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62 Cards in this Set
- Front
- Back
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immunoperoxidase staining for what
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insulin and glucagon in islets of langerhans
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significance of C-peptide
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exogenous insulin vs pancrease secreting too much
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prediabetes
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if caught here can driv ethem abck from diabetes proigression
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<100 mg/dl
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normal
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100-125mg/dl
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prediabetes
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?126 mg/dl
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diabetes
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fasting glucose test
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>126 = diabetes
100-125 prediabetes 2 separate days tests to be positive to confirm has diabetes |
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random glucose
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diabetes > 200 mg
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oral glucose test
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drink 75 gm glucose beverage and measure glucose 2 hrs later;
>200 mg/dl x 2 |
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HbA1c
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>6.5% diabetes
6-6.5 prediabetes <6 normal |
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glycosylated hemoglobin
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bc rbc float around for 120 days HbA1c can measure average blood glucose levels over previous 2-4 months;
HbSS = increased rbc turnover = transfusion requirements |
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HgA1C corelates well w mean palsma glucose levels
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5 = 100
6 = 135 7 = 170 |
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type 1 DM
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B cell destruction; 5-10% of all cases; absolute deficiency in insulin
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type 2 DM
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peripheral resistance and impaired secretory response; 90-95% of diabetic pts have type 2 diabetes; most are overweight
prevalence in childrena nd adolescents has shown a marked increase |
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type 1 genetic susceptibility
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chromosome 6p21
HLA DR3 and DR4; DQ8 highest risk for type 1 DM |
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how many b cells must be destroyed before symptoms
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90% or greater of B cells must be destroyed before hyperglycemia and ketosis before seymptosm occur; disease processes take awhile to kick in bc of large reserves
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mechanisms of B cell destruction in type 1
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failure of self tolerance in T cells; also often seen in asymptomatic family members; predictive markers for type 1 DM;
unknown if these ab are cause of injury or are produced as aresult of injury |
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type 2 DM pathogenesis
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beta cell hyperplasia to make more insulin;
environmental factors: diet and sedentary lifestyle VERY important polygenetic loci |
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de elopment of type 2 DM
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adipokines, FFAs and inflammation generated from obesity; leads to insulin resistance (B cell hyperplasia leads to B cell failure)
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nonesterfied fatty acids
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inverse relationship between insulin sensitivyt and fawtsing plasma NEFA
FA build up, produce toxic intermediates, lead to decreased signaling insulin signaling normally inhibits hepatic gluconeogenesis; body makes more glucose bc dec insulin signaling = more hyperglycemia |
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adipokines
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collection of proteins that can be released by adipocytes
pro-hyperglycemia adipokines antihyperglycemic adipokines; leptin, adiponectin (decreased in obesity) |
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inflammation and insulinr esistance
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obesity leads to inflammation (TNF, IL6, etc) -> adipocytes secrete proinflamamtory cytokines; inflammation increases insulin resistance (all just from obesity) causing insulinr esistance
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PPAR gamma
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nuclear receptor and transcription facctor in adipose tissue; activates promtotion/secretion of anti hyperglycemic adipokines; shifts NEFA deposition away from lvier and seketlal muscle and towards adipose tissue
thiazolindiadione = ligands for PPAR gamma; mutations in PPARG may result in monogenic diabetes |
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amyloid is seen in which type of DM
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type 2' also seen in medullary thyroid carcinoma; high calcitonin levels
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AGE
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advanced glycation end products; sugars combine w proteins; results in signaling of proinflammatory cytokines and growth factors
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excess glucose is metabolized to what
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NADPH; used by glutathione reductase and generates reduce glutathione; hyperglycemia reduces NADPH = opens you up to oxiaxdative damage
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pancreas morphology
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w type 1 diabetes = insulinitis
also know the amyloid in type 2 |
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diabetic microangiopathy
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thickened basement membrane; skin, muscle, retina, glomeruli, renal medulla
all these small vessels soak in high sugar levels damaged capillaries become leaky; plasma proteins get out despite the thickening (just bc theyre getting thicker doesnt mean they're getting better) |
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nodular glomeruler sclerosis (diabetic nephropathy)
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also called Kimmelstiel wilson dz; ovoid spherical nodules due to DM
globs of PAS positive balls (christmas ball dz); acellular PAS psoitive nodules and diffuse increase in mesangial matrix |
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which vessels in kidney does diabetes hit
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hyaline arteriolosclerossi in both afferent and efferent arteriole; due to chemistry of blood sugars
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pyelonephritis
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necrotizing papillitis 2 to DM
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aldose reductase
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converts glucose -> sorbital
