Diabetes Milletus Flashcards
1
Q
- Most common endocrine disorder
A
Diabetes Mellitus
2
Q
- Chronic condition
A
Diabetes Mellitus
3
Q
- A group of metabolic disease
characterized by inappropriate
chronic hyperglycemia with
disturbances of carbohydrates, fats and protein metabolism resulting from defect in insulin secretion, insulin action or both
A
Diabetes Mellitus
4
Q
- Infantile or
Childhood - Young
- Adult
- Elderly
A
1965
5
Q
- Insulin
dependent DM - Non-Insulin
Dependent DM - Other Types
A
1985
6
Q
- type 1
- type 2
A
1999
7
Q
- type 1
- type 2
- specific type due to other causes
- gestational diabetes
A
2023
8
Q
- Destruction of pancreatic beta cell
responsible of insulin production - Associated with autoimmune disease
- Usually develops in children and
young adult - Associated with a faster onset of
symptoms, leading to dependency on
extrinsic insulin for survival
A
type 1 DM
9
Q
- More common type of diabetes
- Occurs in adults older than 40 years
- Peaks onset between 60 and 70
years - Caused by a relative insulin
deficiency and the body’s inability to
effectively use insulin - Symptoms are slower in onset and
less marked than those of Type 1 DM
A
Type 2 DM
10
Q
- Hyperglycemia that is first detected during pregnancy, usually
diagnosed during the 2nd or 3rd trimester
A
Gestational diabetes
11
Q
- Hyperglycemia in pregnancy is associated with adverse
outcomes, including hypertension or pre-eclampsia, fetal
macrosomia or fetal death
A
Gestational diabetes
12
Q
adverse outcomes from hyperglycemia in pregnancy
A
pre-eclampsia, fetal macrosomia, fetal death
13
Q
Diabetes is a result of a pre-existing condition
A
Specific Type due to other causes
14
Q
Acute, symptomatic
A
Type 1 DM
15
Q
Slow, often asymptomatic; symptoms occur when condition is already chronic
A
Type 2 DM
16
Q
Weight loss, polyuria,
polydipsia, polyphagia
A
Type 1 DM
17
Q
If symptomatic, similar with T1DM + obese, strong family history of T2DM, PCOS
A
Type 2 DM
18
Q
body burns fat for energy instead of glucose
A
ketosis
19
Q
Ketosis: Almost always present
A
Type 1 DM
20
Q
Ketosis: Usually absent
A
Type 2 DM
21
Q
Biomarker that indicates how much insulin your body has
A
C-peptide
22
Q
C-peptide: Low or absent
A
Type 1 DM
23
Q
C-peptide: Normal or elevated
A
Type 2 DM
24
Q
Antibodies
- Positive: Islet Cell Antibodies
(ICA), ICA 512, Anti-Glutamic
Acid Decarboxylase (Anti-GAD)
A
Type 1 DM
25
Antibodies
- Negative: Islet Cell Antibodies (ICA), ICA 512, Anti-Glutamic Acid Decarboxylase
(Anti-GAD)
Type 2 DM
26
Insulin
Type 1 DM
27
Lifestyle modification, Oral anti-diabetic agents, Insulin
Type 2 DM
28
Associated auto-immune
diseases: yes
Type 1 DM
29
Associated auto-immune
diseases: No
Type 2 DM
30
Glucose enters the cell via theGLUT 2 transporter → glycolysis → ATP (by product) will bind to ATP sensitive K-channels →K-channel will close, preventing K efflux → depolarization due to increased K → signal Ca channel to open → entry of Ca inside cell→ stimulation of insulin production through a vesicle → bloodstream
main pathway
31
Glutamic acid -> Glutamic acid decarboxylase -> GABA -> insulin
alternative pathway
32
inhibits formation of GABA and will lead to Type 1 DM
Anti-GAD antibodies
33
Hormones affecting sugar
levels in the body
- insulin
- counterregulatory hormones
- incretin hormones
- amylin
34
Regulates CHO, CHON and
lipid metabolism by
promoting glucose uptake
into the cell
Insulin
35
Promotes conversion of
glucose to glycogen
Insulin
36
Facilitates cellular uptake of
