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PHAR 121 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What two roles does the pancreas have? What does each do?

A

Exocrine function = secretes digestive enzymes directly into the GI tract

Endocrine function = secretes hormones from the islets of Langerhans
Insulin – from β-cells
Glucagon – from α-cells

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2
Q

Describe glucose and insulin homeostasis. (Draw a graph representing it)

A

Homeostasis maintains a balance of large upswings and downswings of blood sugar due to eating; not a straight line

Insulin release follows a similar pattern, released in response to high BG levels

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3
Q

What is insulin’s role in glucose homeostasis?

A

Released in response to HIGH blood sugar
Promotes the uptake, utilization, and storage of glucose (glycogen) → lowers blood glucose concentration

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4
Q

What is glucagons role in glucose homeostasis?

A

Released in response to LOW blood sugar
Increases the hepatic glucose output → increases blood glucose concentration

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5
Q

What is the structure of insulin?

A
  • 51 amino acids (A, B chain connected by 2 disulfide bonds)
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6
Q

When is insulin release stimulated?

A

Elevation of blood glucose (i.e. eating)
Other circulating fuels like amino acids or fatty acids
Hormones: GLP-1, GIP, epinephrine, adrenergic and cholinergic stimulation, and estrogen

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7
Q

What antagonizes insulin?

A

In times of stress, cortisol, glucagon, and growth hormone antagonize insulin

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8
Q

Describe how insulin works?

A

The endocrine hormone that regulates blood sugar
Causes rapid uptake, storage, and use of glucose by insulin sensitive tissues
Muscle, adipose, liver, brain*
*Brain is the only organ that doesn’t need insulin to use glucose this explains hypoglycemic symptom progression later

Serum glucose goes down because it enters cells to be used
Suppresses endogenous glucose
Inhibits glucagon release

Insulin is a “key” for the glucose to get into the cells

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9
Q

What cells does glucose enter into in the pancreas? How does it do this?

A

A human eats food and it is broken down into glucose
Glucose enters the beta cells in the pancreas via GLUT2 transporters

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10
Q

How does the pancreas know how much insulin to release?

A

Each glucose molecule is broken down to ATP (i.e. energy) and it attaches to an ATP-sensitive K channel and CLOSES IT
This causes depolarization – and the amount of depolarization determines how many Ca channels will open to try to balance out the charges
Calcium enters the cell and facilitates exocytosis of the pre-made insulin

Continual process and a proportional amount of insulin is dtermined by the amount of gucose that enters the cell

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11
Q

How does insulin allow glucose uptake in cells? (Insulin signal transduction)

A

Insulin binds to the insulin receptor (a D-R interaction)
Cascade of protein activations and translocation of GLUT4 to the cell membrane
Glucose enters the cell
Cell converts to whatever the cell needs (fat, glycogen, or just energy in the form of ATP to use)

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12
Q

What is the basal release rate of insulin? (actual numbers)

A

Basal release rate of 0.5 – 1.0 unit / hour
Oscillates every 3-6 minutes

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13
Q

What is the bolus rate of release of insulin?

A

Rate of release increases when blood glucose (BG) > 5.5mmol/L (in response to eating - bolus)

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14
Q

Define basal release

A

Beta cells secrete small amounts of insulin
throughout the day.

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15
Q

Define bolus release

A

At mealtime, insulin is rapidly released in response to food.

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16
Q

What are the two incretin hormones? What are their role? What enzyme inhibits them?

A

GLP-1 and GIP: hormones secreted by the GI tract at a baseline level all day (basal) and surges with eating a meal (bolus)
Sent to the pancreas to release insulin

DPP-4 is the enzyme that inactivates them (incretin hormones)

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17
Q

How does insulin resistance occur? Explain its correlation to obesity?

A

Strong correlation between obesity and insulin resistance
Excess nutrition inevitably leads to storage of free fatty acids as triglycerides in adipose tissue – peripherally then viscerally – which causes:

Enhanced sensitivity to counter-regulatory hormones by expressing more 𝛃 receptors and activating more cortisol
Lowers insulin receptor affinity

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18
Q

Define diabetes

A

A metabolic disorder characterized by the presence of hyperglycemia due to defective insulin secretion, insulin action, or both

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19
Q

Define Type-1 Diabetes

A

Type 1 – due to defective insulin secretion
Caused by an auto-immune disease (beta-cells destroyed by immune system –> mainly in youth, but not exclusive)
Pancreas not making any insulin
Insulin declines quickly and steadily
Trigger of immune response is unknown

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20
Q

Define Type-2 Diabetes

A

Type 2 – due to insulin resistance, eventually leading to defective insulin secretion (no autoimmunity) –> High correlation btwn obesity and type 2 but not causational

  • Slower than type 1
  • Due to environmental influences (overweating, sedentary lifestyle) on a genetically susceptible individual (COMBINATION OF BOTH)
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21
Q

What are the macrovascular complications of diabetes?

