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Metabolism and Nutrition > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Differentiate the acute from chronic complications of diabetes

A

Acute: Hyperglycemia (DKA, HONKS), Infections, hypoglycemia
Chronic: Retinal disease, weight gain, hypertension, neuropathy, nephropathy, macrovascular disease (CHD, cerebrovascular, peripheral vascular)

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2
Q

What proportion of Canadians does diabetes mellitus affect? How much does it cost the Canadian healthcare system?

A

> 7%; >$7 billion

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3
Q

What are the diagnostic criteria for diabetes?

A

Fasting plasma glucose ≥ 7.0 mM; or
Casual plasma glucose ≥ 11.1 mM combined with classic symptoms of diabetes; or
2h PG in a 75g oral glucose tolerance test ≥ 11.1 mM; or
Hb A1C ≥ 6.5%

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4
Q

What were the threshold levels of PG established based on?

A

Retinopathy. Can be divided into nonproliferative retinopathy (early), proliferative retinopathy (late, w/vasculogenesis), macular edema, cataracts, glaucoma.

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5
Q

What are the classic signs of diabetes?

A

Polyuria, polydipsia, unexplained weight loss

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6
Q

At what plasma glucose concentration does glucose spill into urine to cause osmotic polyuria?

A

PG ≥ 10 mM

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7
Q

What’s type 1 diabetes?

A

Caused by autoimmune destruction of beta cells -> leads to inability to produce insulin

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8
Q

Understand that there is a remission period during the progression of T1DM

A

After initial symptoms, but eventually stops, and full-blown T1DM ensues.

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9
Q

What happens to fatty acid when there’s a depletion of blood glucose? What about glucose production?

A

Increase FFA mobilization; increase glucose production

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10
Q

How does insulin interact with hormone sensitive lipase? How does diabetes impact the downstream pathway of HSL?

A

Insulin inhibits. Lack of insulin during diabetes causes increase FFA mobilization from adipocytes. This creates more acetyl CoA, which is used for energy by conversion to ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone)

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11
Q

Which ketone bodies does acetyl-coa produce?

A

Acetoacetate, which becomes beta-hydroxybutyrate and acetone

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12
Q

Name consequences of ketoacidosis (metabolic acidosis). Complications?

A 
Weakness, fatigue, lethargy, malaise.
Kussmaul breathing (deep breathing).
Fruity breath.
Nausea, vomiting, abdominal pain.
Increase WBC (from catecholamines).

Complications:
hypotension, depressed sensorium, coma, cerebral edema, electrolyte abnormalities

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13
Q

Name the 5 steps of managing diabetic ketoacidosis

A 
Prevent hypokalemia by giving lytes.
Restore ECF with normal saline
Correct metabolic acidosis with IV insulin
Manage hyperosmolality (fluids)
Identify precipitating cause and treat
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14
Q

Name risk factors for insulin resistance

A 
Age
Obesity
Sedentary lifestyle
Ethnicity
Family history
PCOS
Gestational diabetes (caused by underlying abnormal production, superimposed with the effects of human placental lactogen)
Hypertension, dyslipidemia, etc.
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15
Q

What are other types of diabetes?

A

Beta-cell function defects
Genetic deficits causing insulin resistance
Diseases of the pancreas
Endocrinopathies
Drug or chemical induced
Infections (congenital rubella, cytomegalovirus, coxsackie)
Uncommon forms of immune-mediated diabetes
Other genetic syndromes
Gestational

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16
Q

In diabetic nephropathy, which part of the kidney is damaged?

A

Glomerular basement membrane.

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17
Q

How many DM patients die of macrovascular disease?

A

80%

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18
Q

What are the two main clinical trials that defined the threshold values of diabetes?

A

DCCT (Diabetes Control and Complications Trial; type I)

UKPDS (UK Prospective Diabetes Study; type II)

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19
Q

What were the results of the DCCP trial?

