Diabetes Patho Flashcards
Diabetes mellitus
Metabolic dx char by inc blood sugar from relative or absolute insulin deficiency; assoc with long-term damage to multiple systems when uncontrolled
Where carbs are broken down primarily
Duodenum and proximal jejunum
Blood glucose level pattern in normal people
Increase when carbs taken in, then decrease
Liver’s role in blood sugar
Liver extracts glucose from blood, synthesizes it into glycogen and can break down glycogen in glycogenolysis if needed; peripheral fat and muscle extracts glucose if needed
Pancreas role
Produces insulin and controls blood sugar with the liver
Exocrine function of pancreas (UNIMPORTANT)
Secrete directly into ducts (not blood)
Endocrine function of pancreas and location
Cells secrete insulin directly into blood; occurs in islet of langerhans (cell island in pancreas with several types of cells)
Alpha cells
Part of islet of langerhans; secrete glucagon in response to low blood sugar
Glucagon
Stimulates liver to release stored glucose (glycogen) into blood
Beta cells
Located in islet of langerhans; make insulin which decreases glucose levels by stimulating the movement of glucose into body tissue
Insulin
Stimulates uptake, use and storage of glucose by acting like a key to open cells in the liver so they can store glucose as glycogen; ultimately decreases blood plasma concentrations of glucose (Dec blood sugar)
Hormones that increase blood glucose levels
Glucagon, epinephrine, glucocorticoids, growth hormone
What role does insulin play in lipid metabolism?
- promotes synthesis of fatty acids in the liver after the liver has been saturated with glycogen
- inhibits b/d of fat in adipose tissue—build up of TGs in fat cells;
- in healthy, ins has fat-sparing effect and drives cells to use carbs instead of fat for energy
What happens if you lack insulin?
Can’t b/d carbs well, decrease glucose use by the cells, rapid increase of blood glucose—hyperglycemia, cells use fatty acids instead
Insulin deficiency causes…
Dec glucose uptake by the cells (Hyperglycemia), Proteolysis (protein b/d), lipolysis (fat b/d)
Impaired fat metabolism
Occurs from insulin deficiency; causes increased lipolysis (fat breakdown) and decreased lipogenesis (fat synthesis) which causes free fatty acids (FFA) in the blood
Free fatty acid use
Converted to cholesterol and phospholipids in the blood; breaks down into acetyl-CoA (used by the liver to make acetic acid, which can turn into KETONE BODIES)
Short-term effect of ketone bodies
Causes KETOSIS; short-term increase in serum ketones in the blood and urine that can cause severe metabolic ACIDOSIS and COMA
Long-term effects of ketone bodies
Increased risk of atherosclerosis bc high serum lipid levels
Impaired protein metabolism
- protein not stored like normal
- protein synthesis stops and proteolysis begins
- muscle atrophy, inc amino acids circulating in blood cells and used for energy
- gluconeogenesis and glucogenolysis to compensate
Results of abnormal protein catabolism
Muscle wasting, multiple organ dysfunction, aminoacidemia, inc BUN (urea nitrogen)
Effect of insulin deficiency on fluid/electrolytes
Inc serum glucose levels—>increased plasma oncotic pressure—>fluid shifts intravascularly to balance out the high glucose levels—>intracellularly dehydration and increased peeing
Glycosuria and when does it occur?
Peeing out sugar; occurs when hyperglycemia increases beyond what the kidneys can absorb, causing increased acetones in the urine (can use a urine dipstick to test—rare now)
3 Ps of diabetes—more common in Type 1
Polyphagia (excess hunger), polydipsia (excess thirst), polyuria (excess urination)
Why does polyphagia occur?
B/d of fat and protein—cell starvation
Why does polydipsia occur?
B/c increase serum osmolality; glucose is very concentration in blood so fluid moves out of cells and into space to balance it out
Why does polyuria occur?
