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Overview of DM
Clinical Medicine II
| Question | Answer |
|---|---|
| Whas DM type 1 | Absolute insulin deficiency |
| What is type 2 DM | relative insulin Deficiency, insulin resistance |
| What is Diabetes | lack of cellular access to glucose→↓ cellular glucose utilization, accumulation of glucose in plasma |
| What happens at the liver in DM | unmitigated hepatic glucose production, can be not eating and glucose still rises |
| Why do we need insulin | need it to uptake glucose in the cells (except the brain), results in micro and macro |
| What is the fxn of the pancreas | primary endocrine gland of glucose homeostasis, B-cells produce insulin, alpha: glucagon, delta: somatostatin |
| What happens in the liver during the fed state | extracts glucose from blood, glycogen synthesis, FA and TG synthesis |
| Liver fxn during fasted state | ↑ hepatic glucose production, glycogenolysis, gluconeagensis |
| What is the main glucose producer | liver |
| Does the liver, skeletal muscle, adipose tissue and brain need insulin for glucose uptake? | only the skeletal muscleand adipose tissue |
| What happens in skeletal muscle for fed state and fasted state | fed: extracts glucose for glycogen sythensis and ATP production, Fasted: provides AAs and lactate to liver for gluconeaogensis |
| Fxns of adipose tissue in fed and fasted state | fed: extracts glucose for energy storage as TG, fasted, released FA for oxidation and energy, LT fast: ketones |
| Are fatty acids a source of glucose | NO! |
| Why are ketones produced in LT fast | d/t B-oxidation, Aceytyl co-A produces ketones |
| 4 inhibitory fxns of insulin | gluyconeolysis, gluconeogenesis, HGP, lipolysis |
| 4 fxns of glucagon in the liver | stimulates HGP, glycogenolysis, gluconeogenesis, FA release from adipose |
| Stimulates glucose production from glycogen (liver & muscle) and FA release from tissue | epinehhrine |
| Functions of cortisol | AA release from muscle, glucose production from glycogen in liver/muscle, FA release from adipose |
| Fxns of GH | Circadian rhythms, nocturnal rise in GH→insulin resistance, AM hyperglycemia |
| Know the chart of insulin def | pg 2 |
| Nl fasting plasma glucose | 70-100mg/dL |
| What is necessary for brain fxn | 40 mg/dL |
| What level of blood glucose will cause glucose in the urine | >180mg/dL |
| When are most type 1 DM diagnosed | 5-15, around puberty previously called “juvenile diabetes” |
| What causes type 1 DM | genetic, environmental, autoimmune dysfx-more prone to have another autoimmune dz |
| How does type 1 DM show up later in life in it is a complete insulin deficiency | there is a gradual destruction f the b-cell in the pancreas |
| What % of the b-cells need to be gone prior to clinical dz | 90% loss prior to symptomatic |
| What are some environmental exposures/triggers | infections/viruses, chemicals, infant feeding practices (bovine proteins?) obesity?, starts the autoimmune cascade |
| What is the honeymoon phase | in type I DM giving some insulin induces insulin production in the pancreas for some time, but will eventually d/c and need full time insulin replacement |
| What % of the U.S. POPULATION has type2 DM | 7%! |
| What ethnicities see ↑ in DM type 2 | NA, AA, Hispanics,Polynesian, asians |
| What causes type 2 | GENETIC!: obesity!!, RF’s |
| BMI > what will usually result in DM | >35 72% will have DM! |
| What are 6 genetic factors in type 2 DM | Obesity, FH, metabolic syndrome, Race, GDM, SGA |
| RF’s for DM | overweight, inactivity, insulin resistance, pre-dm, concomitant factors: HTN and hyperlipidemia (TG) low HDL, AGE: pancreatic burnout theory |
| What is IDDM | insulin dependent DM aka type 1 DM |
| DKA | diabetic ketoacidosis |
| Patho of type 2 DM | relative insulin deficiency (resistance), receptor and post-receptor defects, perpetuated by hyperinsulinemia, with a progressive secretory defect |
| Symptoms of type 1 DM | polydipsia, polyuria, polyphagia, wt loss |
| Symptoms of type 2 DM | often asymptomatic, present w/ comorbidities (HTN, CVD, stroke, dyslipidemia) |
| Insulin in Type 1 and2 | 1: usually absent, severely diminished 2: low, nl, high |
| Test to distinguish b/w type 1 and type 2 | C-peptide, 1: decreased 2: normal or increased |
| Why do we give insulin to patients with insulin resistance | it takes more insulin to get the same response to a non-insulin resistant patient. |
| What are other disease that can cause problems with the pancreas | pancreatitis, cystic fibrosis |
| What are some disease that DM can be secondary to | Cushing’s disease, acromegaly, hyperandrogenism, PCOS |
| Classification of DM | monogenetic diabetic syndrome, neonatal DM, Maturity onset diabetes of the young, genetic b-cell dysfx for insulin receptor defect, medication induced |
| What are signs of prediabetes | abnl oral glucose tolerance test, 20% progress to type 2 |
| Why does GDM occur | HCG and progesterone, estrogen, lactogen ↑ insulin degradation and resistance |
| How often do we see GDM | 7% of all pregnancies! (↑blacks and Hispanics: obesity) |
| What ↑ risk of perinatal morbidity and morbidity | macrosomia and post-natal hypoglycemia |
| What are nl, pre and DM FPG | nl: 70-100, pre: 100-125, DM>126 |
