DM review for MedSurg Flashcards
T1 is caused by
destruction of beta cells in the pancreas d/t t cell mediated disease
T2 is caused by
beta cells wear out -> cells in body become immune or resistant to insulin -> liver increases gluconeogenesis b/c cells think they need more insulin -> liver makes more insulin but body cannot respond appropriately -> elevated BS
Type 1 Review
-more common in younger people
-S/s are abrupt
-less common
-no endogenous insulin produced, must have insulin replacement
-3 Ps: polyphagia, polydipsia, polyuria
Type 2 review
-more common in adults
-can go undx for years, screen based on risk factors
-insulin resistant, oral/subQ diabetic meds
-only some will need insulin replacement
non modifiable risk factors for T2
-fam hx
->45 y/o
-race/ethnicity
-hx of gestational DM
modifiable risk factors for T2
-physical inactivity
-high body fat or wt
-high BP
-high cholesterol
what is considered a fasting blood glucose
no food or drinks in the last 8 hrs
dx of DM
(at least 1 of the following)
1. A1c >/6.5
2. FBG >126
3. OGTT 12hr level >200mg/dl
4. 3 Ps, random glucose >200 or hyperglycemic crisis
1-3 need repeat testing for dx
T1 needs islet cell autoantibody
what urine ketone level is considered an emergency
> 300 mg/dl
A1c levels
normal: ~5
preDM: 5.7-6.4
diabetes: >/6.5
FBG
normal: </99
preDM: 100-125
diabetes: >/126
OGTT
normal: </139
preDM: 140-199
diabetes: >/200
DM sick care
-if on steroids, may need to adjust basal dosage and increase scheduled dosage bc steroids inc BG
-check BG more frequently
-continue to take oral meds even if V/d bc they are long term drugs
sick w/ DM teaching points
-notify HCP
-check BG every 2-4 hrs
-take dm meds
-prevent dehydration
-meet carb needs
-rest
when does a sick person w/ DM need to call their HCP
-urine ketone present
-BS >250
-fever >101.5 that doesn’t respond to meds
-feeling confused/disoriented
-rapid breathing
-persistent N/V/D
-inability to tolerate liquids
-illness lasting longer than 2 days
hypoglycemia can cause
seizures
hypoglycemia range
BS<70
if person lives at a high level, hypoglycemia can be seen at a higher number
diabetes
metabolic disorder characterized by hyperglycemia that results from defects insulin secretion, insulin action or both & is associated w/ extensive long term damage when uncontrolled to multiple organ systems
where are carbs broken down
in the duodenum and proximal jejunum
regulating glucose depends on the
liver
-extracts glucose
-synthesizes it into glycogen (energy storage)
-glycogenolysis (breakdown of glycogen)
what organ secretes glucagon & insulin
the pancreas
two major functions of the pancreas
1) exocrine: pancreatic cells secrete directly into the ducts (not blood stream)
2) endocrine: cells secrete insulin directly into the blood stream
what cells make up the endocrine function of the pancreas
islets of langerhans
alpha cells: secrete glucagon in response to low blood sugar which stimulates the liver to release stored glucose into the blood
beta cells: produce insulin, which lowers glucose levels by stimulating the movement of glucose into body tissue
what hormones raise BG
-glucagon (islets)
-epinephrine (adrenal medulla)
-glucocorticoids (adrenal cortex)
-growth hormone (anterior pituitary)
complications of impaired fat metabolism: short term
-increased serum ketones
-ketosis
-if severe, metabolic acidosis / coma
complications of impaired fat metabolism: long term
atherosclerosis bc of high serum lipid levels
insulin deficiency effect on protein
body is unable to store protein effectively -> increased protein catabolism & cessation of protein synthesis -> increase use of amino acids as energy and muscle wasting
protein catabolism CM
-muscle wasting
-multiple organ dysfunction
-aminoacidemia
-increase BUN
more typical in T1
insulin deficit & fluid/lytes
increased serum glucose levels -> increased plasma oncotic pressure -> fluid shifts into intravascular compartment -> intracellular dehydration