B/c osmotic diuresis; excreting water and electrolytes
Diabetes diagnosis
6.5% A1C (3 month average of diabetes), fasting glucose of 126 or above, OGTT 200+
Prediabetic criteria (3 tests)
- A1C 5.7-6.4%
- 100-125 fasting average
- 140-199 OGTT
Why use OGTT for pregnant?
Don’t want preg women to fast, 3 month average is too long for 9 month preg period
Type 1 DM
- Autoimmune disease with genetic and enviro factors
- slowly progressive T-cell mediated destruction of beta cells after autoantigen formation on the beta cells
- complete lack of endogenous insulin
DM1 prevalence and diagnosis age
5-10% cases in US; usually diagnosed around age 12
Clinical manifestations of type 1 diabetes
Often kids 11-13; long preclinical period of sx until almost no insulin produced; hyperglycemia and 3Ps with weight loss, recurrent infection, fatigue
DM type 2
Insulin resistance and some decreased insulin secretion; receptors lose sensitivity so insulin stops working as the key to let glucose into the cell; genetic and environmental combo
Nonmodifiable risk factors for diabetes
Family, age over 45, race, history of gestational diabetes
Modifiable risk factors for diabetes
Physical inactivity, high body fat and weight, high BP, high cholesterol
Sx of DM2
Blurry vision, tired, dry skin, reoccurring infection, prolonged infection, feel ill, loss of feeling in feet
Metabolic complications associated with DM2
Impaired insulin secretion (B-cells exhausted), peripheral insulin resistance (inc visceral fat), inc hepatic glucose production, altered production of hormones and cytokines by adipose tissue
Why does hepatic glucose production occur?
Impaired suppression of gluconeogenesis in the liver (which results from proteolysis); body thinks it is hungry so it releases more glucose when really it needs more insulin; releases glucose instead of storing it
Diabetic ketoacidosis (DKA)
Acute complication of diabetes (especially in Type 1) where you get super high sugar (400, 500, 600) and get hyperglycemia, acidosis, ketonuria; can cause coma and death
Hyperosmolar hyperglycemic syndrome (HHNS)
Acute complication of type 2 (bc you need some insulin to cause it) where you get sugar in the 600, 700, 800s and big problems with osmolality where blood becomes so concentrated that body begins to shut down (fluid shifting problems)
Hypoglycemia
Rapid onset, blood sugar below 55-60; usually related to meds (excess insulin); can be symptomatic of this with a higher blood sugar if your normal blood sugar is higher (like 150); symptoms pallor, tachy, palpitation, hunger, restless, tremor, convulse, coma
Chronic complications
Poorly controlled diabetes; insulin resistance/deficit, chronic hyperglycemia, accumulation advance glucagon end products, activate metabolic pathway that cause tissue damage; microvascular and macrovascular
Microvascular complications
Damaged capillaries, retinopathies, nephropathies, neuropathies caused by lesions whose frequency and severity are proportional to duration of disease; hypoxia and ischemia in eyes, kidneys, nerves and microangiopathy (small vessel disease with capillary membrane thickening)
Diabetic neuropathy
Most common complication of diabetes; ischemia and demyelination of nerves causing neural changes and delayed conduction; loss of pain, temperature, vibratic sensation; results in ulcer, infection, amputation
Diabetic retinopathy
Leading cause of blindness; hypoxemia, damage to retinal BVs, RBC aggregation and HTN; small vessel infarction and death
Nephropathy
- CKD and ESKD very common (50% w/ DM)
- glomerular basement thick and hard
Macrovascular complications
Damage to big vessels causing atherosclerosis and coronary artery disease, PVD, stroke, inc risk of infection; caused by oxidative stress and stuff
Diabetes and infection
- less feeling
- tissue hypoxia and impaired skin
- pathogens feed on excess glucose - less circulation of WBCs (less effective and abnormal)
- fungal, yeast, UTI, gangrene
