patho unit 8- diabetes

is the pancreas an endocrine or exocrine organ

both

delta cells secrete

somatostatin

alpha cells of pancreas

secrete glucagon

beta cells of pancreas

secrete insulin

glucoenogenesis

making glucose from fats and proteins when there is no available glucose, often at night

glucagon

hormone from pancreatic alpha cells, stimulates the breakdown of glycogen to glucose to raise blood glucose levels, activates lipase to breakdown lipids for energy, enables protein to be converted to energy (last resort)

glycogen

stored glucose in the liver

glycogeneis

formation of glycogen from glucose, putting glucose in storage

glycogenolysis

breakdown of glycogen to glucose, taking out of storage

lipolysis

breaking down of lipids for use as energy

role of insulin

promotes uptake of glucose into cells, stimulates glycogenesis for storage of glucose, if carbs are available insulin decreases glucogenesis, decreases breakdown of proteins for energy

hormones involved in blood sugar regulation

insulin and glucagon, amylin, incretin, epinephrine

amylin

secreted with insulin from beta cells of pancreas, turn off alpha cells

incretins

hormone secreted by gastric cells to increase insulin release after food is consumed, decreases gastric emptying (stay full for longer), can be used for weight loss

GLP-1

glucagon like peptide, same thing as incretins

epinephrine effect on glucose levels

increase blood sugar and increase lipolysis for energy

somatostatin as GH inhibitor

slows GI transit time, allows more time to absorb nutrients

somatotropin (GH)

growth hormone; helps fat be used for energy, increases blood sugar levels, higher amounts seen in children

Glucocorticoid hormones

released under stress from hypothalamus, can also be exogenous as medication, can lead to steroid induced hyperglycemia

type 1 diabetes mellitus (DM1)

beta cells are not secreting endogenous insulin, glucose cannot get into cells to be used as energy

effects of DM1 on pregnancy

can impact palcental blood flow leading to more premature babies

type 2 diabetes mellitus (DM2)

hyperglycemia and hyperinsulinemia, body is resistant to insulin so glucose isn't entering cells, much more common than type 1

gestational diabetes mellitus (GDM)

hyperglycemia brought upon by pregnancy

etiology of DM1

mostly autoimmune in nature, immune cells destroy the beta cells of the pancreas, can be genetic or due to infection OR idiopathic which has a more abrupt onset and no autoimmune cause which can indicate genetic links

risk factors for type 1 diabetes

white people for autoimmune, idiopathic cause is more common among African Americans or asians, one of the most common childhood diseases

manifestations of DM1

polyuria, polydipsia, polyphagia with weight loss, glycosuria, hyperglycemia, fatigue, infections and poor wound healing

treatment of DM1

neee to balance diet, activity and insulin treatments

etiology of DM2

cells become resistant to insulin, and over time increased levels of glucose in blood can overwork then beta cells secreting insulin and cause them to not function properly so insulin may not be secreted anymore

how well are beta cells functioning at time of diagnosis of DM2

usually about 50% of beta cells have already died off due to exhaustion

risk factors for DM2

obesity, age greater than 45, women with history of gestational diabetes, lifestyle

pre-diabetes

impaired glucose tolerance

manifestations of DM2

polyuria, polydipsia, polyphagia, hyperglycemia, glucouria (usually go unnoticed due to gradual onset) fatigue, recurrent infections, dry itchy skin (from fluid loss), neuropathy, poor wound healing

treatment of DM2

lifestyle changes, diet to control carbohydrate intake, OHAs, insulin if needed

OHAs

oral hyperglycemia agent

metabolic syndrome symptoms

central obesity (waistline over 45 in males or 35 in females), hypertension (135-185), hyperlipidemia (elevated cholesterol) or fasting blood sugar over 126

labs to diagnose diabetes

FBG, A1C, U/A 2 hour post prandial BS

FBG

fasting blood glucose, over 126 indicates diabetes, can be seen on BMP if fasting or can be done randomly (if over 200 when not fasting indicates diabetes)

HgbA1C

Hemoglobin A1C, used both for diagnosing and evaluating diabetes management, average glucose levels over past 3 months

HgbA1C 5.7-6.4%

pre diabetic

HgbA1C 6.5-8%

diabetic

HgbA1C over 8%

uncontrolled diabetes

U/A

urinalysis, can show glucose and ketones in the urine that indicates diabetes

2 hour post prandial blood sugar

(OGTT) glucose tolerance test, assess glucose spikes with eating, after 2 hours blood sugar should come back down, should be less than 200

risk factors aka pre-diabetes

impaired fasting glucose and impaired glucose tolerance

impaired fasting glucose

elevated blood sugar when patient wakes up and has been fasting seen on FBS

impair glucose tolerance

seen on OGTT, fasting blood sugar is normal but blood sugar increases rapidly when eating (doesn't hit 200 yet) but stays high for a long time

fluid movement of diabetes

hyperglycemia pulls fluid from interstitial spaces, causing increase urine output and dehydration

glycerinated hemoglobin test

monitors glucose control similar to A1C

can type 2 diabetics have a normal fasting glucose

yes, their fasting glucose can appear normal but blood glucose increases rapidly when eating

FBS less than 100

normal

FBS 100-125

borderline aka impaired glucose tolerance

FBS over 126

indicated diabetes

2 hour post prandial blood sugar= 139

normal

2 hour post prandial blood sugar 140-199

impaired glucose tolerance

2 hour post prandial blood sugar over 200

diabetes

random fasting blood sugar over 200

indicates diabetes