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Week 13 Concept Questions
Terms in this set (21)
Dysfunction in two types of tissues generally underlie many of the other types of tissue dysfunction that occur in diabetes - what are these two?
Vasculature and Peripheral Nerves
Why does the retina generate new blood vessels in diabetes and why doesn't this work?
Blood vessels within retina swell, leak and are prone to thrombotic ischemia
Angiogenesis of new blood vessels, where density of new vessels further occlude vision. New vessels are prone to microbleeds and can extend improperly into vitreous.
What are the causes of diabetic neuropathy?
-Axons tend to regress back from sensory tissues they enervate
-Intracellular and extracellular hyperglycemia
-Impaired vasculature results in hypoxia
-Ascending and descending pain modulation are affected by persistent hyperglycemia, exacerbating the degree of pain transmitted by dysfunctional first order neurons
Are peripheral nerves insulin dependent or independent?
insulin independent for glucose but insulin provides survival and neurotrophic signals that maintain healthy function of axons
How does insulin play a role in diabetic neuropathy?
Peripheral nerves are "insulin independent" for glucose but insulin provides survival and neurotrophic signals that help maintain healthy function of axons
Experimental systems show that proper insulin signaling can mitigate the effects of chronic hyperglycemia without changing the amount of glucose within the neurons
What is the reason diabetic patients experience bowel problems?
High blood sugar levels from type 1 and type 2 diabetes can lead to diabetic neuropathy, or nerve damage. Damage to the nerves controlling the digestive tract can lead to constipation, diarrhea, and incontinence.
Diabetic neuropathy as well as vascularization problems!!
What is the reason diabetic patients experience inability to concentrate?
The inability to get glucose and metabolites to the area where they are needed.
In DKA, why doesn't Acetyl CoA from FFA oxidation go into the TCA cycle?
For Acetyl-CoA to enter TCA cycle, it must condense with oxaloacetate which is generated from pyruvate during glycolysis
Without glycolysis, not enough pyruvate = shortage of oxaloacetate and Acetyl-CoA can't go into TCA cycle with oxaloacetate shortage so it is diverted into formation of ketones
For DKA, what cells are specifically implicated in generating the ketones and why would they be generating ketones when there is hyperglycemia?
Mitochondria in the liver
Hyperglycemia increases serum osmolality, thirst is induced and osmotic diuresis occurs then to control pH, there is an increase in blood K+ and lowering of intracellular K+ which causes dangerous affect on electrical potential and cell repolarization causing the liver to metabolize FFAs into ketone bodies as an alternate energy source.
Why would DKA patient exhibit tachypnea or Kussmaul respirations?
Extra ketones in your body cause acid to build up in your blood. Because of this, your respiratory system is triggered to start breathing faster.
If acidosis is present under these circumstances, what kind would it be?
What are the pancreatic contributions to digestion?
Secretin secretion by duodenum cells stimulates pancreas to release digestive cocktail
Neutralizes acid from stomach
Hydrolyze proteins (proteases)
Hydrolyze carbohydrates (amylases)
Hydrolyze fats (lipases)
What would you expect in terms of nutrient absorption if the pancreas wasn't contributing?
There would be inadequate digestion as the pancreas works to break down nutrients
What are the hepatic contributions to digestion?
Stored in gallbladder until eating
Incorporate into lipids (fats)
Assist lipase action
Facilitate fat absorption
Bacterial deactivation in colon
What would you expect in terms of nutrient absorption if the liver wasn't contributing?
Fats would not be as readily absorbed and there would be less detoxification
What is difference in tissue damaged between acute & chronic PUD?
Acute: superficial erosion that causes mucosal erosion but does not penetrate muscularis mucosae
Chronic: penetration of muscularis mucosae that damages blood vessels, often causes hemorrhages and can result in scar tissue.
What are the two major causes of PUD and describe the mechanisms for each.
H. Pylori: Prompts chronic inflammatory immune response in gastric mucosa by inducing IL 8, IL-1b which recruit macrophages, neutrophils and other immune cells
NSAIDS:By blocking prostaglandin synthesis = more H+ put into stomach and less mucosal protection causing less foveolar cell activity and more parietal cell
How does urease help H. pylori?
Secretes enzyme that produces ammonia which neutralizes stomach pH
How do NSAIDS, H. pylori & autoimmunity cause gastritis and account for the symptoms?
They all erode the mucosal barrier.
H. pylori and NSAIDS via mucus loss first
Autoimmune via inflammation first
Describe molecular mimicry as it relates to autoimmune gastritis?
H+, K+ ATPase autoreactive T‐cells also activate against H. pylori antigens meaning that H. pylori antigens are similar, or mimic, ATPase epitopes and generate an acquired response
How could you tell the difference between gastritis and reflux gastritis?
Reflux gastritis is evidenced by presence of bile and pancreatic enzymes in stomach
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