DM Tx Flashcards
(106 cards)
1
Q
Antibodies associated w/ T1
A
GAD-65 antibodies
Islet Cell antibodies
2
Q
Factors leading to hyperglycemia
A
impaired insulin secretion increased glucagon secretion increased hepatic glucose production neurotransmitter dysfunction decreased glucose uptake increased glucose reasbsorption increased lipolysis and reduced glucose uptake decreased incretin effect
3
Q
Dx of DM
A
fasting >126
OGTT >200
HbA1C >6.5
Random glucose >200 + symptoms
- confirm w/ additional test
4
Q
Other tests to consider for DM
A
antibodies (GAD-65 and islet cell antibodies)
fasting insulin, C-peptide (how bad)
urine ketones and albumin excretion
5
Q
Comorbidities
A
ASCVD Hypothyroidism CKD Hyperlipidemia Hypertension
6
Q
ASCVD
A
CHD: MI, angina, revascularization
cerebrovascular disease: stroke, TIA
PAD
7
Q
Risk factors for ASCVD
A
obesity dyslipidemia HTN smoking family hx of CAD CKD Albuminuria Diabetes
8
Q
How often do you screen for ASCVD risk factors
A
yearly
9
Q
Leading cause of morbidity/mortality for people w/ DM
A
ASCVD
10
Q
What drugs reduce CV events?
A
Empagliflozin
Liraglutide
Canagliflozin
Dulaglutide and semaglutide = reduce CV events, but not all cause mortality
11
Q
DM Management goals:
A
HbA1C Urine microalbumin BP Lipids Coagulopathy
12
Q
HbA1C goals
A
<6.5% (AACE)
<7% (ADA)
13
Q
Drugs if you note urine microalbuminuria
A
ACE/ARB
14
Q
BP goals
A
<140/90 (ADA)
<130/90 (AHA)
15
Q
DM lipid management
A
high intensity statin: DM + ASCVD (atorvastatin and rosuvastatin)
moderate intensity stati: >40 w/ DM
16
Q
High intensity statins
A
atorvastatin
rosuvastatin
17
Q
Anti-platelet therapy
A
ASA (75-162mg/day) in patients w/ ASCVD and DM
18
Q
ASVD drug regimen
A
High intensity statin
Anti-platelet
+/- ACE/ARB
19
Q
Tx for T1 DM
A
Insulin!!! - Basal/Bolus, fixed dose
20
Q
Tx guidelines
A
A1C <9: Monotherapy (metformin)
A1C >9: Dual therapy
A1C >10 or blood glucose >300 or very symptomatic: consider combo injectable therapy
21
Q
AACE HbA1C goals
A
<6.5 w/o other disease or ris of hypoglycemia
>6.5 w/ concurrent illness and risk of hypoglycemia
22
Q
AACE guidelines of Tx
A
A1C <7.5: mono
>7.5 Dual (proceed to triple if don’t reach goal by 3 mo)
>9 + sx: insulin + other agents
>9 w/o sx: dual/triple therapy
23
Q
1st line for DM
A
Metformin
24
Q
MOA of metformin
A
decreased hepatic glucose production decreases intestinal absorption increase insulin sensitivity! increase glucose utptake decrease FFA
25
Benefits of metformin
decrease CV death
| decrease LDL, increase HDL
26
how metformin works:
lipid accumulation normally stimulates PKC which then inhibits insulin receptor (resistance)
Metformin: stimulates AMPK to produce ACC-1 and ACC2- --> ACC2 lowers FFA --> no FFA to stimulate PKC so no inhibitition
27
Contra for metformin
```
CKD
GFR 30-45 avoid
GFR <30 C/I
Hepatic Disease
Acute/unstable HF
Metabolic acidosis/lactic acidosis/DKA
```
28
SE for metformin
GI (DIARRHEA)! - decreased w/ ER
Black box warning: lactic acidosis - hold before contrast
deplete B12- neuropathy
29
Monitor for metformin
GFR
CBC
LFT
B12
30
TZD drugs
pioglitazone
| rosiglitazone
31
MOA of TZD
bind PPAR=gamma and lead to increased insulin receptor synthesis -- INCREASE INSULIN SENSITIVITY
32
When to consider TZD
early DM and high insulin resistance
33
SE of TZD
edema, fluid retention, weight gain
CHF! - monitor for excessive weight gain, dyspnea, or edema
Reduces bone density - may increase fractures in women!
