Carbs Flashcards
medications for type 2
metformin/ glucophage: help reduce amount of sugar made by liver– eliminates through the urine and turn receptors inward
-will find glucose in the urine
-will not make more insulin
IF metformin/ glucophage doesn’t work go to
glipiZIDE or Januvia
GlipiZIDe/ Januvia
helps pancreas produce insulin
-eliminate sugar though urine
if previous dont work go to
victoza/ trulicity/ ozempic (last resort)
victoza/ trulicity/ ozempic actions
slows down bodies metabolism/ slow down sugar into blood stream
-prevents liver from making glucose and secretes more insulin
gestational diabetes if increased sugar intake
baby is also producing more insulin
-so after birth and cord is cut baby will have abrupt stop of sugar but its still increased amount of insulin — severe risk for becoming hypoglycemic
moms that are gestational diabetic have increased risk of
fetal lung immaturity
what week will baby have normal lung development
37
gestational babies lungs fully developed
40
what week are mothers tested for gestational diabetes
24-28
home glucose monitoring system
hand held glucose measure glucose
-about 10-12 % lower than actual draw would be
-interstitial fluid mixes and dilutes
high hematocrit
decreases blood glucose levels falsey bc RBC are using glucose
CGM- continuous monitoring system
-monitor all the time
-probe under skin
-will be diluted? checks done
-can be used in both types
microalbumin
-looks for small amount of albumin
-looks for renal failure (early stages)
- if kidney loses function can’t reabsorb protein- albumin first to leak
-done twice a year on diabetic
1 testing specimen for microalbumin
24 hour urine
normalbumin
<30
microalbumin
30-300
MACROalbumin
> 300
if doing random urine for microalbumin use
albumin to creatine ratio
what test is done if HgB A1C can’t be done
frutosamine
what occurs in the fructosamine test
glucose sticks to albumin in blood (glycosylated proteins) will stay for 2 weeks
another good time to do fructosamine test
if a diabetic is starting new medication or gestational diabetic
when can’t do fructosamine test
liver failure (increases values) and kidney failure (not enough albumin)
normal fructosamine levels
205-285
lactose intolerant
inability to breakdown lactose
lactose intolerant occurs because
deficient or absent lactase enzyme
babies aren’t lactose intolerant at birth
because breast milk contains lactose – need lactase enzyme
lac. intolerance occurs
changes in gut flora/ introduction of antibiotics
amount of processed foods we eat affect
gut flora
ways to diagnose lac. intolerance
elimination diet, lactose hydrogen breath test, standard lactose tolerance
elimination diet
eat no foods with lactose
if symptoms go away= lactose intolerant
lactose hydrogen test
consume 25-50 g of lactose liquid
-breath samples taken 30 min- 3 hours
increase in hydrogen indicates malabsorption of lactose (can have false negatives)
standard lactose intolerance
blood lactose levels
-if no decrease in lactose shows body isn’t breaking down it
if diagnosed type 2
-doctor will want baseline insulin levels
AS medications change doctors will look at insulin levels
increase in insulin but normal glucose
can be pancreatic tumor secreting insulin
glycogen storage disease
inherited
-once stored body can’t break down glucose
von gierke disease
defect in glucose 6 phosphate
-can’t break down glycogen into glucose
-become hypoglycemic -no storage breakdown
-go into metabolic acidosis
-hepatomegaly- bc main site of glycogen storage
short in height, intellectual disabilities
avoid glycogen buildup
limit sugar intake, small amount of food
-body will utilize sugar= no excess storage
galactosemia
-mentally slow, liver damage, vomitting
-aminoacidopathy
-infants tested
-enzyme deficiency in galactokinase
CAN’T breakdown galactose
for years did clinitest for reducing sugars but now
-GENETIC testing
hexokinase
gold standard for glucose amounts (enzymatic rxn) specific glucose
END product: NADPH; proportional to amount of glucose in speciment
glucose oxidase
-glucose specific
-more interfering substance– Hgb and BILLI
2 step process
1) measured amperometrically– oxygen consumption measures trinder rxn
2) photometric analyze
hydrogen peroxide mixed with chromagic (color production)
proportional to amount of glucose
main source of energy for cells
carbs
where are carbs stored
liver and muscle
what is carbs stored as in the muscle
glycogen
structure of carbs
carbon double bonded to oxygen and alcohol group
most important monosaccharides
glucose, fructose, and galactose
most important disaccharides
lactose, maltose, sucrose
lactose components
glucose and galactose
sucrose components
glucose and fructose
maltose components
glucose and glucose
polysaccharides
starch and glycogen
carbs are hydrates of
aldehyde and ketone groups
only hormone that can decrease blood sugar
insulin
what enhances formation of lipids and proteins
insulin
insulin inhibits breakdown of
glycogen
another regulator of blood sugar
glycogen
glucagon is produced by the ______ cells in the pancreas
alpha
what is the main hormone for rapid increase of blood sugar
glucagon
glucagon will tell the liver to break down _____ then fat
glycogen
what does cortisol do
inhibit insulin and rapidly increases glucose
cortisol finds new ways to get glucose through
fats and proteins
finding new ways to get glucose in the body
gluconeogenesis
metabolism of glucose
taken in as starch or glycogen
1)amylase- enzyme found in salivary glands or pancreas
2) gastric juices released and break down into usable sugars
normal metabolism
sources of sugar– diet and hepatic output
after we take in sugar insulin levels rise
If we fast– breakdown of glycogen first, fats second, proteins last
Glycogenesis– control levels
When BS levels rise the liver will stop releasing glucose
-take in too much sugar – stored as glycogen and fat
abnormal
hyperglycemia all the time
-either no insulin or insulin resistant
continued production of hyperglycemic state
no glucose= go to fat; leads to increased production of triglycerides
can get insulin from recombinant insulin -manufactured
3 major ketones
acetate
acetoacetate
2-hydroxybutyric acid
sodium imbalance
decreased because water comes out of cell to dilute glucose and also dilutes Na
potassium imbalance
normally increases in DKA
-when cells open up K comes out a cell with water and blood levels rise
-body tries to drive hydrogen back into cell and K comes out
potassium increases risk of heart attack
bicarb imbalance
increased because acid increased and bicarb fixes this (tums)
chloride imbalance
increase levels
-1 time Na and Cl don’t follow each other
-some bicarb is used up so Cl is trying to reabsorb
if you give insulin
need to watch potassium because it will drive back into cell to drive now glucose
anion gap
(Na + K) - (Cl + HCO3)
normal : 9-16
no potassium: 8-12
1 reason anion gap increased
DKA
serum osmolarity
2Na + glucose/20 + BUN/3
normal= 275-300
type 1 is also
lactic acidosis
fasting specimen
10-12 hours
use serum or heparinized plasma
seperate cells asap or else cells keep using glucose
gray top stable for 72 hours
Hgb A1C can’t do
after hemolytic event
need Hemoglobin A
-sickle cell can’t do this bc Hgb S
Norm <6
check twice a year
-can be increased due to injury
specimen= EDTA