A

Intensive treatment was able to reduce Hb A1C to 7%, whereas conventional treatment was stuck at 9%. Relative risk reduction for retinopathy and nephropathy progression/incidence were decreased mightily.
Adverse events: more frequent hypoglycemia. Slight weight gain (10lbs)

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20
Q

What’s EDIC?

A

Epidemiology of Diabetes Interventions and Complications. A continuation of the DCCT trial. It showed that intensive therapy also decreased chances of heart attack/stroke, and kidney disease

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21
Q

What were the results of the UKPDS trial?

A

After 10 year trial, reduction in:

Diabetes related endpoints, microvascular, MI, cataract, retinopathy, albuminuria

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22
Q

How to treat type 2 diabetes? 3 steps:

A

1: Improve insulin sensitivity (diet, exercise, metformin)
2: Counter insulin deficiency (secretagogues)
3: Administer insulin therapy.

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23
Q

What do biguanides do?

A

Decrease glucose production. E.g. metformin.

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24
Q

What do thiazolidinediones do?

A

Increase glucose uptake by fat and muscle by activating PPARgamma receptors. E.g. Rosiglitazone, pioglitazone

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25
Q

What do sulfonylureas do?

A

Block potassium channels to increase insulin release from pancreatic beta cells. Secretagogue. E.g. glyburide.

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26
Q

What do meglitinides do?

A

Increase insulin secretion. Shorter-acting than sulfonylureas, so good for patients with erratic eating habits. Secretagogue. E.g. repaglinide.

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27
Q

What do incretins do?

A

Boost GLP-1 production, which helps everything. E.g. exenatide.

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28
Q

What do DPP-IV inhibitors do?

A

DPP-IV breaks down GLP-1, so inhibiting allows more GLP-1 to be around. E.g. sitagliptin.

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29
Q

What do sodium-glucose cotransporter 2 inhibitor class drugs do?

A

Increase renal clearance of glucose through urine. E.g. -liflozin suffix.

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30
Q

Name primary symptoms of hypoglycemia (adrenergic)

A

Anxiety, hunger, confusion, sweating, tremor, agitation, tachycardia

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31
Q

Name secondary symptoms of hypoglycemia (neuroglycopenic)

A

More confusion, coma, somnolence, seizure, death

32
Q

Name long-acting insulin analogues

A

Glargine, detemir, degludec

33
Q

Name rapid-acting insulin analogues

A

Aspart, lispro, glulysine

34
Q

Name 6 stimulators of insulin secretion

A

Glucose, amino acids, free fatty acids, GLP-1, glucagon, acetylcholine

35
Q

Name 3 inhibitors of insulin

A

Somatostatin, insulin, norepinephrine

36
Q

How does insulin affect FA and TAG?

A

Increases FA synthesis and TAG deposition; inhibits their breakdown by inactivating HS-lipase and perilipin

37
Q

How does insulin affect glucokinase?

A

Upregulates it

38
Q

How does insulin affect amino acid uptake?

A

Upregulates it. Increases protein synthesis as well

39
Q

Which glucose receptor does insulin affect?

A

GLUT4 (mostly in muscle and fat)

40
Q

Which receptor mechanism does insulin work on?

A

Tyrosine kinase -> insulin receptor substrate

41
Q

Which receptor mediates glucose absorption in the liver?

A

GLUT2

42
Q

Where is GLP-1 secreted?

A

Endocrine cells of small intestines

43
Q

What does GLP-1 do?

A

Stimulates insulin release and inhibits glucagon release

44
Q

Where is GLP-2 secreted?

A

Intestinal endocrine cells

45
Q

What does GLP-2 do?

A

Inhibits food intake

46
Q

Which proteins can be coded by proglucagon?

A

Glucagon, GLP-1, GLP-2

47
Q

What does amylin do?

A

Slows emptying of stomach and acid secretion, decreases food intake, decreases glucagon secretion. Can also increase serum calcium and renin activity

48
Q

How does the body respond to falling glucose?

