EXAM 2 Flashcards
carbohydrate
simple sugars, broken down in duodenum and proximal jejunum
the liver + glucose
liver extracts glucose and synthesizes it to glycogen (energy storage), glycogenolysis (break down glycogen)
muscles and fat extract glucose for their energy need
pancreas
with the liver controls the bodies fuel supply
exocrine cells
pancreatic cells release into ducts
endocrine cells
secrete insulin into blood stream
islet of lagnerhans
small islands of cells in pancreas that make up endocrine function
alpha cells
secrete glucagon in response to low sugar, glucagon stimulates liver to release stored glucose into blood
beta cells
produce insulin, lowers glucose by moving glucose into body tissues
hormone that lowers blood glucose
insulin
hormones that raise blood glucose
glucagon, epinephrine, glucocorticoids, growth hormone
glucagon is secreted by
islet of langerhans
epinephrine is secreted by
adrenal medulla and chromatin tissues
glucocorticoids are released by
adrenal cortex
growth hormone is secreted by
anterior pituitary
insulin
hormone secreted by beta cells that stimulates glucose uptake, utilization, and storage (glycogen)
insulin and lipids
insulin promotes fatty acid synthesis in the liver, insulin is fat sparing, tells cells to use carbs instead of fat
consequences of having no insulin
carbs cannot be broken down, glucose is unused by cells, builds up in blood cells, cells use fatty acid for energy, fat cant breakdown correctly so there are increased fatty acids in blood
ketones
composed of products of acid breakdown
the problem with impaired fat metabolism
increased serum ketones which causes sever metabolic acidosis. long term: atherosclerosis due to high lipid levels in blood
insulin deficiency and protein metabolism
body cannot correctly store protein, increased protein breakdown, increase use of amino acids as energy source
protein catabolism
muscle wasting, organ dysfunction, increased BUN
glycosuria
excretion of sugar in urine, sugar is too high and kidneys cant keep up, increased acetones
clinical picture of insulin deficiency
polyphagia, polydipsia, polyuria
polyphagia
increased hunger due to breakdown of fat and protein
polydipsia
increased thirst due to serum osmalality
polyuria
excessive urine, loss of K, Na, Cl
Type one diabetes
autoimmune process dye to genetic predisposition and environment, beta cells are destroyed, complete lack of endogenous insulin, 5-10% cases
clinical manifestations of type I diabetes
symptoms start and progress until there is no insulin production, 3 P,s, weight loss, fatigue, infections, itching, vision changes
Type II diabetes
risk factors age, obesity, htn, inactivity, family hx, insulin resistance
clinical manifestations of type II
B cell exhaustion, insulin resistance, increased visceral fat
DKA
common in type one, hyperglycemia, acidosis, ketonuria
hyperosmolar hyperglycemic syndrome
type II, high sugar and osmolality, less profound than type II
hypoglycemia
less than 55-60 rapid hr, sweating, palpitations, hunger, restless
neuropathy
ichemia, demylelination, impaired conduction, loss of feeling
retinopathy
leading cause of blindness, small vessels become occluded
nephropathy
chronic kidney disease, glomerulus thickens and becomes non functional, common in diabetes
macrovascular diabetes complications
common in t2, atherosclerosis (hardening of large arteries) result of oxidative stress, endothelial disfunction
diabetes and infections
diminished warning signs, tissue hypoxia, bacteria feed on the high glucose
liodystrophy
skin indentation at insulin injection site
somogyi effect
too much insulin drops glucose, overcorrection causes hyperglycemia
insulin vial storage
30 days at room temp
rapid acting insulin
-lispro, humalog, novolog
-onset 15 mins
-peak 1 hour
-duration 2-4 hr
given with meals
short acting insulin
-human regular, humulin/novolin
-onset 30-60
-peak 2-6
-duration 3-8
-usually given prior to meals, used in insulin infusions
intermediate insulin
NPH, humulin N
-onset 2-4
-peak 4-10
-duration 10-20
-cloudy=shake up
-usually given 2x/day, can be mixed with rapid or short
long acting insulin
glargine/lantus
1x/day
onset 70 mins
do not mix
sulfonureas
glypizide, glyburide
MOA: binds and closes K-ATP cells, which stimulates insulin secretion
SE: hypoglycemia (more likely with kidney or liver issues)
DO not take when pregnant
side effects worsened by: alcohol, NSAID, sulfa abx
biguanides
metformin
MOA: decrease glucose production in liver, enhances glucose uptake by muscles. does not promote insulin release
peaks 2-4 weeks
