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3.D Flashcards

1
Q

What is the normal exocrine and endocrine function of the pancreas?

A

exocrine: secretes digestive enzymes into the GI tract
endocrine: secretes hormones from the islet of Langerhans

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2
Q

Which hormones are released from the islets of Langerhans?

A

B cells: insulin
a cells: glucagon

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3
Q

Describe glucose and insulin homeostasis?

A

homeostasis maintains a balance of large upswings and downswings of blood sugar due to eat; not a straight line
insulin release follows a similar pattern; released in response to high BG levels

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4
Q

When is insulin released and what is its role?

A

released in response to high blood sugar
promotes uptake, utilization, and storage of glucose (lowers BG concentration)

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5
Q

When is glucagon released and what is its role?

A

released in response to low blood sugar
increases the hepatic glucose output (increases BG concentration)

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6
Q

What can stimulate insulin release?

A

elevation of blood glucose
amino acids or fatty acids
GLP-1, GIP, epinephrine, adrenergic and cholinergic stimulation, estrogen

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7
Q

During times of stress, what can antagonize insulin?

A

glucagon
cortisol
growth hormone

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8
Q

What are the insulin sensitive tissues?

A

muscle
adipose
liver
brain

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9
Q

Which organ does not require insulin to get glucose?

A

brain

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10
Q

What is the simple way to describe insulin?

A

insulin is a “key” for glucose to get into cells

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11
Q

Describe insulin release.

A
  1. person eats food and its broken down into glucose
  2. glucose enters beta cells in pancreas via GLUT2 transporter
  3. each glucose is broken down to ATP and attaches to an ATP-
    sensitive K channel and closes it
  4. causes depolarization-amount of depolarization=amount of
    Ca channels that open
  5. Ca enters and facilitates exocytosis of insulin
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12
Q

How does the pancreas know how much insulin to release?

A

proportional amount of insulin is released is determined by the amount of glucose that enters the beta cell

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13
Q

Describe insulin signal transduction.

A
  1. insulin binds to the insulin receptor
  2. cascade of protein activations and translocation of GLUT4
  3. glucose enters the cell
  4. cells converts to whatever is needed
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14
Q

Differentiate between the basal and bolus release rate.

A

basal: constant release rate, every 3-6min
bolus: at mealtime, insulin is rapidly released in response to
food

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15
Q

What are the incretin hormones?

A

GLP-1 and GIP
-secreted by GI tract at basal level or bolus
DPP-4
-inactivates the above

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16
Q

True or false: there is a strong correlation between obesity and insulin resistance

A

true

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17
Q

What causes insulin resistance?

A

excess nutrition leads to storage of triglycerides in adipose tissue, peripherally then viscerally which causes:
-enhanced sensitivity to counter-regulatory hormones by
expressing more B receptors and activates more cortisol
-lowers insulin receptor affinity

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18
Q

What is diabetes mellitus?

A

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

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19
Q

Differentiate between type 1 and type 2 diabetes.

A

type 1: due to defective insulin secretion (auto-immune)
type 2: due to insulin resistance, eventually leading to
defective insulin secretion

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20
Q

What is diabetes insipidus?

A

more of a kidney disease, deficiency of vasopressin
unrelated to pancreas
only thing in common is polyuria

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21
Q

What are the complications of diabetes?

A

macrovascular: dyslipidemia, hypertension, CAD, stroke, ED
microvascular: nephropathy, retinopathy, peripheral
neuropathy

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22
Q

What causes type 1 diabetes?

A

autoimmune destruction of pancreatic beta cells, causing lack of insulin secretion

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23
Q

What are the signs and symptoms of type 1 diabetes?

A

hyperglycemia
fatigue
polyphagia
weight loss
polyuria
glucosuria
polydipsia

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24
Q

What happens with severe, undiagnosed type 1 diabetes?