A

ACTH and GH release leads to cortisol+epinephrine

49
Q

How does high blood tonicity affect potassium levels?

A

Can lead to hypokalemia, due to solvent drag.

50
Q

How does consumption of food affect blood glucose in diabetics?

A

Inhibition of glucagon release from alpha cells, so no liver gluconeogenesis. No insulin leads to poor glucose absorption.

51
Q

How does adding protamine to an insulin formulation affect its release?

A

Slows it down - promotes aggregation of insulin

52
Q

what are the adverse reactions to insulin?

A

hypoglycemia, local lipodystrophy, allergy and resistance, insulin presbyopia, edema

53
Q

How do biguanides work?

A

Decrease ATP production, so increase glucose uptake and decrease glucose production in liver

54
Q

How do sulfonylureas and meglitinides work?

A

Block K channel; more calcium influx to cause insulin release. Meglitinides are faster acting and shorter duration

55
Q

How do thiazolidinediones work?

A

Activate PPARgamma receptors to cause differentiation of adipose stem cells. New fat cells are active in glucose absorption and are insulin-sensitive

56
Q

How do SGLT2 inhibitors work?

A

Block Na/glucose transporter from the kidneys. Prevent glucose reabsorption, so renal excretion of glucose.

57
Q

How do glucosidase inhibitors work?

A

Inhibits the starch breakdown at the brush border, so delays glucose uptake

58
Q

Eating 1000 kcal less per day leads to how much weight loss per week?

A

1000 g loss per week

59
Q

How do vegetable omega-3 fatty acids work?

A

Decrease VLDL and TG

60
Q

What is linkage disequilibrium?

A

Measure of whether or not there is a marker for a certain disease

61
Q

What is the transmission disequilibrium test?

A

Evaluate the linkage between a genetic marker and a trait, within a family

62
Q

How does Turner’s syndrome affect growth?

A

Shorter women

63
Q

Name deformities in patients with SHOX deficiencies

A

High arch palate, cubitus valgus, Madelung deformity, genu valgum

64
Q

How to treat kids with SHOX deficiency?

A

Give growth hormone

65
Q

What is testotoxicosis?

A

Activating mutation of the LH receptor, causing early puberty (growth plates close quickly, leading to short stature)

66
Q

How many calories in 1kg of adipose tissue?

A

8000 kcal

67
Q

What are recommended dietary measures for metabolic syndrome, overweightness, and obesity?

A

Follow food guide, reduce energy intake, increase activity, modify lifestyle and behaviour, target 5-10% weightloss over 6-12 months

68
Q

What’s the definition of metabolic syndrome?

A

Waist under 102cm, HDL under 1, TG over 1.7, BP over 130/85, glucose around 6.1-6.9 in men. In women, waist over 88cm and HDL under 1.3.

69
Q

Name a few more factors of metabolic syndrome

A

hi uric acid, hi clotting, hi growth factors, low adiponectin (hi fat redistribution, decreased PPAR agonist), hi CRP

70
Q

Name the steps in cryptogenic cirrhosis

A

normal, non-alcoholic fatty liver (NAFL), non-alcoholic steatohepatitis (NASH), cryptogenic cirrhosis

71
Q

How does insulin contribute to hypertension?

A

Increases sodium reabsorption at the distal tubule

72
Q

What do nutritionists look at for their focused physical exams?

A

Skin, nails, hair, eyes, teeth, tongue

73
Q

What’s the nutritional intake goal for someone malnourished?

A

Ensure po intake is >75% of CFG requirements

74
Q

If a patient needs to be fed for <30 days on a tube, what kind is best?

A

Nasoenteric

75
Q

If a patient needs to be fed for >30 days on a tube, what kind is best?

A

Percutaneous or surgical gastrostomy/jejunostomy

Metabolism and Nutrition (7 decks)

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