Exam #4- DM Flashcards
(98 cards)
1
Q
physiologic difference between diabetes type 1 and type 2
A
type 1= pancreas attacks cells that produce insulin- body CAN’T make insulin
type 2= body is resistant to insulin- body MAKES insulin, but body doesn’t respond to it
2
Q
natural hx DM2
A
insulin resistance, insulin secretory defect that is NOT auto-immune related, and increase in glucose production by the liver
3
Q
clinical presentation for type 1 DM
A
polyuria
polydipsia
polyphagia
weight loss
weakness
dry skin
ketoacidosis
4
Q
clinical presentation for type 2 DM
A
possibly asymptomatic
polyuria
polydipsia
polyphagia
fatigue
weight loss
most are discovered while performing urine glucose screening
5
Q
A1C parameters for diagnosis of DM and prediabetes
A
DM: >6.5
prediabetes: 5.7-6.4
6
Q
fasting BG parameters for diagnosis of DM and prediabetes
A
DM: >126
prediabetes: 100-125
7
Q
goals of DM management
A
lower A1C<7%, decrease microvascular complications and macrovascular dx
stringent goals (<6.5%) for some pts
less stringent goals (<8%) for pts. w/hx of severe hypoglycemia, limited life expectancy, or other conditions that make <7% hard
8
Q
1st line agent for DM unless CI
A
biguanides (metformin)
9
Q
MOA of biguanides/metformin
A
decreased hepatic glucose production
increased insulin mediated peripheral glucose uptake
10
Q
efficacy of biguanides/metformin
A
decreases fasting plasma glucose 60-70 mg/dL
decreases A1C 1-2%
11
Q
ADE of biguanides/metformin
A
diarrhea/abdominal discomfort
12
Q
BBW for biguanides/metformin
A
LACTIC ACIDOSIS (rare renal failure and tissue hypoxia)
no weight gain w/possible modest weight loss
may cause small decrease in LDL cholesterol level and triglycerides
13
Q
contraindication for biguanides/metformin
A
**pts w/impaired renal function (Cr>1.4)
HOLD 24 hrs before and 48 hours post-
IV dye load
14
Q
MOA of sulfonylureas
A
increases endogenous INSULIN SECRETION (secretagogue) by binding to receptors on pancreatic beta cells
leads to insulin secretion
15
Q
efficacy of sulfonlylureas
A
decreases fasting plasma glucose 60-70
decreases A1C by 1-2%
16
Q
ADE of sulfonylureas
A
hypoglycemia risk (increased w/other agents)
weight gain
rash
HA
N/V
photosensitivity
caution in renal/hepatic impairment (avoid in CrCl<50)
17
Q
MOA of thiazolidinediones (TZDs)
A
decreases insulin resistance by increasing muscle and fat sensitivity to insulin
also suppresses hepatic glucose production
18
Q
efficacy of TZDs
A
decreases fasting plasma glucose 35-40
decreases A1C 0.5-1%
6-12 weeks for effect
19
Q
ADE of TZDs
A
weight gain
edema
hypoglycemia
increased fracture risk
20
Q
BBW for TZDs
A
**CI in HF pts (class III and IV)
21
Q
considerations for TZDs
A
caution in hepatic impairment
may improve HDL and triglycerides
22
Q
MOA of meglitinides
A
similar to sulfas- more rapid onset and shorter acting
stimulate insulin secretion (rapidly and short duration)
most effective in presence of glucose (has to be given with meals)
23
Q
efficacy of meglitinides
A
decreases peak postprandal glucose
decreases plasma glucose 60-70
decreases A1C 0.5-1% (depends on glucose for activity)
24
Q
ADE of meglitinides
A
hypoglycemia
weight gain
rare SJS
no significant effect on plasma lipid levels
25
CI of meglitinides
not given w/gemfibrozil
caution in hepatic dysfunction
26
MOA of alpha glucosidase inhibitors
work in the gut- block enzymes that digest starches in small intestine
slows glucose absorption
27
efficacy of alpha-glucosidase inhibitors
decreases peak postprandial glucose 40-50
decreases A1C 0.5-1%
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ADE of alpha-glucosidase inhibitors
flatulence
diarrhea
abdominal discomfort
no specific effect on lipids or BP
no weight gain
hypoglycemia risk w/ secretagogue
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CI for alpha-glucosidase inhibitors
in pts w/ IBD or cirrhosis
30
MOA of dipeptidyl peptidase-4 inhibitors (DPP-4 inhibitor)
inhibits breakdown of glucagon-like peptide-1 (GLP-1) secreted during meals
31
SQ form of dipeptidyl peptidase-4 inhibitors (DPP-4 inhibitor)
mild increase in glucose-mediated insulin release
suppresses glucagon secretion
delays gastric emptying
promotes satiety
32
efficacy of DPP-4 inhibitor
0.5-0.8% A1C reduction
33
ADE of DPP-4 inhibitor
decreases risk of hypoglycemia (**except when given w/sulfa drugs**)
pancreatitis
N/V
hypersensitivity- angioedema, anaphylaxis, caution in renal insufficiency
34
sitagliptin (DPP-4 inhibitor)
r/t SJS
caution in renal insufficiency
35
meds in the DPP-4 inhibitor class end in what?
