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patho exam 2
ch 38 - diabetes mellitus and its comp
| Question | Answer |
|---|---|
| pancreas consists of | cells that form clusters known as pancreatic islets, or islets of Langerhans |
| main cells are | alpha and beta cells |
| alpha cells | produce glucagon |
| beta cells | produce insulin |
| when glucose levels rise, | beta cells secrete insulin, stimulating transport of glucose across plasma membranes |
| when glucose levels decline, | alpha cells release glucagon, stimulating glucose release by liver |
| diabetes is a | chronic disease that occurs either when the pancreas does not produce enough insulin and/or when the body cannot effectively use the insulin it produces |
| number of people with diabetes is hard to estimate because | it is always increasing |
| people with diabetes in 1980 | 108 million |
| people with diabetes in 2023 | 529 million |
| people with diabetes in the US | 11.6% |
| how many adults aged 18 or older with diabetes | 38.1 million |
| hyperglycemia common Dx when | pt is diabetic |
| hyperglycemia is | high blood glucose |
| hyperglycemia has | acute symptoms |
| hyperglycemia acute symptoms | increased thirst and urination, weight loss |
| what things can lead to chronic complications | hyperglycemia, insulin resistance, insulin deficiency |
| Type 1 diabetes mellitus percent of pop | 1-5% |
| Type 1 diabetes mellitus condition | autoimmune condition, still trying to identify why |
| what causes Type 1 diabetes mellitus | pancreas unable to make insulin, destruction of pancreatic beta cells, pharmacologic insulin therapy needed for survival |
| Type 2 diabetes mellitus percent of pop | 90-95% |
| Type 2 diabetes mellitus is caused by | insulin resistance and defects in insulin secretion - slowly develop T2D |
| is Type 2 diabetes mellitus dependent on insulin secretion | no, but maybe need insulin therapy or other medications |
| monogenic DM precent of pop | 0.6-5% |
| monogenic DM types | neonatal diabetes mellitus (NDM) maturity-onset diabetes of young (MODY) |
| neonatal diabetes mellitus (NDM) | born with it |
| maturity-onset diabetes of young (MODY) | pt develops when ready to mature |
| gestation diabetes mellitus (GDM) onset is when | during pregnancy, only |
| gestation diabetes mellitus (GDM) treatment | dietary treatment, oral medications, exogenous insulin |
| what can result in fetal and maternal complications | hyperglycemia |
| type 2 diabetes Dx | glycated hemoglobin (A1C) fasting peripheral glucose (FPG) |
| glycated hemoglobin (A1C) test | gold standard test, is pricey so Dr don't frequently order |
| how does A1C test work | determining the percentage of hemoglobin in the red blood cells that is attached to glucose |
| normal A1C value | below 5.7% |
| prediabetic A1C value | 5.7% - 6.5% |
| diabetic A1C value | above 6.5% |
| fasting peripheral glucose (FPG) | measures your blood sugar after you have fasted for at least 8 hours |
| normal FPG value | below 100 mg/dL |
| prediabetic FPG value | 100 mg/dL - 126 mg/dL |
| diabetic FPG value | above 126 mg/dL |
| pt with FPG above 126... | you need to ask for further tests, for example - oral glucose tolerance test |
| oral glucose tolerance test (OGTT) tests | ability for pt to respond to insulin |
| oral glucose tolerance test (OGTT) is a | two hour test that checks your blood glucose levels before and two hours after you drink a 50-75g glucose drink |
| OGTT normal value | below 140 mg/dL |
| OGTT prediabetic value | 140 mg/dL - 200 mg/dL |
| OGTT diabetic value | above 200 mg/dL |
| prediabetes causes | an increase risk for developing Dm, primarily T2D |
| what can prevent T2D if you are prediabetic | exercise and diet or drugs that can help decrease body weight (ozempic) |
| two things associated with prediabetes | impaired fasting glucose and impaired glucose tolerance |
| impaired fasting glucose (IFG) | fasting blood glucose level or hemoglobin A1C higher than normal but not diagnostic of DM |
