Diabetes Care Flashcards
1
Q
insulin
A
- release from beta cells of pancreas
- basal rate - small pulses
- bolus rate - larger amounts to cove meals
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
3
Q
gluconeogenesis
A
formation of glucose
4
Q
glycogenolysis
A
- transformation of glycogen to glucose
5
Q
type 1 diabetes
A
- 10%
- destruction of beat cells
- insulin
6
Q
type 2 diabetes
A
- 85%
- defective beat cells and decreased insulin sensitivity
- lifestyle modifications and PO hypoglycemics
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
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
9
Q
honeymoon period
A
- when first started on insulin may need lower doses as beta cells are kickstarted
- 3-12 months
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
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)
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
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
14
Q
how many people with type 2 DM eventually require insulin
A
50%
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)
16
Q
insulin secretagogues
A
- increase insulin production by pancreas
- hypoglycemics risk
- can speed pancreas exhaustion
- sulfonylureas and nonsulfonylureas
- *sulfa allergy
17
Q
beta blockers and diabetes
A
- blocks epinephrin resulting in hypoglycemics unawareness
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
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
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
21
Q
alpha glucosidase inhibitor
A
- decreases GI carb absorption
- prandase
22
Q
chronic complications
A
- microvascular and macrovascular
- optimal glucose control = less complications but more hypoglycemics events
23
Q
macrovascular complications
A
- CAD
- CVA
- PVD
- changes to coronary, cerebral, and peripheral vessels
- atherosclerosis increased and earlier
- abnormal clotting factors
24
Q
recommendations for macrovascular complications
A
- ASA, platelet aggregate inhibitor, ACE inhibitor, anti HTN
- cholesterol decreasing meds
- stress test & lifestyle modifications
25
microvascular complications
- decreased tissue perfusion of smaller vessels
- neuropathy (peripheral, autonomic NS, genitourinary)
- retinopathy
- nephropathy
- infections
- foot issues
26
peripheral neuropathy
- pain caused by tissue hypoxia
- segmental demyelination of nerve cells
- sensory and motor
27
autonomic NS neuropathy
- vasomotor reflection defects (dizzy, syncope, ortho HTN)
- silent MI
- decreased intestinal motility
28
genitourinary neuropathy
- bladder & sexual dysfunction
| - increased risk of renal problems
29
retinopathy
- leading cause of acquired blindness
- changes in retinal blood vessels
- changes in acuity, depth, colour, peripheral, or night vision
30
nephropathy
- 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
infections
- altered neutrophil function
| - increased risk and frequency
32
foot injury
- from angiopathy, neuropathy, and infections
33
acute DM complications
- hypoglycemia
- DKA
- HHS
34
counter regulatory hormones
- 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
4 counter regulator hormones
1) glucagon
2) epinephrine
3) cortisol
4) growth hormone
36
glucagon
- release from alpha cells in pancreas
- aids in gluconeogenesis and glycogenolysis
- prevents BG from dropping <4mmol/L
37
epinephrine
- causes S&S of hypoglycemia
- inhibits pancreatic insulin release
- causes glycogenolysis
- decreases use of glucose by tissues to conserve it for brain
38
cortisol
- 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
growth hormone
- released by pituitary in response to hypoglycaemia and growth
- can increase BG 50-100%
- hyperglycaemia during childhood/adolescence = treat w increase insulin
40
dawns phenomenon
- growth hormone is released early am, so sometime pts can wake up hyperglycemic
41
hypoglycemia
- always and emergency
- S&S
- causes
- treatment
- education
42
hypoglycemia S&S
- 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
hypoglycaemia causes
- commonly insulin/food mismatch
- missed meal
- too much insulin
- exercise
44
hypoglycemia treatment if pt can swallow
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
what can be given as 15g of sugar for hypoglycemia
- 4 glucose tablets
- 3/4 cup of juice or pop
- 1/2 popsicle
- 6 lifesavers/jelly beans
- 1tbs honey
46
hypoglycemia treatment if pt cant swallow
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
somogyi effect
- 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
glucometer reading
- call MD in 2 consecutive 14+ BG readings
49
diabetic ketoacidosis (DKA)
- type 1
- often present at diagnosis
- onset over a few days
- moderately to severely ill
- results form CRH and not enough insulin
50
why does DKA not occur in type 2
there is enough insulin to prevent the breakdown of fats for energy
51
what happens with DKA
- 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
why is plasma K+ increased in DKA
- K+ out of cells and H+ into cells
53
DKA S&S
- 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
DKA treatment
- 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
K+ replenishment for DKA
- 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
sick day rules
- 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
hyperosmolar hyperglycemia state (HHS)
- 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
why does dehydration occur in DKA
- dehydration occurs from BG in blood being so high that fluid is pulled from cells/ECF and excreted in urine
