol/L if on insulin

45
Q

Describe the different severities of hypoglycemia.

A

mild:

  • autonomic symptoms
  • person is able to self-treat

moderate:

  • autonomic and neuroglycopenic symptoms
  • person is able to self-treat

severe:
- requires assistance of another person
may be unconscious
plasma glucose is <2.8mmol/L

46
Q

What are the 5 steps to adress hypoglycemia?

A
  1. recognize autonimic/neuroglycemic symptoms
  2. confirm blood glucose < 4mmol/L
  3. treat with fast sugar (simple carbs), 15g
  4. retest in 15min to ensure BG > 4mmol/L, retreat if needed
  5. eat usual snack or meal due at that time of day or a snack with 15g carbs + protein
47
Q

What is the treatment of severe hypoglycemia in an unconscious person with no IV access?

A
  1. give 1 mg of glucagon subcutaneously or intramuscularly

2. call 911

48
Q

What are the complications of hyperglycemia?

A
  • DKA
  • HHS (hyperosmolar hyperglycemic state)
    volume depletion + electrolyte deficiency + hyperosmolarity
49
Q

Who is at risk of DKA?

A 
<2yo
ethnic minorities
lower socioeconomic status
lack of private health insurance
lower parental education
lower BMI
preceding infection
adolescent girls
50
Q

DKA and HHS?

A

look it up

51
Q

What are the signs and symptoms or hyperglycemia and acidosis?

A

hyperglycemia:
symptoms: polyuria, polydipsia, weakness
signs: ECFV contraction

acidosis:

symptoms: air hunger, nausea, vomiting, abdominal pain
signs: kussmaul respiration, acetone-odoured breath

52
Q

What are urine ketones?

A

important for T1DM, GDM, previous GDM

may indicate impending or even established ketoacidosis

53
Q

When should diabetics test for ketones?

A
  • acute illness with high BG
  • stress
  • consistently high BG (>14mmol)
  • symptoms of ketoacidosis
  • pregnancy
54
Q

Where are ketones normally present?

A

in urine

55
Q

When are ketones normally found?

A

during fasting and in first morning urine of pregnant women

56
Q

What are false positives and false negatives?

A

+
several sulfhydryl drugs

-
test strips exposed to air for extended periods of time or highly acidic specimens

57
Q

Which is the preferred method to check for ketone bodies?

A

through blood test, not urine

58
Q

What is the most common cause of DKA?

A 
insulin omission
but also:
new diagnosis of diabetes
infection/sepsis
MI
thyrotoxicosis
drugs
59
Q

What percentage of reduction of A1C reduces the risk of complications?

A

1%

60
Q

What are the vision complications of diabetes?

A

retinopathy
glaucoma
cataracts

61
Q

What are 2 things associated with retinopathy?

A
  • loss of pericytes

- changes in the retinal vasculature

62
Q

When do you initiate screening for retinopathy in T1DM and T2DM?

A

T1: 5 years after diagnosis if >15yo
T2: at diagnosis

63
Q

What is neuropathy?

A

the presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after the exclusion of other causes

accelerated by smoking, lack of exercise, alcohol

64
Q

What are the 2 types of neuropathy?

A

diffuse: peripheral & autonomic
focal: eyes, face, mouth, hearing, pelvis

65
Q

What is nephropathy?

A

20-30% of diabetic
leading cause of renal failure
earliest clinical evidence is persistent microalbuminuria

66
Q

What are 4 types of macrovascular complications?

A

heart disease
hypertension
peripheral vascular disease
atherosclerosis

67
Q

Are are the mechanisms of hyperlipidemia in type 1 and type 2 diabetes?

A

T1DM: hyperTG defective removal of CM and VLDL resulting from impaired LPL activity (insulin dependent)
HDL and LDL may be normal

T2DM: hyperTG due to elevated de novo synthesis from glucose
low HDL (due to obesity)
LDL may be normal

68
Q

Who should receive statins?

A
  • clinical CVD
  • > 40yo
  • microvascular complications
  • diabetes >15y duration and >30yo
69
Q

What is the increase of 1% in A1C related to?

A

increased risk of mild cognitive impairement and dementia

70
Q

What is the hypertension threshold for diabetic patients?

A

> 130/80

71
Q

Which type of diabetes is common in people with celiac disease? What is the recommendation?

A

T1DM

A gluten free diet

72
Q

What is the dawn phenomenon?

A

an abnormal early morning increase in blood sugar between 4-8am
more common in T1DM

73
Q

What is somogyi phenomenon? what are the symptoms?

A

Also known as rebound hyperglycemia or post hypoglycemia hyperglycemia
It is a pattern of hypoglycemia’s followed by hyperglycemia

When suspected, patient should wake up between 2 and 4am to monitor blood glucose levels

symptoms: nightmares, sweating, difficulty waking up, morning headaches

74
Q

What is the checklist for diabetes in the elderly?

A 
Assess
Individualize
Avoid
Select/adjust
Give
75
Q

What are the 2 classes of meds accepted to treat obesity in diabetes?

A
  1. Gastrointestinal lipase inhibitor

2. GLP-1 receptor agonist

76
Q

What are the nutrition recommendations if someone has gastroparesis?

A

low fiber
small frequent meals
consume high calorie liquids

**avoid high protein and large-particle meals

77
Q

What are the 2 types of embryopathic meds that pregnant women should stop when pregnant?

A
  • ACEi/ARB

- statins

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