rare hepatotoxicity
34
C/I of TZD
III-IV CHF or symptomatic CHF
| active bladder CA (Pioglitazone)
35
C/i in active bladder CA
pioglitazone
36
Monitor for TZD
LFT (rare risk of hepatotoxicity)
37
Sulfonylurea drugs
glimepiride
glipizide
glyburide
38
MOA of SU
depolarize cell (via closing K+ channel) and STIMULATE BETA- CELL INSULIN RELEASE
39
Increase insulin sensitivity
Metformin
| TZD
40
Increase insulin release
SU
| GLP-1
41
Why are SU good?
inexpensive
| effective in early DM
42
SE of SU
hypoglycemia!
weight gain
lower dose if used w/ insulin or GLP-1
43
C/I of SU
Elderly
| Sulfa allergy
44
DDP-4 Inhibitor drugs
```
-gliptins:
Sitagliptin
Linagliptin
Saxagliptin
Alogliptin - generic
```
45
MOA fo DDP-4 I
inhibit DDP-4 which SLOWS BREAKDOWN OF GLP-1, restores insulin and glucagon to physiological levels
46
Effect of DDP-4 I
Modest decrease in HgA1C
47
SE of DDP-4I
peripheral edema- caution in HF
| Pancreatitis**
48
Edema
TZD
| DDP-4
49
Excretion of DDP-4I
renal: sitagliptin, saxagliptin, alogliptin
Feces: lingagliptin -- OK to use in renal impairment
50
CI
risk of pancreatitis
HF
Renal impairment (except linagliptin)
51
feces excretion
linagliptin
52
GLP-1 drugs
```
Exenatide (daily)
exenatide (weekly)
Liraglutide (daily)
dulaglutide
Dulaglutide (weekly)
Semaglutide (weekly)
```
53
Weekly GLP-1
exenatide (one type)
dulaglutide
semaglutide
54
Daily GLP-1
exenatide
| liraglutide
55
MOA of GLP-1 drugs
activates GLP1 receptor
- increase insulin secretion
- decrease glucagon
- slow gastric emptying and increase satiety (promotes weight loss)
- may increase beta cell mass and function
56
Slow gastric emptying
GLP1
57
weight loss
GLP1
Glycosides inhibitors
SGLT-2
Primantide
58
increases beta cell mass and function
GLP-1
59
Kinetics of GLP-1
injected! - pt adherence,
weekly preps available
exenatide weekly- depot under skin, may take 6-7 weeks for full efficacy
weight loss/appetite control
60
SE of GLP-1
GI - N/v/decreased appetite
titrate slow to improve response
Thyroid C-cell tumor risk**** (black box)
- medullary thyroid carcinoma (MTC)
- family hx of MTC
- multiple endocrine neoplasia syndrome type 2 (MEN2)
61
C/I in MEN2
GLP-1
62
Education for GLP-1
thyroid tumor symptoms
- neck mass
- dysphagia
- dyspnea
- persistent hoarseness
63
Thyroid CA
GLP-1
64
CI for GLP-1
Pancreatitis
gastroparesis (slows emptying)
MEN2?
Exenatide - avoid in GFR <30
65
ASCVD and GLPS1
Liraglutide- reduced CV mortality and all cause mortality
semaglutide and dulaglutide (not all cause mortality)-- not FDA approved red
66
SGLT2 MOA
inhibit sodium-glucose cotransporter 2 in proximal tubule
- reduced renal glucose reabsorption
- increase urinary glucose secretion
67
SGLT2 drugs ("glucoretics")
-gliflozins
canagliflozin
empagliflozin
dapagliflozin
entugliflozin
68
Tests in SGLT2
monitor GFR!!