SE: n/v/d, acidosis in people with elevated creatinine
do not use in people with high ALT levels,
nursing: monitor glucose, give 30 before meals, must be held for 48 hours after IV contrast
not for those with: heart failure, ckd, liver issues, heavy alcohol
therapeutic: sugar control, prevent T2D, treat PCOS
DPP4 inhibitors
linagliptin, sazagliptin, sitagliptan
MOA: inhibits DPP4 which inactivates incretin hormone. result: increase insulin, reduce glucagon, decrease liver glucose, slow digestion
SE: n/d, flu sx, skin issues, increase pancreatitis risk
usually in combo with diet and life change, combo med, low incidence hypoglycemia
GLP 1 agonist
dulaglutide, exenatide, semaglutide
MOA: enhances glucose dependent release of insulin, inhibits postprandial release of glucagon, suppress appetite, slowed gastric emptying
used in combo with metformin or others
plasma peaks 2 hours, half life 2.5
SE: n/v/d, inj. site rxn, URI, weight loss
not for use in pancreatitis pt, hx of medullary thyroid cancer, multiple endocrine neoplasia syndrome type 2, renal disease patient
sodium glucose cotransporter 2
dapagliflozin
MOA: prevents kidneys from reabsorbing glucose, allows kidneys to lower glucose levels by inhibiting reabsorption of glucose
SE: increased uti, genital mycotic infections, hypotension
oral
not for use in end stage kidney disease, not approved for type 1, given in combo
glucagon
oral, sq, IV, IM
oral if awake
MOA: activates glucagon receptors, releases glucose
short duration, may need multiple doses
fingerstick 15 mins after
adipose tissue
insulation and mechanical support
what does adipose tissue secrete
adipokines
adipocytes
fat storing cells, stored as triglycerides
major storage site for fat
subq or peripheral adipose tissue
android obesity
apple shape, htn, diabetes, stroke, heart disease
gynoid obesity
pear shaped, women
adipokines
secreted by adipose tissue, regulate appetite, energy, inflammatory, coagulation
adipokine list
leptin, angiopoietin, angiotensinogen, retinol-binding protein, IL-6, TNF-alpha
adipoponectin
good adipokine, more fat=less adiponectin
increases energy expenditure, enhanced insulin sensitivity
leptin
good adipokine, more fat=more leptin
tells body when it is full, increases insulin sensitivity
bmi for obesity
> 30
obesity and genetics
leptin gene determines leptin resistance, pcos, cushings
obesogens
endocrine disrupting chemicals
underweight bmi
18.5 and less
ideal bmi
18.5-24.9
overweight bmi
25-29.9
obese bmi
30-39.9
extreme obese bmi
40+
ghrelin
stimulates hunger and controls gastric motility and growth hormone, released in obesity
GLP1 w obesity
stimulates insulin secretion, imhibits glucagon release, slows gastril emptying
Peptide YY
decreased in obesity
reduces appetite and increases energy output
CKK
decreases in obesity
increase fullness, reduce intake
obesity medication
orlistat, alli, xenical
MOA: binds to gastic and pancreatic enzymes and blocks, reduces fat absorption
SE: black box liver injury
gas, fecal incontinance, decreases vitamin concentrations
3 months for effects, must be used with diet and exercise, must have already tried
metabolic syndrome criteria overview
high waist circumference, high triglycerides, high BP, low HDL, high fasting glucose
delerium
acute confused state, sudden or gradual onset
hyperactive delerium
acute, often in icu, postop, withdrawal,
risk factors=benzos or narcotics, surgery, infection
restless, shaking, insomnia
remove risk factors
hypoactive delerium
right sides frontal basal ganglion disruption, common in liver and kidney failure
decreased alertness, forgetfull, sleepy
demetia
progressive cerebral function failure
alzheimers
genetic, can be early onset, >65, existing impairment
alzheimers patho
tau protein forms plaques and tangles, kills neurons, loss of synapses, brain atrophies
vascular dementia
cerebrovascular disease, risk is DM, HLD, HTN, smoking
prevent risk
frontotemporal dementia
pick desaese, genetic mutations with tau
cholinesterase inhibitors
donepezil
MOA: increase ach levels by inhibiting achesterase
SE:gi, dizzy, insomnia, cramps, bradycardia, syncope
give with food, must have program for them to stay on track
NMDA receptor antagonist
memantine
MOA: blocks NMDA stimulation
SE: confusion, low bp, headache, dizzy, constipation
pain neurotransmitters
ne, ach, dopamine, serotonin, GABA
endorphines
endogenous opioid
pain transduction
stimuli converted to AP at the receptor
pain transmission
ap move from receptors to spinal cord to brain
a delta fibers
small diameter, myelinated, fast
c fibers
smaller diameter, non myelinated, slow
perception of pain