| Random PG levels | nl <140, Pre: 140-199, DM >200 w/ sxs |
| What is Hgb A1C | Average level of hyperglycemia over 2-3m |
| Hgb surrounded by high glucose levels | causes ↑ A1C |
| Impaired fasting glucose | out of the nl range |
| Pre diabetes levels of A1C | 5.7-6.4 (no classified nl level (usually under 5 but not gold std)) |
| What is the diagnostic criteria for metabolic syndrome | Waste >40, >35, TG’s: < 150 HDL: <40M <50F, BP: >130/85, |
| What are screening guidelines for type 2 DM | Begin 45 yo, every 3 yrs, (more frequent w/ ↑ risk), FPG, OGTT, Hgb A1C |
| WHO do we screen | asymptomatic patients who are overweight (BMI > 25). Who have >1 RFs |
| RF’s DM | BMI>25, inactivity, 1 relative w/ DM, delivery >9lb baby, PCOS, HTN, HDL, H/O CVD, Acanthosis nigracans |
| What is acanthosis nigracans | in NA/AA’s darkening areas of the skin usually around the neck |
| What is the screening for type I DM | there isn’t any, abrupt onset, and too rare for screening (research for potential intervention BEFORE b-cell destruction) |
| How do we detect type 1 DM | immune assays to detect abs |
| Diagnostic criteria for gestational DM: OGTT at 24-28 weeks (everyone), Fasting: >92, 1hr: >180, 2 hrs>153 | |
| What is the post-partum assessment for DM for women | check 6-12 weeks postpartum (test other than A1C), then check q3years if hx of GDM |
| CP of type 1 DM | polyuria, dipsia, phagia, wt loss, blured vision, DKA, Dehydration, ketonuria, glucosuria, ketone breath, C-peptide absence |
| CP of type 2 DM | +/- nl D sxs, vaginal yeast, candida, ↑infx, vision sxs, neuopathy, retinopathy, |
| Lab findings of DM | A1C, FLP, LFTs, microalbuminurea, and micro (creatinine), SCr, estimated GFR, TSH |
| What should we screen for with t1 and t2dm | celiac dz |
| What other endocrine dysfx is often associated/ dm | polycystic ovarian syndrome PCOS |
| Microvascular complications of DM | eye, kidney, nerve |
| Macrovascular complications of DM | cardiac, CVD, PAD |
| Skin manifistationsof DM | acanthosis nigicans,insulin injection sites |
| What is important when giving pt ed for DM | it’s a self-managed dz!! Patient orientated tx |
| Self-montioring guidelines for type 1 | 3 or more injections/day or continuous pump therapy, should have pre and post pradinal insulin dosing, |
| What are indications for continuous glucose monitoring | patients unaware of hypoglycemia |
| Why is there such a chance for hypoglycemia in the diabetic patient | their nl bodies response to insulin decreases, so the insulin continuous to decrease the blood glucose |
| Hgb A1C testing recommendations | 2/year if meeting tx goals, 4x yr if not meeting goals |
| Goal for A1C | <7 % will ↓ micro and macrovascular complications |
| What is the primary target for glycemic control | A1C |
| What populations need special considerations when managing DM | children, pregnant women, elderly |
| Targetgoals for DM A1C, BP, BG, lipids | A1C <7, pre prandial BG 70-130, post prandial or peak <180, BP: 130/80, LDL<100, TG<150, HDL>40M >50F |
| MNT for Type 1 | glycemic control by coordinating CHO intake, exercise, and insulin therapy, also: prevent HTN,CAD |
| Why do we keep BG highter in those younger | more vulnerable to hypoglycemia ` |
| What is the hallmark of DM management | CHO counting and control |
| Does a diabetic need to be on a low CHO diet? | no, just need to distribute it throughout the day |
| What is a diabetic diet | normal healthy eating with a reduction in saturated fats |
| What do we do with a 5 yo type 1 DM going to a birthday party and going to eat cake and ice cream | adjust his insulin dose, but ensure he is actually going to eat this |
| What classifies early stage renal disease | 30-299mg/24 hrs microalbuminuria |
| What is tx for early Early stage renal dz | avoid excess protein (.8-1.0gm/kg) (not a RDA restriction) |
| Management for T2DM | weight management of >25BMI, calorie reduction, Low CHO, mediterranean, exercise, pharm |
| Wt management in T1DM | watch excess wt gain in tightly controlled T1DM |
| What are 3 other nutritional considerations | fiber, ↓ calorie/non-nutritive sweetners,alcohol ↓ |
| Alcohol recommendations for diabetics | on for women, 2 for men 1:15g/carb |
| How can alcohol contribute to hypoglycemia | the liver works on metabolizing alcohol, stops producing glucose |
| Bariatric surgery indications | type2DM w/ BMI >35, comorbid condition, difficult to control w/ LSM and pharm |
| Is gastric bypass rcommended w/ BMI 30-35 | no |
| Why does physical activity help glucose | ↑ muscle, ↑ glucose consumer, ↑insulin sensitivity, wt management, ↓ risk CVD |
| PA recommendations | moderate 150m/week, vigerous 90m/wk, resistance 3x/wk |
| Pharm for t1 and t2dm | 1: insulin, 2: metformin, insulin |
| What are we trying to do w/ drug therapy | cell glucose intake, ↑insulin secretion, ↓HGP, |
| Immunization recommendations | (STOP SMOKING), annual flu >6m old, pneumococcal for al DB>2yr, HBV |
| When do we revaccinate for pneumococcal | >65, >5yr ago, have nephrotic syndrome, CRF, immunocompromised |
| Tx for preDM | ↓kcal, ↑fiber whole grains-helps w/ insulin control, |
| Tx for gestational dm | manage w/ diet, wt loss CI in preggo, pharm: insulin only, non-insulin pharm CI |
Created by:
becker15
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