| impaired glucose tolerance (IGT) | blood glucose level two hours after oral glucose load (OGTT) higher than normal but not diagnostic of DM |
| when is metabolic syndrome developed | prior to T2D |
| does MS or prediabetes have more risk factors for T2D | MS |
| once B-cells are dysfunctional | it is hard to go back to being functional |
| development of T2D starts with | prediabetes: body becomes resistant to insulin, leading to slightly elevated blood sugar levels |
| development of T2D after prediabetes | insulin resistance: cells become less responsive to insulin, requiring more to lower blood sugar. |
| development of T2D after insulin resistance | Pancreas Failure: pancreas gradually loses its ability to produce enough insulin to overcome insulin resistance |
| type 2 diabetes official | High blood sugar levels persist |
| metabolic syndrome AKA | insulin resistance syndrome |
| metabolic syndrome Dx | any 3 of the 5 features!! |
| components for Dx of MS | waist circumference or BMI triglycerides HDL cholesterol blood pressure fasting glucose |
| waist circumference or BMI clinical cutoff values | >102 cm/40 in in men >88 cm/35 in in women >30Kg/m2 |
| triglycerides clinical cutoff values | >150 mg/dL |
| HDL cholesterol clinical cutoff values | <40 mg/dL in men <50 mg/dL in women |
| blood pressure clinical cutoff values | >130 mmHg systolic BP or >86 mmHg |
| fasting glucose clinical cutoff values | >100 mg/dL |
| what is the body's main source of energy | glucose |
| glucose is | obligate fuel for brain and CNS |
| what kind of supply does glucose need | continuous |
| glycolysis the break down of | carbohydrate (CHO) to form ATP |
| aerobic glycolysis | mitochondria and oxygen, forms pyruvate |
| anaerobic glycolysis | no mitochondria and no oxygen, forms lactic acid |
| homeostasis regarding insulin is disturbed when | blood glucose levels increase |
| homeostasis regarding glucagon is disturbed when | blood glucose levels decrease |
| glucose transport | facilitated transport mediated by glucose transporter (GLUT) |
| can glucose cross cell membrane | no |
| where is GLUT4 located in skeletal muscle and adipocytes | the cytosol |
| what do GLUT4 vesicles need | insulin stimuli to translocate to the membrane |
| GLUT2 is located at | cell membrane of several organs, in particular: liver and pancreas |
| does GLUT2 require insulin to be translocated | no |
| GLUT2: Pancreas | GLUT2 transport glucose into the cell and that stimulates a signaling pathway to secrete insulin |
| GLUT2: Liver | GLUT2 transport glucose into the cell and insulin activate a pathway to convert glucose as glycogen |
| what is glycogen | storage form of glucose, present in liver and skeletal muscle |
| what is glycogenesis | conversion of liver and muscle glycogen to glucose, happens when glucose is low |
| insulin sensitivity | body's ability to effectively use insulin |
| insulin resistance | the body's cells become less responsive to the hormone insulin, leading to elevated blood sugar levels |
| lipolysis | process through which triglycerides are hydrolyzed to fatty acids and glycerol |
| gluconeogenesis | formation of glucose or glycogen from non CHO sources |
| gluconeogenesis precursors | pyruvate, amino acids, glycerol |
| ketogenesis | production of ketone bodies (will decrease body pH which is a huge complication of diabetes) - acetoacetate - 3-Hydroxybutyrate |
| fuel metabolism in diabetes mellitus | deficiency in insulin and increase in glucagon and other counterregulatory hormones, hyperglycemia, T1D, T2D |
| T1D fuel metabolism | increase mobilization of FFAs causes increase hepatic synthesis of ketone bodies, diabetic ketoacidosis (DKA) |
| T2D fuel metabolism | ketone bodies not sufficient for development of DKA, hyperosmolarity |
| type 1 diabetes mellitus most common form | T-cell mediated autoimmune destruction of pancreatic beta cell |
| etiology of T1DM | genetics, environment and autoimmunity |