amino acids
Insulin
37
Decreases the breakdown of
fatty acids into ketone bodies
insulin
38
Produced during low glucose
levels to increase the amount
of glucose in the body
Counterregulatory hormones
39
Antagonizes insulin effects
Counterregulatory hormones
40
Promotes conversion of
glycogen to glucose
Counterregulatory hormones
41
glucagon, growth hormones,
catecholamines, cortisol
Counterregulatory hormones
42
Released or secreted after
meal or nutrient intake to
stimulate release of insulin
incretin
43
Inhibits inappropriate glucone
secretion and increases beta
cell growth and reproduction
incretin
44
Suppresses appetite
incretin
45
Gastric inhibitory peptide
(GIP) and Glucagon-like
peptides (GLP)
incretin
46
Co-secreted with insulin
amylin
47
Lowers post-prandial blood
glucose level by prolonging
the gastric emptying time
amylin
48
Reduces post-prandial
glucagon secretion
amylin
49
Suppresses appetite
(2)
amylin
50
Human Leukocyte Antigen (HLA) DQA
and DQB appear to code for either
disease susceptibility or resistance
T1DM Genetics
51
Viral, chemical or dietary
T1DM environment
52
Assigns if person is susceptible or resistant to DM
DQA and DQB
53
- Anti-insulin ,anti-beta cell antibodies
- Antibodies to glutamic acid
decarboxylase
T1DM autoimmunity
54
> 90% concordance rate in identical twins if one has _______
T2DM genetics
55
Improper insulin secretion
T2DM Beta cell dysfunction
56
Post-receptor binding, a decreased number of insulin receptor or defects in insulin receptors can lead to hyperglycemia
T2DM peripheral site defect
57
Risk factors for diabetes
- overweight or obesity (+)
- Maternal history of DM or GDM during the child’s gestation
- Family history of T2 DM in first- or second-degree relative
- Race/ethnicity (Native American, African American, Latino, Asian American, Pacific Islander)
- Signs of insulin resistance or conditions associated with insulin resistance (acanthosis nigricans, HTN, dyslipidemia, PCOS, or small-for-gestational-age birth weight)
58
- Glucosuria
- Polyuria
- Polydipsia
- Polyphagia
- Weight loss
Most common clinical manifestations
59
≥ 126 mg/dL
Fasting Blood Glucose Level
60
≥ 200mg/dL
Random Blood Glucose Level/ Oral Glucose Tolerance Test
61
≥ 6.5%
Hemoglobin A1c
62
- Atherosclerosis
>Stroke, Heart Attack, Artery Disease
- Retinopathy
>Cataract, Glaucoma
- Neuropathy
>Diabetic Foot, nerve endings
- Nephropathy
> liver, nephron damage
Complications associated with Diabetes
63
acanthosis nigricans, HTN, dyslipidemia, PCOS, or small-for-gestational-age birth weight
Clinical conditions with Insulin resistance
64
- Prevent Complications
- Optimize Quality of Life
Treatment goals
65
< 7.0%
A1C - glycemic recommendations for many nonpregnant adults with diabetes
66
80 - 130 mg/dl
pre prandial CPG - glycemic recommendations for many nonpregnant adults with diabetes
67
<180 mg/dl
peak post-prandial CPG (1-2 hours after meal) - glycemic recommendations for many nonpregnant adults with diabetes
68
- Required for glycemic management in individuals with T1DM
- May be used in combination with oral agent or amylin agonist
- May also be initial or adjunctive agent for individual with T2DM
Insulin
69
- Stimulates hepatic glycogen synthesis
- Increase protein synthesis
- Facilitates triglyceride synthesis and storage by adipocytes
- Inhibits lipolysis
- Stimulates peripheral uptake of glucose
MOA of Insulin
70
- inject 10 -15 mins before mealtime
- typically used in conjunction with longer-acting insulin