monitor hydration
monitor hyperkalemia (canagliflozin)
monitor ulcers/pain/infection --Amputation risk
69
CI of SGLT2
GFR <45: canagliflozin, empagliflozin
GFR <60: dapagliflozin, ertugliflozin
C/I GFR <30
70
SE for SGLT-2
dehydration
hyperkalemia (canagliflozin)
AMPUTATION -- avoid canagliflozin or whole class
diuresis - caution in elderly and hypotensive patients
GU/mycotic infections
DKA!! (FDA warning) (euglycemic DKA)
71
Triggers for DKA in SGLT-2
reduced fluid/food intake
reduced insulin doses
hx of alcohol intake
concurrent illness
cause: reduced availability of carbs and reduced insulin
72
Amputation
canagliflozin
73
Risk factors of lower limb amputation
Prior amputation hx
PVD
Neuropathy
Diabetic foot ulcer
74
ACVSD and SGLT-2
empagliflozin- reduced CV death, reduction of hospitilizations in pts w/ CHF
canagliflozin- reduced CV death, MI, stroke; FIRST ORAL TO REDUCE CV EVENTS
75
first oral to reduce CV events
canagliflozin
76
MOA of insulin
stimulates peripheral glucose uptake
inhibits glucose production
inhibits lipolysis
regulates glucose mettabolism
77
When is insulin given
A1C >10%, glucose level >300
option when metformin or multi drug therapies don't work
78
SE of insulin
hypoglycemia
weight gain
hunger
nausea
79
Basal insulin (long-acting)
lowers glucose evenly over 24 hours
glargine
detemir
degludec
80
Intermediate acting insulin
start: 2-4 hrs post injection
peak: 4-12 hrs
last: 12-18 hrs
Drugs: Insulin NPH (Humulin N, Novolin N)
not commonly used
81
Regular/short acting insulin (Bolus)
start: 30 min
peak: 2-3 hrs
last: 3-6 hrs
Drugs: Regular insulin (humulin R, novolin R)
not commonly used
82
Rapid acting insulin ("mealtime" or "correction")
start: 15 min
peak: 1 hrs
last: 2-4 hrs
Drug: lispro, aspart, glulisine
83
Premixed insulin
insulin NPH/insulin regular
insulin lispro protamineinsulin lispro
insulin aspart protamine/insulin aspart
84
When is premixed insulin good
pts stable on insuline
regular diet (same each day)
good choice if they have poor adherence to basal-bolus regimen
85
SE or premixed insulin
hypoglycemia
86
How to treat w/ insulin
fix fasting glucose first - basal insulin (detemir, glargine, degludec) - calculate TDD or starts w/ 10 units QHS (bed time)
87
normal fasting glucose
| A1C elevated
overbasalization
| consider adding meal-time or bolus insulin
88
Overbasalization
assuming beta cell function is well enough to cover meal time insulin
DO NOT KEEP INCREASING BASAL DOSING - risk for hypoglycemia (esp. nocturnal hypoglycemia)
only 1/2 of TDD should be basal
89
Insulin pumps contain
rapid acting (lispro, aspart, glulisine)
90
When to consider pump
- pts who are testing and injecting multiple times/day and cannot achieve normal A1C
- pts w/ frequent hypoglycemia
91
Somogyi effect
morning hyperglycemia in response to undetected nocturnal hypoglycemia
- common w/ exogenous insulin
92
Dawn phenomenon
morning hyperglycemia due to elevated AM hormone levels (HGH, Cortisol, EPI) and decreased insulin action
93
Hypoglycemia tx
oral glucose (avoid fats) - recheck BG in 15 min, follow up with snack
IV glucose
Glucagon (IM) - unwilling to consume orally, train caregivers
94
DKA presentation
rapid onset of:
- hyperglycemia
- ketonemia
- acidemia
95
Etiology of DKA
absence of insulin
elevated counter-regulatory hormones (glucagon, catecholamines, cortisol, GH)
causes extreme metabolic derangement
96
Precipitating events to DKA
inadequate insulin therapy
infection
stress
potentially fatal- requires prompt medical attention
97
Sx of DKA
```
dehydration- mucous membranes
polydipsia, polyphagia
n/v, abdominal pain
weight loss
shock (severe cases)
```
98
PE for DKA
```
kaussmal breathing
"fruity breath"
tachypnea, tachycardia
altered mental status
decreased skin turgor
orthostatic hypotension
```
99
DKA labs
glucose >250
UA- glucose + ketones
Serum ketones +
BMP: elevated anion gap, electrolyte imbalance (K, Na, Cl, Ca)
CBC- elevated WBC
ABG: arterial pH needed to diagnose DKA - venous pH to monitor treatment
100
How to monitor treatment in DKA
venous pH
101
Treatment of DKA
HOSPITILIZE
Restore volume deficit
- IV fluids (D5W when glucose <200)
- avoid rapid fluid/electrolyte replacement esp in peds--> cerebral edema
Resolve hyperglycemia & ketosis/acidosis (IV insulin)
Correct Electrolyte abnormalities
Treat underlying cause (infection?)
102
Overall DKA tx
IV fluids
Insulin
Tx electrolytes and underlying cause
103
Non-ketotic hyperglycemic hyperosmolar syndrome (NKHS) or (HHS)
profound hyperglycemia >600!
osmotic diuresis (due to hyperglycemia)
NOT ACIDOTIC
absent or minimal ketones in UA/blood
104
Etiology of NKHS
insulin deficiency + increased counterregulatory hormones
Infection may precipitate (PNA or UTI)
More common in older type 2 diabetics (rare but deadly)
105
Presentation of NKHS
```
AMS
Polyuria, polydipsia
weakness
tachycardia
decreased BP, dehydration, shock
```
106
Tx for NKHS
HOSPITILIZE
| IV fluid, IV insulin, electrolyte correction