A

Cardiovascular disease (dyslipidemia, hypertension, coronary artery disease, stroke, erectile dysfunction)

22
Q

What are the microvascular complications of diabetes?

A
  • Small blood vessels

Nephropathy  kidney impairment  kidney failure
Retinopathy  blindness
Peripheral neuropathy  infection  amputation

23
Q

Type 1 Diabetes Symptoms

A

Hyperglycemia – no insulin, so glucose can’t enter cells

Fatigue – cells aren’t getting energy
Polyphagia – cells are starving so they signal for hunger
Weight loss – use up stored energy instead*

Polyuria – kidney tries to help clear the excess glucose
Glucosuria – the pee has more glucose than normal
Polydipsia – we are thirsty because of peeing so much

24
Q

What can undiagnosed type-1 diabetes lead to?

A

Severe, undiagnosed Type 1 Diabetes usually presents as diabetic ketoacidosis (DKA)
The body breaks down *ketones for energy instead (because it can’t use the glucose)  produce keto acids  coma  death

25
Q

What are the signs of diabetic ketoacidosis?

A

nausea, vomiting, severe abdominal pain, thirst, excessive urine production, dry mouth, hypotension, tachycardia, deep and laboured breathing (acetone), confusion

Can monitor for ketones in urine (will ‘spill over’ into urine when high level in blood) – Ketostix®

26
Q

How is type-1 diabetes treated?

A

We give patients insulin and do our best to mimic normal pancreatic function with products we have available

27
Q

How is type-1 treated? What is it classfied as? What are the benefits of this?

A

Our insulin is made within bacterial cells (e. coli) as a biologic, which means:
Less allergies and resistance
More effective
Can be modified to have desired results on blood glucose levels

28
Q

Signs and symptoms of type-2 diabetes?

A

Entirely depends how far the disease has progressed

Can be asymptomatic at diagnosis
Possibly any Type 1 signs and symptoms
Often overweight or obese but not all (~85%)
May have already developed complications at presentation
Macro – signs of cardiovascular disease
Micro – kidney disease, retinopathy, peripheral neuropathies

29
Q

Where is the problem in Type-1? Where is the problem in Type-2?

A

Type-1 –> Pancreas –> Insulin sensitive tissues not affected
Type 2 –> Begins at the insulin sensitive tissues (pancreas may die out eventually)

30
Q

How is type-2 diabetes treated?

A
  • Lifestyle and healthy diet –> can effectively delay progression
  • Oral hypoglycemic (or antihyperglycemic) drugs
  • Patients may eventually need insulin
31
Q

What is the goal of treatment for both type-1 and type-2?

A

By giving patients insulin or oral medications, we attempt to mimic the normal production and release of insulin by the pancreas as much as possible to accomplish glucose homeostasis

In order to do this, we need to recognize the signs and symptoms of both hyperglycemia and hypoglycemia
Hypoglycemia is very dangerous as well – we need a balance

32
Q

How can we measure blood glucose>

A

Fasting
Post-prandial
Hemoglobin A1C

33
Q

Fasting Glucose Measurement

A

Fasting (FPG) (mmol/L)= technically no caloric intake for at least 8h

This term is sometimes used to indicate a BG reading right before a meal (pre-prandial)

  • The lowest reading, only a snapshot in time
34
Q

Post-Prandial Glucose Monitoring

A

Post-Prandial (PPG) (mmol/L) = 2 hours after a meal

In someone without diabetes, the glucose has entered the cells by then

  • Just a snapshot –> No info about past or present
35
Q

Hemoglobin A1C Glucose Measurement

A

Hemoglobin A1C (%) = measures an average of blood glucose control over the last 3 months

Measures the % of hemoglobin that has been glycosylated, which is correlated with blood glucose levels

A hemoglobin cell lives ~3 months, and glycosylation is irreversible (i.e. it does not exist in an equilibrium)

  • Not a snapshot –> gives us a look back over the last 3 months
  • Does not tell us how high or how low
36
Q

What is the A1C target for most patients?