RAPID acting
71
Inject at least 20-30 minutes before mealtime
SHORT acting
72
- commonly used twice daily
- often combined with rapid or short acting insulin
INTERMEDIATE acting
73
- covers insulin needs for 24 hrs
- if needed, often combined with rapid or short acting insulin
LONG acting
74
- combination of intermediate and short acting insulin
- commonly used twice daily before mealtime
PRE-MIXED
75
Long acting no peak
Lantus or Glargine
76
Amylin Receptor Agonists
Pramlintide
77
Enhance post-prandial control in individual with
T1DM and T2DM
Amylin Receptor Agonists indication
78
Gastric motility disorder
Amylin Receptor Agonists contraindication
79
- Slow gastric emptying time
- Decrease post-prandial glucagon secretion
- Suppresses appetite
MOA of Amylin Receptor Agonists
80
GLP-1 agonist
Incretin mimetics
81
Incretin mimetics
Exenatide, Liraglutide, -glutides
82
Management of T2DM
Indication of incretin mimetics
83
Severe GI motility, pancreatitis, renal or hepatic impairment
Contraindication of incretin mimetics
84
- Increase glucose-dependent insulin secretion,
- Decrease hepatic glucose output
- Increase beta cell growth and replication
- Slow gastric emptying time
- Enhance satiety or feeling of fullness to suppress appetite
MOA of Incretin mimetics
85
Dipeptidyl peptidase IV (DPP IV) inhibitors
Sitagliptin, Saxagliptin, Linagliptin
86
Patients with T2DM with normal or impaired
hepatic and renal function
Indication of Dipeptidyl peptidase IV (DPP IV) inhibitors
87
Pancreatitis
Contraindication of Dipeptidyl peptidase IV (DPP IV) inhibitors
88
- Prevents the inactivation of incretin hormones by the
enzyme DPP IV during hyperglycemia
- Inhibits the breakdown of GLP-1 allowing increased
insulin secretion and decrease hepatic glucose production
MOA of Dipeptidyl peptidase IV (DPP IV) inhibitors
89
- Targets fasting blood glucose level
- Binds to and inhibits the ATP-sensitive potassium channels to increase the beta cell sensitivity to glucose and stimulate the secretion of insulin
- Protein-bound
- Prone to drug-drug interactions
Sulfonylureas
90
- Typically not prescribed since 2nd gen has fewer ADR
- Associated with thrombocytopenia, agranulocytosis, hemolytic anemia, hyponatremia, SIADH, disulfiram-like reactions
1st Generation Sulfonyureas
91
- Tolbutamide, Tolazamide, Chlorpropamide
1st Generation Sulfonyureas
92
Glyburide, Glipizide, Glimepiride
2nd Generation Sulfonyureas
93
Meglitinide
Repaglinide
94
Phenylalanine derivatives
Netaglinide
95
Insulin Secretagogues
Sulfonyureas, Meglitinide, Phenylalanine derivatives
96
- Management for T2DM
- Targets post-prandial glucose control
Indication of Meglitinide and Phenylalanine derivatives
97
Binds to ATP-sensitive potassium channel to stimulate secretion of insulin from pancreatic Beta cell, reduces hepatic glucose output
MOA of Meglitinide and Phenylalanine derivatives
98
Severe renal and hepatic dysfunction
- Used in caution in elderly due to increased risk of fall
Contraindication of Meglitinide and Phenylalanine derivatives
99
Biguanides
Metformin
100
- Used for the glycemic control for management of T1DMand T2DM
- Targets fasting blood glucose
Biguanides
101
First line medication for newly diagnosed diabetes
Metformin
102
Renal disease, Hepatic impairment, HF
Contraindication of Biguanides
103
- Inhibits hepatic glucose output, thus exerting beneficial effects on fasting blood glucose level
- Promotes glucose uptake by fat and muscles, improving insulin sensitivity
