Diabetes Flashcards

(52 cards)

1
Q

What is the pancreas and what does it secrete?

A

-is an endocrine and exocrine gland
-secretes several enzymes into duodenum for digestion (exocrine)
-secretes insulin when glucose increases, glucagon when glucose decreases (endocrine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which pancreatic cells secrete insulin and glucagon?

A

-alpha = glucagon
-beta = insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the islet of Langerhans in the pancreas?

A

group of cells that secrete hormones into blood (endocrine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the pathway when blood glucose is high?

A

high blood glucose -> beta cells in the pancreas release insulin -> liver produces glycogen and cells take up glucose -> blood glucose decreases and no stimulus to release insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the pathway if the blood glucose is low?

A

low blood glucose -> alpha cells in the pancreas release glucagon -> liver breaks down glycogen -> blood glucose rises and no stimulus to release glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is glucose homeostasis?

A

-the reciprocally regulated pathways of glycolysis and gluconeogenesis
- When blood sugar rises, liver combats
-when blood sugar decreases, the liver combats
-keeps the blood sugar relatively steady (90mg/100mL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is type 1 diabetes?

A

-develops suddenly and in young people
-no functional beta cells from autoimmune destruction by T-cells
-does not secrete insulin
-causes episodic hyperglycemia
-10% of primary cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is type 2 diabetes?

A

-occurs in older people
-insulin resistance or deficiency in secretion
-insulin levels are normal or elevated because the body compensates because they are not responding
-also causes hyperglycemia
-90% of primary cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is diabetes mellitus?

A

-a group of metabolic diseases-caused by elevated glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is primary diabetes mellitus?

A

-95% of cases
-type 1 and type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is secondary diabetes mellitus?

A

-5% of cases
-as a result of a disease or medication
caused by:
-endocrine diseases
-chronic pancreatitis
-cushing’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is type 1 diabetes controlled?

A

-insulin injections
-prevents hyperglycemia and ketoacidosis
-mimic basal and reactive insulin secretions to respond to glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is type 2 diabetes controlled?

A

-diet change and exercise
-block liver glucose production
-maintain glucose levels
-prevent long-term complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What factors can lead to type 2 diabetes?

A

-genetics
-aging
-peripheral insulin resistance
-diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What organs can sense insulin?

A

-liver
-muscle
-adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do the insulin-sensing organs do when they are resistant to insulin?

A

-pancreas -> beta cell disfunction
-liver -> increased glucose output (no insulin to stop it)
-muscle -> decrease in glucose uptake
-adipose tissue -> exaggerated lipolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

List some signs/symptoms of hyperglycemia

A

-fasting glucose of >6.5 mmol/L
-polyuria (increased pee)
-polydipsia (thirst)
-glucosuria (peeing glucose)
-weight change
-fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the long-term complications of hyperglycemia?

A

-hypertension
-glaucoma
-hemorrhage
-gangrene
-infections -> amputations
-peripheral neuropathy
-pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the two groups of long-term diabetes complications?

A

-macrovascular: Complications of large and medium-sized vessels ex. stroke, coronary heart disease
-microvascular: complications of small vessels ex. retinopathy, neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What occurs with neuropathy complications?

A

loss of automatic and peripheral neural function
-injuries
-gangrene
-amputations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What occurs with retinopathy complications?

A

-failing eyesight
-blindness
-glaucoma

22
Q

what is nephropathy?

A

-chronic kidney disease
-renal disease
-microalbuminuria

23
Q

What is cerebrovascular disease?

A

-stroke
-ischaemic attacks

24
Q

What occurs with coronary heart disease?

A

-angina
-hypertension
-heart failure

25
What is insulin?
-peptide hormone -precursor -> proteolytic cleavage -> dipeptide and protein C -beta cell secretes both insulin and pro-insulin -biggest anabolic enzyme in the body
26
What are the levels of pro-insulin in a type 2 diabetic and how is it measured?
-high levels -easier to measure levels of protein C to estimate insulin levels -each have antibodies
27
What regulates insulin release?
1. glucose, AA, FA, ketones -> stim release 2. glucagon and somatostatin -> inhibit release 3. a-adrenergic stim -> inhibits release 4. b-adrenergic stim -> promotes release 5. elevated intracellular Ca -> promotes release
28
What are the difference glut receptors?
-glut 1 in brain is insulin insensitive -muscle = glut 4 = insulin sensitive -beta cell = glut 2
29
What is the pathway of insulin release?
-glut 2 takes up glucose -> respiration -> ATP produced -> ATP:ADP increases -> closes K channel -> Ca channel opens -> Ca enters -> pushes out insulin
30
What is the difference between oral and IV glucose?
-oral glucose: more insulin secretion -IV: less insulin secretion -why?: oral elicits gut hormones which augment the insulin response
31
Where is insulin catabolized?
-by kidney -by insulinase
32
What does an influx of calcium do to insulin?
-ca influx = pulsatile secretion of insulin -activation of transcription factors for insulin
33
What was the first insulin from and what is it now?
-beef or pork insulin -now usually human insulin = fewer allergies, less resistance
34
Which insulin form is rapid and which is prolonged?
-rapid: humalog -prolonged: lantus
35
How do insulin preparations vary?
-onset of action -time to peak -duration -route of admin
36
What are the different ways insulin can be administered?
-SC -Insulin pump -powder inhaler -IV
37
he will ask to name each of the types, two of each, don't need to know rest
38
What are the names of the Rapid-acting analogs? Clear or cloudy?
-Humalog (lispro) -Novorapid (aspart) -both are clear
39
What are the names of the regular/fast-acting analogs? Clear or cloudy?
-Humulin-R -Novolin GE toronto -clear
40
What are the names of the intermediate-acting analogs? Clear or cloudy?
-Humulin N & L -Novolin GE NPH -cloudy
41
What are the names of the long-acting analogs?
-Humulin-U -cloudy
42
What are the names of the extended-acting analogs?
-Lantus (glargine) -clear
43
What are the names of the premixed insulin?
-Humalog Mix25 -Novolin GE 10/90 -cloudy
44
What does the proportions on premixed insulin mean?
-ex. Novolin GE 20/80 -% rapid or fast / % intermediate
45
What makes the insulin types cloudy?
-additives -zinc analogs -makes it long-acting
46
What is the structure of human insulin?
-51AA -two chains connected by 2 disulfide bridges
47
What is the half-life of human insulin and what is it degraded by?
-5-10 min -deg. by glutathione-insulin transhydrogenase (insulinase)
48
What is the structural difference between human, bovine, and pork insulin?
-human: 51 AA -bovine: differs in 3 AAs from human -pork: differs in 1 AA from human
49
What are the effects of rapid insulin?
-incr. GLC tranport, AA, K+ into insulin sensitive cells
50
What are the effects of intermediate insulin?
-stim. protein synth -Inhibit protein breakdown -activate glycogen synthase -inhibit gluconeogenic enzymes
51
What are the effects of delayed insulin?
-incr. mRNA for lipogenic enzymes = lipogenesis
52