| genetic etiology of T1DM | familial predisposition, HLA genes on short arm of chromosome |
| autoimmunity etiology of T1DM | autoantibodies against pancreatic beta-cell components |
| pathogenesis of T1DM | environmental factors trigger immune response, autoantibodies and antigens develop, honeymoon period follows (period of endogenous insulin secretory recovery), insulin production ceases |
| treatment of T1DM | exogenous insulin |
| T2DM is | most common form is DM |
| etiology of T2DM | genetics: if both parents have T2D, kid has 75% chance ethnicity: disproportionately affects minority populations |
| non-modifiable risk factors for T2D | family history of diabetes, age over 45, race and ethnicity (AA and latino) and Hx of gestational diabetes |
| modifiable risk factors for T2D | physical inactivity, high body fat or body weight, tobacco use/pollution, unhealthy diet |
| treatment for T2D | lifestyle modifications, medications, glucose monitoring |
| lifestyle modifications for T2D: balanced diet | more fiber-rich fruits/vegetables, brown rice, brown bread, whole wheat less white rice, white bread, pastas, sodas, candy less |
| lifestyle modifications for T2D: exercising | aerobic exercise- 150 minutes/week (walk, run, bike) resistance exercise- 2-3 times/week (weights, yoga) |
| medications for T2D: oral | metformin, glipizide, pioglitazone, dapagliflozin, sitagliptin, acarbose |
| medications for T2D: insulin | typically "basal" insulin is used, intermediated or long acting forms, insulin regimens vary |
| glucose monitoring for T2D: HbA1c test | measures average blood glucose level over past 2-3 months, goals vary but may be </= 6.5-7% |
| glucose monitoring for T2D: fingersticks | finger-stick glucose testing may be performed daily or multiple times per day depending on the treatment plan |
| acute complications of diabetes | diabetes ketoacidosis, hyperosmolarity syndrome, hypoglycemia |
| DKA absolute of relative insulin deficiency | characterized by hyperglycemia, metabolic acidosis, ketonemia most commonly associated with T1D |
| most common causes of DKA absolute of relative insulin deficiency | disruption of insulin treatment, new onset of T1D |
| DKA insulin deficiency and CHO metabolism | Hyperglycemia Glycosuria and osmotic diuresis Dehydration and hemoconcentration Periperipheral circulatory failure progressing to shock, hypotension, anuria Coma and death |
| quick diagnostics of DKA insulin deficiency and CHO metabolism | high blood glucose and acidic urine |
| DKA insulin deficiency and fat metabolism | Mobilization of depot in the blood, lipemia Secondary hypertriglyceridemia; FFAs made in LDLs - Ketone bodies develop into ketonemia - Progressive metabolic acidosis - Ketonuria - Cardiovascular collapse - Decrease in protein synthesis |
| DKA insulin deficiency and protein metabolism | Decreased protein synthesis Overall protein catabolism, particularly in muscle (break down muscle) Elevated levels of blood urea nitrogen (BUN) Net loss of K+ |
| diagnosis of DKA | laboratory criteria - hyperglycemia, ketosis, metabolic acidosis |
| treatment of DKA | Supportive measures, IV insulin therapy, IV fluids, IV electrolyte replacements |
| hyperglycemic hyperosmolar syndrome (HHS) | severe hyperglycemia and coma but without ketosis |
| risk factors of HHS | IGT or T2D |
| etiology and pathogenesis or HHS | Ready access to fluids not available; excessive unreplaced fluid losses Severe hyperglycemia and hyperosmolarity Glycosuria, osmotic diuresis, urinary electrolyte losses Reduction in GFR from dehydration |
| does metabolic acidosis develop with HHS | No |
| CMs of HHS | Related to hyperglycemia, dehydration, serum hyperosmolarity more severe than in DKA Plus neurologic symptoms (bc of excess glucose in neurons) and vascular thrombosis |
| diagnosis of HHS | laboratory criteria, profound dehydration and alteration in consciousness |
| treatment for HHS | is same is DKA - Supportive measures, IV insulin therapy, IV fluids, IV electrolyte replacements |
| hypoglycemia is | low blood glucose levels |