brain says it hurts
modulation
synaptic transmission is altered and blocks pain before it reaches brain
prostoglandin
promotes inflammation and fever, affects gi and kidney fxn
nociceptive pain
pain in response to stimuli
neuropathic pain
due to injury to nerve
tramadol
centrally acting analgesic
MOA: binds opioid receptors and inhibits reuptake of norepi and serotonin
SE: drowsy, dizzy, constipation, headache, respiratory depression, possibly seizures
gabapentin or pregablin
MOA: unknown, maybe surpresses neuronal firing
to compliment opioids
SE: drowsy, dizzy, can be partially reversed w naloxone
NSAID moa
anti prostoglandin, blocks COX
COX 1
protects gastric mucosa and platelets
COX 2
responsible for inflammation and fever
non selective cox
aspirin, ibuprofen, naproxen, ketorolac
cox 1 and 2 blocked,
se: gi, stomach ulcers, gi bleed, kidney failure
cox 2 selective
celecoxib
mucose protected, no platelet impact
associated with serious cardiovascular thrombolytic events
aspirin
salicylate poisoning, n/v/ seizures, cerebral edema, ringing ears
reyes syndrome
do not give aspirin to kids as it causes brain and liver damage
ketorolac
potent NSAID
IV, IM, sometimes po
only 5 days or less
SE: ulcers or renal dysfunction
acetaminophen
MOA: maybe decreases prostoglandin synthesis
not anti inflammatory
large amount causes hepatic necrosis
Large amount: jaundice, liver failure, LFT, creatinine
lortab/norco
hydrocodone and acetaminophen
percocet
oxycodone and acetaminophen
iv tylenol
ofirmev
list of opioids
morphine, hydromorphone, fentanyl, meperidine, codeine, oxycodone, hydrocodone, narcan
things to assess before opioid admin
LOC, BP, pulse, resp rate
morphine
MOA: my agonist, mimics endogenous opioids
PO, IV, epidural
interactions:alcohol and CNS depressants
SE: resp depression, constipation, drowsy, dry mouth
PO dose=30mg
IV=1-4mg
hydromorphone
similar to morphine but more potent, iv and PO
fentanyl
synthetic opioid
PO, IV, IM, Transdermal
extremely potent
merperdine
synthetic opioid, shorter duration than morphine, less resp depress, repeated doses cause a toxic metabolite
SE: potential seizures
codeine
PO
can reduce coughing, only for use in 18+
Se:nausea
oxycodone
po only
more potent than codeine, high abuse
hydrocodone
cough suppressant
usually combo med
methadone
opioid detoxn
naloxone
opioid receptor antagonist, clogs receptors, raises BP
overall nursing considerations for opioids SE
constipation, nausea, vomitting
seizure
episode of abnormal electrical activity
motor, sensory, cognitive
convulsion
seizure characteristic, involuntary
epilepsy
chronic seizures, no evidence of cause, electrical storm
myoclonic
brief shock like jerks of muscles
patho of seizures
group of neurons that spontaneously fire
gliosis
scar tissue from neurons firing during seizures
primary seizures
unknown cause
secondary seizures
chemical imbalance -drugs, BG
fever
TBI, stroke, menengitis, tumors
3 features of seizure classification
area of origin, level of awareness, motor or no motor involvement
generalized onset seizure
originates in both hemispheres, tonic clonic or absence seizures
tonic clonic
tonic-contraction
clonic-alternating muscle contraction and relaxation, jerking
focal onset seizures
one lobe of the brain
prodromal
signs of seizure, jerking, lethargy, mood change
aural phase
sensory warning
ictal phase
seizure
post ictal phase
recovery
status epilepticus
multiple seizures with no recovery, 30+ mins
can cause resp arrest, hypoxia
anti-epileptic drugs
control and prevent seizures, cannot abruptly stop, usually no meds after just one seizure,
require therapeutic monitoring
traditionally used: barbiturates, hydantoins, iminostilbines, valporic acid
MOA of anti epileptic drugs
increase threshold in motor cortex
limit spread by suppressing impulses
decrease speed of impulses
black box of anti epileptic drugs
increase of suicide, depression
adverse effects of anti epileptic meds
dizziness, drowsy, GI upset, teratogens
phenytoin/dilantin
indicated for: tonic clonic, focal seizures, first line for epilepsy
po or IV
lots of adverse effects, lethargy, confusion, gingival hyperplasia, osteoporosis
valporic acid
absence, myoclonic, tonic clonic
PO or IV, highly protein bound
contraindicated for liver disease or urea cycle disorters
hepatatoxicity, pancreatitis
topiramate, topamax
partial and secondary seizures, tonic clonic
PO
SE: cns depression, gi upset, visual changes
can interact with contraceptive meds
keppra, levetiracetam
partial seizures with and without generalization
po and IV
rapid seizure management
diazepam, lorazepam