A

diabetic ketoacidosis
-ketones for energy–>keto acids–>coma–>death

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25
What are the distinguishing side effects of diabetic ketoacidosis?
deep and laboured breathing breath smells like acetone
26
What is the treatment of type 1 diabetes?
biological insulin
27
True or false: type 2 has more distinct phases of progression and is slower than the progression of type 1
true
28
What causes type 2 diabetes?
environment (overeating, sedentary lifestyle, aging) genetic predisposition
29
What are the signs and symptoms of type 2 diabetes?
*depends on stage of progression* can be asymptomatic at diagnosis any type 1 signs overweight or obese (85%) may have developed complications
30
What is the treatment of type 2 diabetes?
lifestyle and healthy diet alone or in addition to oral hypoglycemic, may eventually need insulin
31
What is the goal of giving diabetics oral medications or insulin?
to mimic the normal production and release of insulin to accomplish glucose homeostasis
32
What is fasting glucose?
no caloric intake for at least 8h, used to indicate BG before a meal (pre-prandial) mmol/L snapshot in time
33
What is post-prandial glucose?
2 hours after a meal mmol/L snapshot in time
34
What is hemoglobin A1C?
an average of blood glucose control over the last 3 months % of Hb that has been glycosylated, correlates with BG levels Hb cell lives ~3 months, glycosylation is irreversible
35
What are the targets of diabetics?
A1C (%): <7.0 (<6.5 or 7.1-8.5 for some ppl) FPG: 4.0-7.0 PPG: 5.0-10.0, 5.0-8.0 if A1C not met
36
What is considered to be hyperglycemia? What does it look like?
FPG>7.0mmol/L polyuria, polydipsia, polyphagia, glucosuria, fatigue
37
What is considered to be hypoglycemia? What does it look like?
FPG<4.0mmol/L mild-->moderate-->severe-->coma/death autonomic-->neurological changes
38
What are the characteristics that vary with insulin treatment?
onset of action time to peak glycemic effect duration of action appearance
39
What is the faster acting bolus insulin?
insulin aspart (Fiasp)
40
What are the rapid acting bolus insulin analogues?
insulin lispro (Humalog) insulin aspart (NovoRapid) insulin glulisine (Apidra)
41
What are the rapid acting insulins?
insulin, regular U100 (Humulin R & Novolin Toronto) -bolus insulin regular U500 (bolus and basal)
42
What is the intermediate acting basal insulin?
insulin, NPH (Humulin N & Novolin NPH)
43
What are the long acting basal insulin analogues?
insulin detemir (Levemir) insulin glargine (Lantus) insulin degludec (Tresiba)
44
Which insulin has a cloudy appearance?
insulin, NPH (Humulin N & Novolin NPH)
45
Describe how insulin detemir works.
after injection, self-associates and binds to albumin-->slowly released from subcutaneous tissue into blood stream, at a slow, predictable rate
46
Describe how insulin degludec works.
forms multihexamers following SC injection, leading to a depot-->delayed absorption from SC tissue and also binding to albumin leads to longer time profile
47
Describe how insulin glargine works.
an acidic product in the vial, once injected SC the acidic solution is neutralized, and forms micro-precipitates-->slow dissolve at a slow, predictable rate
48
What are the routes of administration for insulin?
subcutaneously-layer of fat (most common) with an insulin pump (continuous subcutaneous) IV (R or Toronto, emergency only)
49
True or false: all insulins can be mixed
false
50
What are the devices for insulin administration?
insulin pens (user-friendly, simple) insulin pumps (intense management needed)
51
What is lipodystrophy?
abnormal distribution of fat (atrophy and hypertrophy) repeated injections of insulin into the same tissue over and over causes the tissue to adapt
52
What can worsen lipodystrophy?
frequent needle re-use
53
What is the suggestion for insulin injection sites?
rotate injections systematically within the same anatomical region (abdomen, thigh, under arm, love handles) -rate of absorption remain similar -reduces chances of lipodystrophy
