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ABSN > DM review for MedSurg > Flashcards

DM review for MedSurg Flashcards

1
Q

T1 is caused by

A

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

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2
Q

T2 is caused by

A

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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3
Q

Type 1 Review

A

-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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4
Q

Type 2 review

A

-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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5
Q

non modifiable risk factors for T2

A

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

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6
Q

modifiable risk factors for T2

A

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

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7
Q

what is considered a fasting blood glucose

A

no food or drinks in the last 8 hrs

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8
Q

dx of DM

A

(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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9
Q

what urine ketone level is considered an emergency

A

> 300 mg/dl

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10
Q

A1c levels

A

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

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11
Q

FBG

A

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

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12
Q

OGTT

A

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

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13
Q

DM sick care

A

-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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14
Q

sick w/ DM teaching points

A

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

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15
Q

when does a sick person w/ DM need to call their HCP

A

-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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16
Q

hypoglycemia can cause

A

seizures

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17
Q

hypoglycemia range

A

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

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18
Q

diabetes

A

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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19
Q

where are carbs broken down

A

in the duodenum and proximal jejunum

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20
Q

regulating glucose depends on the

A

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

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21
Q

what organ secretes glucagon & insulin

A

the pancreas

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22
Q

two major functions of the pancreas

A

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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23
Q

what cells make up the endocrine function of the pancreas

A

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

24
Q

what hormones raise BG

A

-glucagon (islets)
-epinephrine (adrenal medulla)
-glucocorticoids (adrenal cortex)
-growth hormone (anterior pituitary)

25
Q

complications of impaired fat metabolism: short term

A

-increased serum ketones
-ketosis
-if severe, metabolic acidosis / coma

26
Q

complications of impaired fat metabolism: long term

A

atherosclerosis bc of high serum lipid levels

27
Q

insulin deficiency effect on protein

A

body is unable to store protein effectively -> increased protein catabolism & cessation of protein synthesis -> increase use of amino acids as energy and muscle wasting

28
Q

protein catabolism CM

A

-muscle wasting
-multiple organ dysfunction
-aminoacidemia
-increase BUN
more typical in T1

29
Q

insulin deficit & fluid/lytes

A

increased serum glucose levels -> increased plasma oncotic pressure -> fluid shifts into intravascular compartment -> intracellular dehydration

30
Q

3 P’s

A

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

31
Q

T1DM s/s

A

-3 Ps
-wt loss
-fatigue
-recurrent infections
-prolonged wound healing
-general pruritis
-visual changes
-parathesias
-cardiovascular symptoms

32
Q

T2DM s/s

A

vague & non specific
-fatigue
-recurrent infections
-visual changes
-prolonged wound healing

33
Q

metabolic comps w/ T2DM

A

-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

34
Q

DKA is characterized by

A

hyperglycemia, acidosis & ketonuria

35
Q

HHNS is characterized by

A

extremely high hyperglycemia & osmolality w/ a normal pH + significant fluid deficiency

36
Q

hypoglycemia S/s

A

-pallor
-sweating
-tachycardia / palpitations
-hunger
-restlessness
-anxiety
-tremors
-convulsions
-coma

37
Q

microvascular comps of DM

A

-damage to capillaries
-retinopathy, nephropathy, neuropathy
-microangiopaathy (small vessel disease)
lesions appear, hypoxia & ischemia, & capillary membrane thickening

38
Q

macrovascular comps of DM

A

-damage to large vessels (coronary artery, peripheral & cerebral vascular)
atherosclerosis

39
Q

diabetic neuropathy

A

-related to metabolic & vascular factors
-cause ischemia & demyelination
-loss of pain, temp, & vibration sensation
-can lead to ulcer, infection & possible amputation

40
Q

diabetic retinopathy

A

-leading cause of blindness
-results from relative hypoxemia, damage to retinal blood vessels, red blood cell aggregation & htn
small vessels become occluded causing infarction

41
Q

diabetic nephropathy

A

-most common cause of CKD & end stage kidney disease
-glomerular basement membrane thickens and becomes sclerosed (thick, hard & nonfunctional)

42
Q

DM & infection

A

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)

43
Q

if a person has preDM

A

no sx may be present but long term damage can be occurring
teach lifestyle mods, encourage close BG monitoring, monitor for sx, & diet mods

44
Q

pharm mgt: oral meds

A

-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

45
Q

pharm mgt: insulin

A

-mock normal body cycle
-basal of glargine/detemir/degludec at bedtime
-bolus of lispro/aspart/glulisine or regular before each meal

46
Q

rapid acting insulin

A

lispro & aspart
onset: 10-30 mins
peak: 30-3hr
duration: 3-5hr

47
Q

short acting insulin

A

regular
onset: 30-1hr
peak: 2-5 hr
duration: 5-8 hr

48
Q

intermediate acting insulin

A

NPH
onset: 1-4 hr
peak: 4-12 hr
duration: 12-18 hr

49
Q

long acting insulin

A

glargine & detemir
onset: 0.8-4 hr
peak: less define/no peak
duration: 16-24 hr

50
Q

rule of 15

A

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

51
Q

DM diet

A

-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

52
Q

when should a diabetic person not exercise

A

if glucose levels are <80 or >250

53
Q

DM & exercise

A

-PA lowers BG
-best to do after a meal
-if more than 1hr post meal, eat another carb snack
-wear med alert bracelet

54
Q

stored version of glucose

A

glycogen

55
Q

breakdown of glycogen occurs by

A

glycogenolysis

56
Q

what does glucagon do

A

Stimulates the liver to release stored glucose into the blood

57
Q

How does the liver release glucose in response to glucagon

A

Glycogenesis

ABSN (161 decks)

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