3 P’s
1) polyphagia d/t catabolism of fat & protein + cellular starvation
2) polydipsia d/t increased serum osmolality
3) polyuria d/t osmotic diuresis, excreting water & loss of lytes
T1DM s/s
-3 Ps
-wt loss
-fatigue
-recurrent infections
-prolonged wound healing
-general pruritis
-visual changes
-parathesias
-cardiovascular symptoms
T2DM s/s
vague & non specific
-fatigue
-recurrent infections
-visual changes
-prolonged wound healing
metabolic comps w/ T2DM
-impaired insulin section d/t b cell exhaustion
-peripheral insulin resistance d/t inc visceral fat
-inc hepatic glucose production d/t impaired suppression of gluconeogensis within the liver
-altered production of hormones & cytokines by adipose tissue
DKA is characterized by
hyperglycemia, acidosis & ketonuria
HHNS is characterized by
extremely high hyperglycemia & osmolality w/ a normal pH + significant fluid deficiency
hypoglycemia S/s
-pallor
-sweating
-tachycardia / palpitations
-hunger
-restlessness
-anxiety
-tremors
-convulsions
-coma
microvascular comps of DM
-damage to capillaries
-retinopathy, nephropathy, neuropathy
-microangiopaathy (small vessel disease)
lesions appear, hypoxia & ischemia, & capillary membrane thickening
macrovascular comps of DM
-damage to large vessels (coronary artery, peripheral & cerebral vascular)
atherosclerosis
diabetic neuropathy
-related to metabolic & vascular factors
-cause ischemia & demyelination
-loss of pain, temp, & vibration sensation
-can lead to ulcer, infection & possible amputation
diabetic retinopathy
-leading cause of blindness
-results from relative hypoxemia, damage to retinal blood vessels, red blood cell aggregation & htn
small vessels become occluded causing infarction
diabetic nephropathy
-most common cause of CKD & end stage kidney disease
-glomerular basement membrane thickens and becomes sclerosed (thick, hard & nonfunctional)
DM & infection
can be deadly
-diminished warning signs
-tissue hypoxia so when skin is impaired, healthy cells cannot get to the site to heal
-rapid proliferation of pathogens d/t excess sugar (fungal/yeast/UTI/gangrene)
if a person has preDM
no sx may be present but long term damage can be occurring
teach lifestyle mods, encourage close BG monitoring, monitor for sx, & diet mods
pharm mgt: oral meds
-start at low dose & increase gradually based on A1c levels & FBG
-if hospitalized, stop oral meds and put on insulin for tight control
-hold metformin before procedures
pharm mgt: insulin
-mock normal body cycle
-basal of glargine/detemir/degludec at bedtime
-bolus of lispro/aspart/glulisine or regular before each meal
rapid acting insulin
lispro & aspart
onset: 10-30 mins
peak: 30-3hr
duration: 3-5hr
short acting insulin
regular
onset: 30-1hr
peak: 2-5 hr
duration: 5-8 hr
intermediate acting insulin
NPH
onset: 1-4 hr
peak: 4-12 hr
duration: 12-18 hr
long acting insulin
glargine & detemir
onset: 0.8-4 hr
peak: less define/no peak
duration: 16-24 hr
rule of 15
only if conscious and able to swallow
give 15g simple carb (4oz juice or regular soda, 3 glucose tabs, 8oz milk) -> wait 15 mins then recheck BG -> repeat until normal & once normal eat regular meal
avoid sugars w/ fat d/t delayed absorption
DM diet
-Balanced w/ high fiber, low fat, low chol
-carbs should be grains, fruits, legumes & milk
-limit simple carbs (pasta & bread)
-carbs should be 45-65% of total daily intake
-protein should be 15-20%
-limit alc to 1/d for women & 2/d for men
when should a diabetic person not exercise
if glucose levels are <80 or >250
DM & exercise
-PA lowers BG
-best to do after a meal
-if more than 1hr post meal, eat another carb snack
-wear med alert bracelet
stored version of glucose
glycogen
breakdown of glycogen occurs by
glycogenolysis
what does glucagon do
Stimulates the liver to release stored glucose into the blood
How does the liver release glucose in response to glucagon
Glycogenesis