gliptin
36
MOA of glucagon-like peptide-1 agonists (GLP-1 agonist)
analog of GLP-1: binds to GLP-1 receptors
increases glucose mediated insulin release (when you eat)
suppresses glucagon secretion
delays gastric emptying
promotes satiety
37
how are GLP-1 agonists given?
via SQ injection
38
efficacy of GLP-1 agonists
0.9-1.1 A1C reduction
39
ADE of GLP-1 agonists
weight loss
low risk hypoglycemia
GI s/s
pancreatitis
**caution in renal dysfunction and severe gastroparesis**
40
MOA of SGLT2 inhibitors
block renal glucose resorption
glucosuria (pee out the sugar, so it's not in blood)
41
efficacy of SGLT2 inhibitors
decreases fasting glucose and post-prandial glucose
0.5-1% A1C reduction
42
ADE of SGLT2 inhibitors
**GU infections* (because you're peeing out sugar)
weight loss
polyuria
osmotic diuresis
dehydration
CI in severe renal impairment
fracture risk (bone density loss)
dose related increase in LDL
43
how are amylin analogs (pramlintide) given?
SQ immediately prior to meal
44
MOA of amylin analogs (pramlitidine)
binds to amylin receptors
slows gastric emptying (like GLP1 analogs)
**used in BOTH DM1 and DM2**
suppresses glucagon secretion
delays gastric emptying
suppresses appetite
45
efficacy of amylin analogs (pramlintide)
0.5-1% A1C reduction
effective post-prandial glucose reduction
46
ADE of amylin analogs (pramlintide)
**BBW in DM1 for increased risk of hypoglycemia**
**CI in hypoglycemic unawareness and/or frequent hypoglycemia**
**you need to decrease short acting insulin (prandial) dose by 50% when starting** (i.e. you usually give 10 units lispro before dinner- when starting an anylin analog, you need to decrease the dose to 5 units lispro before dinner)
caution in gastroparesis
nausea, HA, cough
47
MOA of bile acid sequestrants
bile acid binder
decreases glucose via unknown mechanisms
48
efficacy of bile acid sequestrants
minimal
49
ADE of bile acid sequestrants
constipation
indigestion
flatulence
hypersensitivity reactions
large pills (dysphagia is a problem)
can make hypertriglyceridemia worse
not systemically absorbed
pregnancy category B
50
principles of insulin therapy in DM1
starting dose is based on weight
daily dosing (basal-single injections and prandial-determined by estimating carb content of meal)
higher total daily insulin needed for obese pts, sedentary lifestyle, and during puberty
51
action profile of endogenous insulin
spikes high and drops rapidly
52
action profiles of bolus insulins (lispro, aspart, glulisinine, regular)
spikes high and then drops off after 4-8 hours
53
action profiles of basal insulins (NPH, detemir, glargine, degludec)
does not spike as high but lasts for 17-20 hours
degludec lasts for 42 hours
54
injection pens
fast and easy
increased pt adherence
accurate dosing mechanisms
55
insulin pumps
for motivated pts
expensive
continuous
only use rapid acting insulin
programmed to give basal and bolus doses
hx feature
lots of support and education
56
modern meters
accurate
check FS intermittently
57
continuous glucose monitoring
benefits: more complete glucose profile than traditional SMBG, tracking of meal related glycemic trends, detection of nocturnal hypoglycemia, facilitation of changes in insulin regimens, alarm for highs and lows
challenges: daily SMBG still required, not suited to many pts, limited accuracy (esp hypoglycemia), glycemia pattern results confusing and subject to interpretation
58
weight gain on insulin
reverses catabolic effect of DM
glycosuria decreased
risk of hypoglycemia
pts increase caloric intake and avoiding exercise
risk of weight gain decreases w/more physiologic insulin admin
flexible insulin dosing to meet dietary and exercise needs
59
physiologic multiple injection regimen
BASAL=BASELINE. controls glucose production between meals and overnight. near constant level.
