DM review for MedSurg Flashcards by Jane Daum

T1 is caused by

destruction of beta cells in the pancreas d/t t cell mediated disease

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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

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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

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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

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non modifiable risk factors for T2

-fam hx
->45 y/o
-race/ethnicity
-hx of gestational DM

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modifiable risk factors for T2

-physical inactivity
-high body fat or wt
-high BP
-high cholesterol

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what is considered a fasting blood glucose

no food or drinks in the last 8 hrs

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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

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what urine ketone level is considered an emergency

> 300 mg/dl

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A1c levels

normal: ~5
preDM: 5.7-6.4
diabetes: >/6.5

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FBG

normal: </99
preDM: 100-125
diabetes: >/126

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OGTT

normal: </139
preDM: 140-199
diabetes: >/200

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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

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sick w/ DM teaching points

-notify HCP
-check BG every 2-4 hrs
-take dm meds
-prevent dehydration
-meet carb needs
-rest

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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

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hypoglycemia can cause

seizures

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hypoglycemia range

BS<70
if person lives at a high level, hypoglycemia can be seen at a higher number

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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

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where are carbs broken down

in the duodenum and proximal jejunum

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regulating glucose depends on the

liver
-extracts glucose
-synthesizes it into glycogen (energy storage)
-glycogenolysis (breakdown of glycogen)

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what organ secretes glucagon & insulin

the pancreas

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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

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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