| when does hypoglycemia frequently occur | happens to pt being treated with insulin |
| hypoglycemia medical emergency | decreased blood glucose levels (<60 mg/dL), autonomic NS and neuroglycopenic symptoms (pt acts drunk) |
| etiology and pathogenesis of hypoglycemia | complication of T1D and insulin treated T2D, glucose-stimulated decline in plasma insulin levels, precipitating factors |
| precipitating factors of hypoglycemia | incorrect amount (too much) or type of insulin, missing meals and snacks, exercise |
| CMs of hypoglycemia | ANS symptoms prompt eating which raises blood glucose level, neuroglycopenic symptoms result from glucose deprivation to CNS |
| treatment of hypoglycemia | glucose! this will invert hypoglycemic conditions |
| long term complications in multiple organs from hyperglycemia | microvascular complications and macrovascular complications |
| microvascular complications | limb amputation -> neuropathy kidney failure -> nephropathy blindness -> retinopathy |
| macrovascular complications | hypertension induces heart attack and then stroke heart attack -> heart disease stroke -> cerebrovascular disease |
| microvascular complications are | diseases of smaller vasculature |
| macrovascular complications are | diseases of large vasculature |
| proposed pathogenesis of microvascular complications | hyperglycemia primary factor retinopathy neuropathy nephropathy |
| proposed pathogenesis of macrovascular complications | aggressive and accelerated rates of stroke, cardiovascular disease, peripheral disease hyperglycemia insulin resistance |
| insulin resistance examples | reduced HDLs, increase triglycerides, increase LDLs FFA induced increase in ROS polyol pathway, hexosamine pathway, PKC, AGE precursors atherosclerotic macrovascular disease |
| diabetic retinopathy is | disease of retina resulting in loss of vision |
| diabetic retinopathy: etiology and pathogenesis | excessive vascular occlusion or vascular permeability subsequent macular edema, neovascularization, fibrous tissue proliferation, vitreous hemorrhage |
| diabetic retinopathy: CMs | temporary blurring of vision, refractory changes increase risk of cataract formation |
| diabetic retinopathy: management | glucose control well-controlled blood pressure |
| diabetic neuropathy is | damage to kidneys |
| what is the leading cause of death in DM pts | diabetic neuropathy |
| class of renal changes in diabetic neuropathy | glomerulosclerosis structural vascular changes tubulointerstitial disease |
| glomerulosclerosis | loss of epithelial cells in kidneys, CT will replace lost cells but are not as functional |
| structural vascular changes | small arterioles |
| tubulointerstitial disease | tubular region cells die and filtrate leaks into interstitial space |
| diabetic neuropathy: CMs (if present) | presence of microalbuminuria (presence of protein in urine) |
| does diabetic neuropathy or diabetic retinopathy get more money from the government? | diabetic retinopathy because diabetic neuropathy pts just die |
| diabetic neuropathy is | high blood glucose that damages nerves and microvascularity |
| diabetic neuropathy: pathogenesis | increase polyol pathway activity Na retention, edema, myelin swelling, nerve degeneration |
| what does acute muscle contraction induce | glucose uptake |
| association between exercise and blood glucose | exercise is effective in decrease blood glucose by making your body more sensitive to insulin |
| acute effect of exercise | adipose release FFA, FFA used by muscle, muscle uses FFA to make ATP |
| increase mitochondria number and size | increase the capacity of muscle to metabolize glucose and lipids |
| increase GLUT4 concentration | increase insulin sensitivity and the capacity of uptake glucose |
| decrease intracellular lipid accumulation | decrease the impairment on insulin pathway |
| increase the size of the muscle fiber | increase the site for glucose clearance under insulin stimulation |
Created by:
leh195