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DKA
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more common in 1; insulin deficiency; not getting enough sugar so release epinephrine; stimualte gluconeogenesis which makes hypoerglycemia even worse; pee alot due to somotic; then dehydrated diabetic; DKA = abdoluste emergency, dehydrated diabetic
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hyperosmolar nonketotic coma
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Type 2; non ketosis bc have enough insulin to shut down the process of having to convert to ketone bodies; hyperglycemia = osmolar effect = dehydration, can kill you as well but for different reaons
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microalbuminemia
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smalla mount of albumin in urine; lets you know youre headed towards significant renal damage
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neovascularization
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secondary to hypoxia induced overexpression of VEGF in DM
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glove and stocking
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hands, legs, feet afected by neuropathy; parathesias/weakness in distal extremities
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old man in office w impotence
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consider diabetes
bowel dysunctinon, bladder dysfunction, other autonomic problems |
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footdrop, wrist drop, isolated cranial nerve palsies
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diabetic mononeuropathy
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infections
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pyelonephritis, pneumonia, TB, skin infections; pts w diabetes are immunocompromised
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insulinoma
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pancreatic endocrine neoplasm, MSOT COMMON; can secrete enough insulin to cause hypoglycemia;
pt w very low blood sugars usually benign high levels of insulin w high insulin/glucose ratio (q to differentiate hypoglycemia) |
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gastrinoma
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zollinger-ellison syndrome;
tumors produce gastrin; originate in pancreas, duodenum, peripancreatic soft tissue associated w hypersecretion og gastric acid and severe peptic ulceration (dont respond to therapy and are in unusual places w multiple ulcers) related to MEN1 syndrome diarrhea (30% of pts will presentw diarrhea0 |
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ulcers that dont respond to therapy, unusual places, multiple ulcers
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gastrinoma; ulcers 2 to increased gastrin release
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high VIP assocaited w what symptom
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secretory diarrhea
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major cause of hypoglycemia
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mcc is pts who take too much insulin or agents that increase insulin secretion; know whipples triad to dx hypoglycemia
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whipples triad
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symptoms w hypoglycemia, low plasma glucose level, relief of symptoms when the glucose level is raised
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neurogenic
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increased autonomic nervous system activity; things you feel peripherally
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neuroglycopenic
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things you feel in your brain
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pt comes in hypoglycemic; pt w access to insulin, inject themselves and through some factitious method theyre trying to get their blood glucose level low; difference between exogenous insulin and insulinoma
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exogenous insulin mixtures do not contain C-peptide; high c peptide in an insulinoma, but exogenous insulin is going to be low
this is how you differentiate exogenous from insulinoma sulfonylurea; forces body to make insulin normally so youll pump out C peptide as well; if palsma sulfonylurea levels are high you know this is the cause of the hypoglycemia |
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xanthelasma
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yellow plaque on eyelid, consider type II: (familial hypercholesterolemia)
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arcus senilis
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rim of white around the outer part of the cornea
consider increased LDL if a young pt or normal age related change if older patient |
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eruptive xanthomas
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yellow papular lesions over the body; due to increased triglyceride: type IV (hypertriglyceridemia)
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achilles tendon xanthoma
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familial hypercholesterolemia (II)
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draw blood = turbid, what is it?
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triglyceride
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two fractions that carry TG
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chylomicrons and VLDL
chlylomicrons: carry saturated fat (LCFA); broken down by lipases, reassembled in enterocytes and stuck in chylomicrons |
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do you have to fast for TG or cholesterol?
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TG: increased chylomicrons falses elevated TG
dont have to for cholesterol bc less than 3% cholesterol for chylomicrons dont have to fast for HDL level (bc we're measuring HDL cholesterol) |
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endogenous triglycerides
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VLDL
made in live from glycerol 3 phosphate which came from glucose; increased in alcoholics (bc of NADH pushing DHAP -> glycerol 3 phosphate) |
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are chylomicrons or VLDL more dense?
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VLDL; because has some protein in it (chylomicrons has little, so it floats on supernate)
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fast to decrease what
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triglycerides derived from diet
no fasting for accurate cholesterol or LDL |
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achiles xanthoma in pt w family history of death by CAD by 20 yrs of age
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familial hypercholesterolemia (type II)
AD w absent LDL receptor; all LDL supposed to be going into cells builds up in other places get first coronary by 18 and dead shortly there after; probably put on HMG-CoA reductase inhibitor at birth |
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hyperplastic arteriolosclerosis
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onion skinned; narrowed lumen
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first thing noticed in diabetic nephropathy
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microalbuminemia; mechanism = NEG
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