54
Rank the ordering of injection sites in speed/consistency of absorption.
abdomen>arm>thigh>buttock
55
What can increase insulin absorption?
exercise heat massage injection into muscle
56
What can decrease insulin absorption?
cold lipohypertrophy decreased blood flow
57
How should insulin be stored?
stored unopened insulin in the fridge in-use vials & cartridges may be stored at room temp for 28d -Humalog (lispro) states not to re-refrigerate pens when in use -insulin detemir (Levemir) stable for 42d not refrigerated avoid freezing or direct sunlight
58
What are the classes of oral hypoglycaemic?
metformin sulfonylureas repaglinide thiazolidinediones acarbose DPP4 inhibitors GLP-1 agonists SGLT-2 inhibitors
59
What is the MOA of metformin?
increases AMPK activity -enhances insulin sensitivity to tissue -decreases hepatic gluconeogenesis -decreases intestinal glucose absorption
60
What is often the first drug prescribed in type 2 diabetes?
metformin
61
What are the main adverse effects of metformin?
nausea (take with food) diarrhea (transient-titrate slowly) lactic acidosis (rare)
62
What are the sulfonylureas?
glyburide gliclazide glimepiride
63
What is the MOA of sulfonylureas?
enhance insulin secretion from the pancreas -inhibits ATP-sensitive K channels to stimulate insulin secretion from the functioning B cells
64
What are the main adverse effects of sulfonylureas?
hypoglycemia (main one) -avoid in elders weight gain nausea rash hepatotoxicity (dont take with alcohol)
65
What is the MOA of repaglinide?
same mechanism as sulfonylureas but works much quicker and less effectively
66
What is required when taking repaglinide?
repaglinide requires the presence of glucose to exert its action must be taken before (30mins) OR with a meal "skip a meal, skip a dose; add a meal, add a dose"
67
What is the main adverse effect of repaglinide?
hypoglycemia (less than sulfonylureas) weight gain
68
What are the thiazolinediones?
rosiglitazone pioglitazone
69
What is the MOA of thiazolinediones?
enhance insulin sensitivity at target tissues like metformin -agonist for PPARy -PPARy: receptor that forces insulin receptor to the surface, combating insulin resistance
70
What are the main adverse effects of thiazolinediones?
edema and fluid retention headache weight gain increased risk of fractures increased risk of CV events
71
What is the MOA of acarbose?
inhibits a-glucosidase, which reduces the rate of absorption of carbohydrates from the GI tract
72
What is required when taking acarbose?
taken with meals
73
What are the main adverse effects of acarbose?
abdominal cramping diarrhea flatulence malabsorption of vits/mins, other drugs
74
What do we give someone who is hypoglycemic while taking acarbose?
glucose tabs milk honey
75
What are the DPP-4 inhibitors?
linagliptin alogliptin sitigliptin saxagliptin
76
What is the MOA of DPP-4 inhibitors?
inhibit the breakdown of incretins, increasing and prolonging their activity instructing pancreas to release more insulin for longer
77
What are the adverse effects of DPP-4 inhibitors?
hypoglycemia cough nasopharyngitis rash hypersensitivity muscle aches/joint pain pancreatitis
78
What are the GLP-1 agonists?
exenatide liraglutide dulaglutide semaglutide lixisenatide
79
What is the MOA of GLP-1 agonists?
mimic endogenous GLP-1 results in increased satiety, reduced gastric emptying, greater insulin secretion
80
What are the SGLT-2 inhibitors?
dapaglifozin empaglifozin canaglifozin ertugliflozin
81
What is the MOA of SGLT-2 inhibitors?
increases excretion of glucose in the kidney by preventing glucose reabsorption, therefore reducing blood glucose levels
82
What are the main adverse effects of SGLT-2 inhibitors?
diuretic effect hypotension polydipsia increased rate of UTIs MUST HAVE ADEQUATE KIDNEY FUNCTION

PHAR121 (17 decks)

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