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Acute Health Challenges > Diabetes Care > Flashcards

Diabetes Care Flashcards

1
Q

insulin

A
  • release from beta cells of pancreas
  • basal rate - small pulses
  • bolus rate - larger amounts to cove meals
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2
Q

glucose metabolism and liver

A
  • low BG sensed by alpha cells
  • glucagon released
  • liver converts glycogen to glucose and release in bloodstream
  • gluconeogenesis and release
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3
Q

gluconeogenesis

A

formation of glucose

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4
Q

glycogenolysis

A
  • transformation of glycogen to glucose
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5
Q

type 1 diabetes

A
  • 10%
  • destruction of beat cells
  • insulin
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6
Q

type 2 diabetes

A
  • 85%
  • defective beat cells and decreased insulin sensitivity
  • lifestyle modifications and PO hypoglycemics
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7
Q

signs and symptoms of DM

A
  • polyphasic - increased hunger
  • polyuria - increased urination
  • polydipsia - increased thirst
  • recurrent utis/yeast infections
  • sore that won’t heal
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8
Q

diabetes diagnosis

A
  • FPG >7.0mmol/L
  • A1C >6.5%
  • 2hPG in a 75g OGTT >11.1mmol/L
  • random PG >11.1mmol/L
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9
Q

honeymoon period

A
  • when first started on insulin may need lower doses as beta cells are kickstarted
  • 3-12 months
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10
Q

short acting/regulat

A
  • onset = 30 mins
  • peak = 2-3 hr
  • duration = 6.5hr
  • only regular can be given IV
  • Humulin R, NPH
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11
Q

rapid acting

A
  • onset = 10-15 mins
  • peak = 60-90 mins
  • duration = 3-5 hrs
  • eat right after
  • often used with CHO counting
  • Humalog (lispro), Aspart (NovoLog), glargine (Apidra)
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12
Q

long acting

A
  • onset = 90 mins
  • peak = no peak as consistently release
  • duration = 24hrs
  • once daily often HS
  • no mixing
  • glargine (Lantus), detemir (Levemir), degludec (tresiba), humulin N
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13
Q

pharmacological treatment of type 2

A
  • start with diet/exercise trial
  • oral hypoglycemics only type 2
  • often combo with insulin
  • 6 classes
  • not given with gestational diabetes or pregnant type 2
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14
Q

how many people with type 2 DM eventually require insulin

A

50%

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15
Q

metformin (Glucophage)

A
  • biguanide
  • suppress hepatic glucose production and increase glucose uptake by cells
  • no hypoglycaemia risk
  • hold for CT dye to let it be excreted by kidneys (48hrs after procedure)
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16
Q

insulin secretagogues

A
  • increase insulin production by pancreas
  • hypoglycemics risk
  • can speed pancreas exhaustion
  • sulfonylureas and nonsulfonylureas
  • *sulfa allergy
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17
Q

beta blockers and diabetes

A
  • blocks epinephrin resulting in hypoglycemics unawareness
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18
Q

incretin agents

A
  • acts on hormone in GI D-PP4 inhibitors and GLP1
  • stimulates pancreas to secrete more insulin and decrease glucose production by liver
  • hypoglycaemia risk
  • GI side effects
  • injection
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19
Q

sodium glucose linked transporter protein inhibitor (SGLT-2)

A
  • new class PO med
  • decrease glucose reabsorption by kidneys
  • no hypoglycaemia risk
  • risk for uti/yeast infection
  • cardiac benefits
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20
Q

insulin sensitizers

A
  • thiazolidinediones (TZD)
  • increases insulin sensitivity at cell receptors = decreased insulin resistance
  • no hypoglycaemia risk
  • increased MI risk, contraindicated in CHF
  • 8-12 wk peak
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21
Q

alpha glucosidase inhibitor

A
  • decreases GI carb absorption

- prandase

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22
Q

chronic complications

A
  • microvascular and macrovascular

- optimal glucose control = less complications but more hypoglycemics events

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23
Q

macrovascular complications

A
  • CAD
  • CVA
  • PVD
  • changes to coronary, cerebral, and peripheral vessels
  • atherosclerosis increased and earlier
  • abnormal clotting factors
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24
Q

recommendations for macrovascular complications

A
  • ASA, platelet aggregate inhibitor, ACE inhibitor, anti HTN
  • cholesterol decreasing meds
  • stress test & lifestyle modifications
25
Q

microvascular complications

A
  • decreased tissue perfusion of smaller vessels
  • neuropathy (peripheral, autonomic NS, genitourinary)
  • retinopathy
  • nephropathy
  • infections
  • foot issues
26
Q

peripheral neuropathy

A
  • pain caused by tissue hypoxia
  • segmental demyelination of nerve cells
  • sensory and motor
27
Q

autonomic NS neuropathy

A
  • vasomotor reflection defects (dizzy, syncope, ortho HTN)
  • silent MI
  • decreased intestinal motility
28
Q

genitourinary neuropathy

A
  • bladder & sexual dysfunction

- increased risk of renal problems

29
Q

retinopathy

A
  • leading cause of acquired blindness
  • changes in retinal blood vessels
  • changes in acuity, depth, colour, peripheral, or night vision
30
Q

nephropathy

A
  • leading cause of end stage renal failure
  • high glucose damages glomerular basement membrane
  • earliest sign in increased microalbuminuria
  • should be on ACEs or ARBs
31
Q

infections

A
  • altered neutrophil function

- increased risk and frequency

32
Q

foot injury

A
  • from angiopathy, neuropathy, and infections
33
Q

acute DM complications

A
  • hypoglycemia
  • DKA
  • HHS
34
Q

counter regulatory hormones

A
  • opposite effect of insulin = increased glucose
  • stimulate liver glucose production and decreases glucose movement into cells
  • decreased BG = CRH to keep glucose in bloodstream
35
Q

