Q6 - DM Flashcards
Pancreas: AGBIADS
Alpha cells - glucagon
Beta cells - insulin/amylin
Delta cells - somatotropin.
Glucagon is a _________ hormone.
Insulin is a ________ hormone
Catabolic (Break down)
Anabolic (BUILD)
Things that stimulate glucagon release:
Inhibit glucagon release:
Stim: low glucose, SNS, amino acids
Inhibit: high glucose, insulin.
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.
Measuring ______ can indirectly measure serum insulin synthesis.
C-peptide (cleaved in insulin synthesis)
things that stimulate insulin?
Inhibit?
Stim: increase in blood glucose. PSNS, amino acids, GI hormones
Inhibit: low blood glucose, high insulin, SNS, prostaglandins.
Insulin in the liver:
_____ glucose uptake
____ glycogenesis
______ Glycogenolysis
____ Glycolysis
_____ gluconeogensis
As an anabolic hormone:
Increase for storage
Increase for storage
Decrease (into glucose in storage)
Increase (into pyruvate for energy extraction)
Decrease (
Cells that don’t require GLUT4 transporters? How is this relavent in DM?
Brain, RBCs, kidneys and lense of eye. Still affected by high blood glucose levels in DM.
Insulin signaling involves _______ receptors on cell surfaces through the body. What things can decrease the sensitivity of this receptor?
Tyrosine Kinase.
Age, weight, abdominal fat
Obesity alters________ which _______ gluconeogenesis, insulin resistance and _______
Adiponectin
Increases
Inflammatory mediators
GLUT4 is the only glucose transporters requiring ____ to fxn. Other GLUTs (1,2,3,5 and SGLT1) are ________
Insulin.
Insulin-independent.
What does amylin do?
Delay gastric emptying, suppress glucagon, satiety. Prevent hyperglycemia and regulate glucose levels.
Pancreatic polypeptide is _____ in pts with DM. What does it do?
Increased.
Decreases pancreatic secretion of fluid and HCO3 which promotes gastric acid secretion and antagonizes cholecystokinin.
What is the incretin effect? What are incretins? How can they be impaired?
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
Gestational GDMA1 - diet controlled insulin issue.
GDMA2 - need intervention to control blood sugar
Symptoms of T1DM appear with loss of _______% of B cells
80-90
adaptive immunity is stimulated and cause Bcell destruction and apoptosis.
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
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
Hyper
Insulin resistance.
B cells secrete insulin and _______.
_______ deficiency causes increased glucagon.
Alpha cells then become less responsive to glucose inhibition.
Amylin
Amylin
Criteria for dx of metabolic syndrome looks at: (3/5)
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
2 ketones form acetylCo-A and used for energy.
Catecholamines, cortisol, glucagon, GH (insulin counterregulatory hormones) are ________ in DKA?
Increased
In DKA, excessive gluconeogenesis by liver using increased fatty acids and glycerol from fat catabolism = hyperglycemia, ketone bodies, low pH, metabolic acidosis
In DKA, Respiratory tries to compensate for acidosis by _______
Kussmaul respirations.
transient ______ in K levels in DKA, then _____ K with treatment (due to H/K pump)
Increase,
Drop/Hypo
HHNS - serum osm 320. - severe dehydration, _______K due to osmotic dieresis then insulin. AKI.
HYPO
What is the polyol pathway?
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.
Body is using all of it’s oxygen to try to convert glucose so there’s end tissue hypoxia
Glycation of mitochondrial respiratory chains by AGEs is a cycle that results in more reactive oxygen species, which damage microvasculature and promote accelerated atherosclerosis
3 stages of Diabetic retinopathy
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.
Kidneys in DM:
Low RBF and filtration, tubulointerstitial fibrosis, hyperfiltration 2* to tubular reabsorption of glucose, loss of autoregulation and anemia = hypoxia.
DM kidney issues lead to microalbuminuria (proteinuria)-> hypoproteinemia, decreased plasma oncotic pressure, = fluid overload, anasarca and HTN
Uremia develops at GFR ________
<10
Somatic neuropathy _____
Autonomic neuropathy _______
Somatic = muscle groups, Charcot arthropathy, distal neuropathies
Autonomic = delayed gastric emptying, diarrhea, bladder dysfxn, impotence, orthostatic, high HRV.