- Minor role in decreasing intestinal absorption of glucose
MOA of biguanides
104
Thiazolidinediones (TZDs)
Pioglitazone, Rosiglitazone
105
Glycemic control in T2DM and primarily affects
fasting blood glucose level
Indication of Thiazolidinediones (TZDs)
106
Hepatic dysfunction, Class III/IV HF, Anemia, Fracture risk
Contraindication of Thiazolidinediones (TZDs)
107
Alpha-glucosidase Inhibitors
Acarbose, Miglitol
108
Management of post-prandial blood glucose
Indication of Alpha-glucosidase Inhibitors
109
IBD
Contraindication of Alpha-glucosidase Inhibitors
110
with serum creatinine of > 2.0mg/dL or
creatinine clearance of < 25mL/min; hepatic impairment
Acarbose
111
Competitive inhibition of alpha-glucosidase in the
intestinal brush border, which leads to slower
absorption of complex carbohydrates
MOA of Alpha-glucosidase Inhibitors
112
Sodium-Glucose Cotransporter Inhibitors
-New class of oral hypoglycemic agent
Canagliflozin, Dapagliflozin, and Empagliflozin
113
Selectively and reversibly inhibits the sodium-glucose
cotransporter which is selectively expressed in the
proximal renal tubule
MOA of Sodium-Glucose Cotransporter Inhibitors
114
T2 DM + Atherosclerotic
Cardiovascular Disease (ASCVD)
Monotherapy of Glucagon-Like Peptide-1 Receptor Agonists (GLP-1 RA) or Sodium Glucose Cotransporter 2 (SGL2) Inhibitors [Canagliflozin, Dapagliflozin, Empagliflozin]
115
T2 DM + Atherosclerotic
Cardiovascular Disease (ASCVD)
> If A1C above target
consider combination therapy or add Thiazolidinediones (TZDs) [Pioglitazone, Rosiglitazone]
116
T2 DM + Heart Failure
Sodium-Glucose Cotransporter 2 (SGL2) Inhibitors [Canagliflozin, Dapagliflozin, Empagliflozin]
117
T2 DM + Chronic Kidney Disease (CKD)
Sodium-Glucose Cotransporter 2 (SGL2) Inhibitors [Canagliflozin, Dapagliflozin, Empagliflozin] OR Glucagon-Like Peptide-1 Receptor Agonists (GLP-1 RA) [Exenatide,
Liraglutide]
118
T2 DM + Chronic Kidney Disease (CKD)
> If A1C above target
consider combination therapy of SGL2I and GLP-1 RA
119
Glycemic Control
Metformin
120
If glycemic control is not achieved
combination therapy with other oral hypoglycemic agents
121
(Efficacy for Glucose Lowering) Very high
- high dose dulaglutide
- semaglutide
- tirzepatide
- insulin
- combination GLP-1RA-Insulin
122
(Efficacy for Glucose Lowering) High
- GLP-1 RA
- Metformin
- SGLT2i
- Sulfonylureas
- TZDs
123
(Efficacy for Glucose Lowering) Intermediate
DPP4 Inhibitors
124
(Efficacy for Weight Loss) Very high
- Semaglutide
- Tirzepatide
125
(Efficacy for Weight Loss) High
- Dulaglutide
- Liraglutide
126
(Efficacy for Weight Loss) Intermediate
GLP-1RA, SGLT2i
127
(Efficacy for Weight Loss) Neutral
- DPP4 inhibitors
- Metformin
128
T2 DM + Weight Control Problems
- Set individualized weight management goals
- Lifestyle modification, nutrition programs,
physical activity, metabolic surgery
129
HbA1c <9%
FBS < 250
- Monotherapy
- Option for combination
130
HbA1c >= 9%
FBS >= 250
- combination
- insulin
131
World diabetes day
Nov 14
132
three things to remember in DM
chronic, uncontrolled, and hyperglycemia
133
Insulin should not be stopped (t or f)
T
134
Blood glucose less than 13 mmol/L (or less than 230 mg/dL)
Continue with current medication
135
Blood glucose 13-22 mmol/L (or 230-390 mg/dL)
Patient should inject insulin by 2 units per injection, even if unable to eat
136
Blood glucose greater than 22 mmol/L (or 390 mg/dL)
Patient should increase his insulin by 4 units per injection, even if unable to eat
