Q6 - DM Flashcards

1
Q

Pancreas: AGBIADS

A

Alpha cells - glucagon
Beta cells - insulin/amylin
Delta cells - somatotropin.

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2
Q

Glucagon is a _________ hormone.
Insulin is a ________ hormone

A

Catabolic (Break down)
Anabolic (BUILD)

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3
Q

Things that stimulate glucagon release:
Inhibit glucagon release:

A

Stim: low glucose, SNS, amino acids
Inhibit: high glucose, insulin.

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4
Q

Glycogenesis - formation of glycogen from glucose
Gluconeogenesis - formation of new glucose from something other than carbs.
Glycolysis - breakdown of glucose into pyruvate
Glycogenolysis - breakdown of glycogen into glucose.

A
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5
Q

Measuring ______ can indirectly measure serum insulin synthesis.

A

C-peptide (cleaved in insulin synthesis)

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6
Q

things that stimulate insulin?
Inhibit?

A

Stim: increase in blood glucose. PSNS, amino acids, GI hormones
Inhibit: low blood glucose, high insulin, SNS, prostaglandins.

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7
Q

Insulin in the liver:
_____ glucose uptake
____ glycogenesis
______ Glycogenolysis
____ Glycolysis
_____ gluconeogensis

A

As an anabolic hormone:
Increase for storage
Increase for storage
Decrease (into glucose in storage)
Increase (into pyruvate for energy extraction)
Decrease (

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8
Q

Cells that don’t require GLUT4 transporters? How is this relavent in DM?

A

Brain, RBCs, kidneys and lense of eye. Still affected by high blood glucose levels in DM.

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9
Q

Insulin signaling involves _______ receptors on cell surfaces through the body. What things can decrease the sensitivity of this receptor?

A

Tyrosine Kinase.
Age, weight, abdominal fat

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10
Q

Obesity alters________ which _______ gluconeogenesis, insulin resistance and _______

A

Adiponectin
Increases
Inflammatory mediators

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11
Q

GLUT4 is the only glucose transporters requiring ____ to fxn. Other GLUTs (1,2,3,5 and SGLT1) are ________

A

Insulin.
Insulin-independent.

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12
Q

What does amylin do?

A

Delay gastric emptying, suppress glucagon, satiety. Prevent hyperglycemia and regulate glucose levels.

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13
Q

Pancreatic polypeptide is _____ in pts with DM. What does it do?

A

Increased.
Decreases pancreatic secretion of fluid and HCO3 which promotes gastric acid secretion and antagonizes cholecystokinin.

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14
Q

What is the incretin effect? What are incretins? How can they be impaired?

A

GIP/GLP1 - increase glucose uptake, increase insulin secretion, decrease glucose production, decrease glucagon secretion). This effect is suspected to be impaired in type II diabetes; DPP-4 enzymes degrade incretins

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15
Q

Gestational GDMA1 - diet controlled insulin issue.
GDMA2 - need intervention to control blood sugar

A
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16
Q

Symptoms of T1DM appear with loss of _______% of B cells

A

80-90

17
Q

adaptive immunity is stimulated and cause Bcell destruction and apoptosis.

A
18
Q

Insulin inhibits glucagon, which is impaired
Insulin normally stimulates fructose 2,6 bisphosphate, which stimulates glycolysis and inhibits gluconeogenesis -> this physiology is impaired
Glucagon normally inhibits 2,6 bisphosphate, which inhibits glycolysis and stimulates gluconeogenesis -> this is exacerbated

A
19
Q

Initially with T2DM, there is a period of ______ insulin secretion caused by _____. You’ll have hyperinsulinemia before all the cells tire out and then start decreasing insulin secretion

A

Hyper
Insulin resistance.

20
Q

B cells secrete insulin and _______.
_______ deficiency causes increased glucagon.
Alpha cells then become less responsive to glucose inhibition.

A

Amylin
Amylin

21
Q

Criteria for dx of metabolic syndrome looks at: (3/5)

A

Waist circumference (>40m and >35F)
Plasma triglycerides >150
Plasma HDL <40M and <50W
BP >130/>85
Fasting glucose >100 <126 A1c >5.7-6.4

22
Q

2 ketones form acetylCo-A and used for energy.

A
23
Q

Catecholamines, cortisol, glucagon, GH (insulin counterregulatory hormones) are ________ in DKA?

A

Increased

24
Q

In DKA, excessive gluconeogenesis by liver using increased fatty acids and glycerol from fat catabolism = hyperglycemia, ketone bodies, low pH, metabolic acidosis

A
25
Q

In DKA, Respiratory tries to compensate for acidosis by _______

A

Kussmaul respirations.

26
Q

transient ______ in K levels in DKA, then _____ K with treatment (due to H/K pump)

A

Increase,
Drop/Hypo

27
Q

HHNS - serum osm 320. - severe dehydration, _______K due to osmotic dieresis then insulin. AKI.

A

HYPO

28
Q

What is the polyol pathway?

A

Conversion of glucose to Sorbitol to fructose
In DM -> all the areas that are affected are not able to use sorbitol, so it accumulates as deposits.

29
Q

Body is using all of it’s oxygen to try to convert glucose so there’s end tissue hypoxia

A
30
Q

Glycation of mitochondrial respiratory chains by AGEs is a cycle that results in more reactive oxygen species, which damage microvasculature and promote accelerated atherosclerosis

A
31
Q

3 stages of Diabetic retinopathy

A

1 - nonproliferative - increased capillary permeability, dilation, micro aneurysm, hemorrhages.
2 - preproliferative. - ischemia leading to “cotton wool spot” infarcts
3 - proliferation (neovascularization, fibrous tissue, poss retinal detachment or hemorrhage into vitreous humor.

32
Q

Kidneys in DM:

A

Low RBF and filtration, tubulointerstitial fibrosis, hyperfiltration 2* to tubular reabsorption of glucose, loss of autoregulation and anemia = hypoxia.

33
Q

DM kidney issues lead to microalbuminuria (proteinuria)-> hypoproteinemia, decreased plasma oncotic pressure, = fluid overload, anasarca and HTN

A
34
Q

Uremia develops at GFR ________

A

<10

35
Q

Somatic neuropathy _____
Autonomic neuropathy _______

A

Somatic = muscle groups, Charcot arthropathy, distal neuropathies
Autonomic = delayed gastric emptying, diarrhea, bladder dysfxn, impotence, orthostatic, high HRV.