A
  • Less than or equal to 7%

A1C –> 6.5% for some patients
A1C 7.1 – 8.5% for some patients

37
Q

When would hyperglycemia occur? What does it look like? What is the numerical value of hyperglycemia?

A

HYPERglycemia would occur if a patient with diabetes did not have enough insulin

It looks like:
Polyuria = peeing
Polydipsia = thirsty
Polyphagia = hungry
Glucosuria = glucose in urine
Fatigue = very tired

FPG > 7.0mmol/L

38
Q

What is hypoglycemia and what doe sit look like?

A

HYPOglycemia would occur if a patient with diabetes had too much insulin, improper timing of insulin, or skipped a meal

FPG < 4mmol/L

It looks like:
Mild –> moderate –> severe symptoms –> coma/death
Autonomic –> neurological changes (periphery –> CNS)

Autonomic –> trembling, sweating, nauseau, tingling
Neuroglycopenic –> Drunk –> Confusion, weakness, diffucluty speaking concentrating, drowsiness
Recurrent episodes of hypoglycemia can impair their ability to sense future episodes – elderly major concern

39
Q

How do insulin preparations vary?

A

Insulin preparations vary by:
Onset of action
Time to peak glycemic effect
Duration of action
Appearance

40
Q

How can insulin be given?

A

Subcutaneously (most common) – layer of fat
Must rotate sites to prevent localized fat deposits (lipodystrophy)
With an insulin pump (continuous subcutaneous)
IV - only regular (R or Toronto) emergencies

41
Q

Lipodystrophy

A

Abnormal distribution of fat (both atrophy and hypertrophy can present H>A)
Repeated injections of insulin into the same tissue over and over again causes the tissue to adapt
Glucose enters cells here at a higher rate due to proximity
Worsened by frequent needle re-use

42
Q

Where should insulin be injected?

A

Rotate injections systematically within the same anatomical region

Rates of absorption remain similar
Reduces chances of lipodystrophy effects

Underarm, around belly button, thigh, love handles

43
Q

What are the classes of hypoglycemics to treat type-2 diabetes?

A

Metformin
Sulfonylureas (Insulin secretagogues)
Repaglinide (Insulin secretagoue)
Thiazolidinediones
Acarbose
Dipeptidyl Dipeptidase 4 (DPP4) inhibitors
Glucagon-like peptide 1 (GLP-1) agonists
SGLT-2 Inhibitors

44
Q

Metformin

A

Mechanism is to increase activity of enzyme AMPK that regulates multiple metabolic processes
Enhances tissue sensitivity to insulin –> reducing insulin resistance
Decreases hepatic gluconeogenesis (amount of glucose the liver us making)
Decreases intestinal glucose absorption

45
Q

Sulfonylureas

A

Enhance insulin secretion from the pancreas (insulin secretagogue)
How? inhibiting ATP-sensitive potassium channels to stimulate insulin secretion from functioning beta cells of the pancreas

46
Q

Repaglinide

A

Same mechanism as sulfonylureas but works much quicker and arguably less effective (insulin secretagogue)

Requires presence of glucose to exert action, therefore MUST BE TAKEN BEFORE (within 30 mins) OR WITH A MEAL
Skip a meal, skip a dose; add a meal, add a dose

47
Q

Thiazolidinediones

A

Enhance insulin sensitivity at target tissues similar to metformin
How? Agonist for PPAR𝛄 – peroxisome proliferator-activated receptor-gamma which forces the insulin receptor to the cell surface, combating insulin resistance

48
Q

Acarbose

A

Inhibits α–glucosidase, which reduces the rate of absorption of carbohydrates from the GI tract, preventing hyperglycemia – therefore TAKE WITH MEALS

49
Q

DPP4 Inhibitor

A

DPP-4 inhibitors inhibit the breakdown of incretins, which increases and prolongs their activity  instructs pancreas to release more insulin for longer

50
Q

GLP-1 Agonists

A

GLP-1 agonists mimic endogenous GLP-1

51
Q

SGLT-2 Inhibitors

A

Increases excretion of glucose in the kidney by preventing glucose reabsorption, therefore reducing blood glucose levels

52
Q

Insulin in type 2?

A

With progression of the disease, eventually β–cells are destroyed and insulin must be started

Begin with a long-acting insulin analogue (glargine or detemir), progress to addition of bolus insulin with meals over time

PHAR 121 (6 decks)

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