BOLUS (mealtime/prandial)- limits hyperglycemia after meals. immediate rise and sharp peak at 1 hour post meal
60
ideal insulin replacement
each component should come from a different insulin w/a specific profile or via insulin pump (w/1 insulin)
you want your insulin peaks to correspond w/meals
61
typical daily insulin requirements in adults
total daily dosage affected by body size, adiposity (fat), physical activity, and remaining endogenous insulin
**daily dosage usually 0.3-0.8 U/Kg in adults**
**daily dosage usually 50% basal/50% bolus insulin**
62
regular +NPH
give 2/3 dose in AM (prior to meal- 2/3 NPH and 1/3 regular)
give 1/3 in PM (prior to meal/bedtime- 1/3 NPH+1/3 regular)
advantage- inexpensive, 2-3 injections/day
disadvantage- does NOT mimic physiologic insulin secretion
63
basal/bolus insulin
physiologic insulin therapy/"poor man's insulin pump"
50% insulin requirement=long acting (controls fasting BG, basal insulin dose)
50% insulin requirements as rapid acting insulin (divide into 3 doses, controls post prandial plasma glucose, bolus insulin doses w/meals)
ex: total requirement= 60 U/day- lantus 30 units QHS and 10 units humalog w/meals
64
basal/bolus insulin considerations
education: need to learn carb counting. must be a motivated/competent patient.
advantages: mimics physiologic insulin secretion, less hypoglycemia, flexible
disadvantages: cost, frequency of injections
65
correction insulin "1800 rule"
used in addition to basal/bolus dosing
assists in controlling post prandial hyperglycemia
"1800 rule"= if pt requires 50 U/day, 1800/50=36. **suggests that 1 unit of rapid acting insulin will decrease BG by 36**
can be more pt specific than regular sliding scale
66
glargine AM, PM, or bedtime with rapid-acting analogue w/each meal
glargine 18 U at bedtime
lispro 6 U before breakfast/lunch/dinner
67
detemir at PM or bedtime, or in AM plus PM or bedtime with rapid-acting analogue w/each meal
detemir 8 U before breakfast
glulisine 6 U before breakfast/lunch/dinner
detemir 10 U at bedtime
68
insulin dose adjustments
**based on glycemic pattern over several days**
***generaly, change only 1 component of insulin at a time!!!***
morning fasting glucose too high/low so increased/decrease total basal insulin by 10%
post-prandial glucose too high/low so adjust carb to insulin ratio
PPG too low so decrease bolus insulin
correction dose insufficient so adjust correction factor
69
ADA/EASD DM 2 tx algorithm
**monotherapy-metformin**
dual therapy if you don't get goal A1C after 3 months of monotherapy- metformin and another drug
triple therapy- metformin and another drug and another drug
70
what medication should you always start with for type 2 DM?