4 counter regulator hormones

A

1) glucagon
2) epinephrine
3) cortisol
4) growth hormone

36
Q

glucagon

A
  • release from alpha cells in pancreas
  • aids in gluconeogenesis and glycogenolysis
  • prevents BG from dropping <4mmol/L
37
Q

epinephrine

A
  • causes S&S of hypoglycemia
  • inhibits pancreatic insulin release
  • causes glycogenolysis
  • decreases use of glucose by tissues to conserve it for brain
38
Q

cortisol

A
  • keeps glucose stable between meals and fasting
  • release by adrenal glands in response to stress
  • increases gluconeogenesis
  • inhibits use of glucose by muscles
  • steroid meds have similar effect
39
Q

growth hormone

A
  • released by pituitary in response to hypoglycaemia and growth
  • can increase BG 50-100%
  • hyperglycaemia during childhood/adolescence = treat w increase insulin
40
Q

dawns phenomenon

A
  • growth hormone is released early am, so sometime pts can wake up hyperglycemic
41
Q

hypoglycemia

A
  • always and emergency
  • S&S
  • causes
  • treatment
  • education
42
Q

hypoglycemia S&S

A
  • fight or flight then CNS
  • fight or flight = increased HR and BP, trembling, dilated pupils, sweating
  • CNS = seems as if they are drunk: confusion, decrease LOC, irritability, trouble concentrating, headache, staggering, diaphoresis, nervousness, pallor, palpitations, visual disturbances, stupor, coma
43
Q

hypoglycaemia causes

A
  • commonly insulin/food mismatch
  • missed meal
  • too much insulin
  • exercise
44
Q

hypoglycemia treatment if pt can swallow

A

1) give 15g fast acting carbs (sugar) to increase BG 2mmol/L in 15-20 mins.
2) retest BG in 15 mins. if <4 mmol/L then give 15g sugar again
3) repeat until BG >4 mmol/L
4) give 15g carbs and a protein if meal is >30 mins away

45
Q

what can be given as 15g of sugar for hypoglycemia

A
  • 4 glucose tablets
  • 3/4 cup of juice or pop
  • 1/2 popsicle
  • 6 lifesavers/jelly beans
  • 1tbs honey
46
Q

hypoglycemia treatment if pt cant swallow

A

1) a) if IV give 50ml 50% dextrose in water over 1-3mins IV push
1) b) if no IV give 1 mg glucagon s/c or IM2
2) retest BG in 15 mins. if <4 mmol/L then give dextrose again
3) complex carb
4) determine cause and educate

47
Q

somogyi effect

A
  • pt goes to bed and wake up in am with high BG
  • may go low in night then CRH take over to increase BG
  • diagnose by testing during night
  • may need to decrease supper or HS insulin
48
Q

glucometer reading

A
  • call MD in 2 consecutive 14+ BG readings
49
Q

diabetic ketoacidosis (DKA)

A
  • type 1
  • often present at diagnosis
  • onset over a few days
  • moderately to severely ill
  • results form CRH and not enough insulin
50
Q

why does DKA not occur in type 2

A

there is enough insulin to prevent the breakdown of fats for energy

51
Q

what happens with DKA

A
  • decreased extracellular volume from osmotic diuresis
  • hyperosmolarity
  • metabolic acidosis from ketones decreasing blood pH (<7.3)
  • electrolyte imbalance from osmotic diuresis and acidosis increasing plasma K+
52
Q

why is plasma K+ increased in DKA

A
  • K+ out of cells and H+ into cells
53
Q

DKA S&S

A
  • dehydration
  • decreased blood pH = increased acidity
  • thirst, warm dry skin, poor turgor, dry mucous membranes
  • weakness, malaise, decreased LOC
  • rapid thready pulse to compensate for hypotension and lack of fluid
  • rapid deep respirations from acidosis trying to exhale CO2
  • N&V, abdominal pain
  • lethargy, coma from dehydration
54
Q

DKA treatment

A
  • VS, LOC, cardiac monitor (Q1hr)
  • monitor BG, electrolytes, and ABG (Q2hrs)
  • regular insulin (humulin R) IV initially then s/c (6 units/hr till BG <15 then 3units/hr
  • IV fluid to rehydrate —> usually N/S with or without K+
  • monitor anion gap to determine level of acidosis goal is <12
  • monitor HCO3 = CO2 goal is >20
  • determine cause, treat, educate, counsel
55
Q

K+ replenishment for DKA

A
  • if K+ above 5.5 then none needed
  • if between 3.5-5.5 then 20mmol KCl/L in N/S
    if below 3.5 then 40mmol/L KCl/L in N/S
56
Q

sick day rules

A
  • treat at home if:
  • can maintain hydration and carb intake
  • frequent BG monitoring (2-4 hrs)
  • check urine for ketones = acidosis
  • continue meds and insulin
  • 8oz calorie free fluid each hour
  • call if vomit >1, diarrhea++, or ketones showing
57
Q

hyperosmolar hyperglycemia state (HHS)

A
  • type 2, gradual onset, precipitating factors
  • similar clinical and labs as DKA but no acidosis
  • similar treatment as DKA = hydration and insulin
  • severe hyperglycaemia (>33mmol/L)
  • profound dehydration, urine and plasma specific gravity increase
  • increased mortality as usually elderly with other illnesses
58
Q

why does dehydration occur in DKA

A
  • dehydration occurs from BG in blood being so high that fluid is pulled from cells/ECF and excreted in urine

Acute Health Challenges (7 decks)

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