metformin unless there's a CI (i.e. women w/Cr of 1.5)
withhold metformin before and after any type of IV dye
71
defect of beta cells
increased insulin available d/t use of secretagogues/exogenous insulin
72
defect of liver
suppressed hepatic glucose production d/t impaired counter regulatory response
73
defect of skeletal muscle
increased glucose uptake d/t exercise
74
defect of alpha cells
suppressed glucagon d/t impaired counter regulatory response
75
defect of brain
hypoglycemia unawareness
76
insulin, glucagon, and glucose homeostasis
brain senses plasma glucose concentration and provides regulatory inputs which leads to homeostasis
77
GLP1
glucagon like peptide 1
stimulates insulin secretion and inhibits glucagon secretion which leads to decreased post meal glucose abnormalities
78
incretin effect in DM2
increases stimulation of insulin secretion from PO glucose
in pts w/DM2, the incretin effect is decreased which leads to increased blood sugars
79
CSII in DM2 pt candidates
absolutely insulin deficient
take 4 or more insulin injections/day
assess BG 4x or more/day
motivated to achieve tighter glucose control
**competency in carb counting, insulin correction, and adjustment formulas**
ability to troubleshoot problems related to pump operation and plasma glucose levels
stable life situation
frequent contact w/HCP's
80
risk factors for hypoglycemia
risk factors: older pt females, AA's, longer duration of DM, neuropathy, renal impairment, previous hypoglycemia, missing meals, increased A1C
81
consequences of hypoglycemia
cognitive changes (confusion, irritability)
accidents
falls
recurrent hypoglycemia and hypoglycemia unawareness
refractory DM
dementia (elderly)
CV events: cardiac autonomic neuropathy, cardiac ischemia, angina, fatal arrhythmias
82
symptoms of hypoglycemia
mild- 50-70: neurogenic- palpitations, tremor, hunger, sweating, anxiety, paresthesia
severe- <50: severe confusion, unconscious, seizure, coma, death
83
higher risk of hypoglycemia with which medications?
metformin+SULFONYLUREAS and INSULIN (basal, basal-plus, premixed)
84
tx of hypoglycemia
conscious: give glucose. repeat Q15 min after episodes
unconscious: glucagon injection and taken to hospital
85
age considerations in making A1C goals for patients
older adults- decreased life expectancy, higher CVD burden, decreased GFR, at risk for adverse events from polypharmacy, more likely to be compromised from hypoglycemia
86
weight considerations in making A1C goals for patients
majority of DM2 are overweight/obese, intensive lifestyle program, metformin, GLP-1 receptor agonists, bari surgery
87
sex/race considerations in making A1C goals for patients
latinos= more insulin resistant
east asians= more beta cell dysfunction
gender may drive concerns (i.e. bone loss from TZDs)
88
comorbid disease in DM
CAD- avoid TZDs!!!
HF- avoid TZDs and metformin!
renal dx- increased risk of hypoglycemia and lactic acidosis, caution w/sulfa, DPP-4- dose adjusted for renal dx, avoid exenatide GFR<30
liver dx- insulin is best option
hypoglycemia
89
ADA guidelines for glycemic, BP and lipid control
A1C<7%
pre-prandial (fasting) 70-130
post-prandial <180
BP< 130/80
lipids:
LDL<100, <70 w/CVD
HDL>40 (men) and >50 (women)
TG<150
90
eye complications of diabetes
microvascular
high blood glucose and high blood pressure can damage eye blood vessels, causing retinopathy, cataracts and glaucoma
91
kidney complications of diabetes
microvascular
high blood pressure damages small blood vessels and excess blood glucose overworks the kidneys, resulting in nephropathy
92
neuropathy complications of diabetes
microvascular
hyperglycemia damages nerves in the peripheral nervous system. this may result in pain and/or numbness.
feet wounds may go undetected, get infected and lead to gangrene.
93
brain complications of diabetes
macrovascular
increased risk of stroke and cerebrovascular disease, including transient ischemic attack, cognitive impairment, etc.
94
heart complications of diabetes
macrovascular
high blood pressure and insulin resistance increase risk of coronary heart disease
95
extremities complications of diabetes
macrovascular
peripheral vascular disease results from narrowing of blood vessels which increases the risk for reduced or lack of blood flow in legs
feet wound are likely to heal slowly contributing to gangrene and other complications
96
what is the foundation of DM2 programs?
diet, exercise, and education
97
after trying metformin first, what is the next step?
combination therapy w/ 1-2 other oral injectable agents is reasonable
98
how often should you evaluate therapy?
Q3 months until stable
