Diabetes mellitus Flashcards
1
Q
Diabetes mellitus
A
is a group of metabolic diseases characterized by hyperglycemia due to defects in insulin secretion or action
2
Q
Diabetes mellitus is often accompanied by hypertension and hypercholesterolemia
A
increasing the risk of complications
3
Q
Type 1 diabetes
A
accounts for less than 10% of cases and results from autoimmune destruction of pancreatic beta cells
4
Q
Type 1 diabetes requires exogenous insulin
A
to control blood glucose and prevent diabetic ketoacidosis
5
Q
The honeymoon phase in type 1 diabetes
A
is a transient period of reduced insulin requirement early in the disease
6
Q
Type 2 diabetes
A
accounts for more than 90% of cases and is initially characterized by insulin resistance
7
Q
Type 2 diabetes risk factors
A
include older age
8
Q
Ketosis in type 2 diabetes
A
is usually prevented by sufficient insulin secretion but can occur during severe stress
9
Q
Other specific types of diabetes
A
include MODY
10
Q
Gestational diabetes mellitus
A
is abnormal glucose tolerance first detected during pregnancy
11
Q
Women with pre-existing diabetes before pregnancy
A
are not classified as having gestational diabetes
12
Q
After delivery in gestational diabetes
A
glucose tolerance usually returns to normal but increases the risk of type 2 diabetes
13
Q
The A1C diagnostic threshold for diabetes
A
is 6.5% or higher
14
Q
Classic diabetes symptoms with random plasma glucose of 200 mg/dL or more
A
confirm a diabetes diagnosis
15
Q
Fasting plasma glucose of 126 mg/dL or higher
A
is diagnostic for diabetes
16
Q
Two-hour plasma glucose of 200 mg/dL or more during an OGTT
A
confirms diabetes diagnosis
17
Q
Prediabetes fasting glucose range
A
is 100-125 mg/dL
18
Q
Prediabetes A1C range
A
is 5.7-6.4%
19
Q
Prediabetes 2-hour OGTT range
A
is 140-199 mg/dL
20
Q
Normal glucose tolerance fasting glucose
A
is below 100 mg/dL
21
Q
Normal glucose tolerance A1C
A
is below 5.7%
22
Q
Management of diabetes involves three steps
A
glycemic control
23
Q
Diabetes treatment goals include A1C
A
below 7.0%
24
Q
Preprandial plasma glucose goal
A
is 90-130 mg/dL
25
Peak postprandial glucose goal
is below 180 mg/dL
26
LDL cholesterol goal in diabetes
is below 100 mg/dL
27
HDL cholesterol goal in diabetes
is above 40 mg/dL
28
Triglycerides goal in diabetes
is below 150 mg/dL
29
Assessment of glycemic control includes
self-monitoring of blood glucose and HbA1c testing
30
HbA1c testing should be done every 3 months
or at least twice a year in well-controlled patients
31
Dietary modification in diabetes
helps maintain ideal body weight and achieve proper nutrition
32
Exercise benefits in diabetes
include improved insulin sensitivity and reduced blood glucose levels
33
Medications for diabetes
are most effective when combined with diet and exercise
34
Type 1 diabetes clinical presentation
includes abrupt onset of polyuria
35
Type 1 diabetes may be triggered
by an unrelated illness or stress on an already-limited islet reserve
36
Diabetic ketoacidosis may be the first presentation
for a minority of type 1 diabetes patients
37
Type 1 diabetes incidence increases in winter
due to respiratory viral infections
38
Puberty and type 1 diabetes
are linked due to insulin resistance from sex and growth hormone secretion
39
Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome
are the two main metabolic decompensation syndromes in diabetes
40
Diabetic ketoacidosis is more common in type 1 diabetes
but can also occur in type 2 under severe stress
41
Precipitating factors for diabetic ketoacidosis
include infection
42
Symptoms of diabetic ketoacidosis
include polyuria
43
Kussmaul respiration and fruity breath odor
are characteristic physical findings in diabetic ketoacidosis
44
Dehydration
respiratory distress
45
Laboratory findings in diabetic ketoacidosis
include elevated plasma glucose
46
Management of diabetic ketoacidosis
requires IV access
47
Fluid replacement in diabetic ketoacidosis
is critical due to severe dehydration of 7-9% body weight
48
Initial fluid resuscitation for diabetic ketoacidosis
should be isotonic (0.9%) saline
49
Insulin therapy in diabetic ketoacidosis
is needed to stop ketogenesis and lower blood glucose
50
A bolus of 10-15 units of regular insulin
should be followed by a continuous infusion in diabetic ketoacidosis
51
Blood glucose reduction in diabetic ketoacidosis
should be 50-75 mg/dL per hour
52
Excessively rapid glucose correction in diabetic ketoacidosis
increases the risk of osmotic encephalopathy
53
Dextrose infusion should start
when plasma glucose reaches 250 mg/dL to prevent hypoglycemia
54
Potassium deficit in diabetic ketoacidosis
should be assumed and monitored regardless of initial plasma levels
55
Bicarbonate therapy in diabetic ketoacidosis
is not routinely needed but may be used in severe acidosis
56
Type 2 diabetes results from
progressive beta-cell failure and insulin resistance
57
Type 2 diabetes patients
can develop diabetic ketoacidosis under severe stress
58
Polyuria
polydipsia
59
Type 2 diabetes may go undiagnosed
for years before symptoms appear
60
Severe hyperglycemia in type 2 diabetes
can present as hyperosmolar hyperglycemic syndrome
61
Type 2 diabetes metabolic defects
worsen over time requiring treatment escalation
62
Early type 2 diabetes
may be managed with diet and weight loss alone
63
Most type 2 diabetes patients
eventually require oral medications or insulin therapy
64
Microvascular complications may be the first sign
of type 2 diabetes in some patients
65
Treatment goals for type 2 diabetes
are the same as for type 1 diabetes
66
Type 2 diabetes treatment requires
individualized therapy with lifestyle and pharmacologic interventions
67
Oral therapy should be started early
if diet and exercise fail to control glucose
68
Monotherapy for type 2 diabetes
includes insulin secretagogues
69
Combination therapy or insulin
is needed if monotherapy fails to control glucose
70
Patients with glucose above 240 mg/dL at diagnosis
should start with combination therapy or insulin
71
Nonketotic hyperosmolar syndrome is a life-threatening complication
of type 2 diabetes
72
In 30%-40% of cases
nonketotic hyperosmolar syndrome is
73
Ketoacidosis is absent in nonketotic hyperosmolar syndrome
due to insulin preventing lipolysis and ketogenesis
74
Precipitating factors for nonketotic hyperosmolar syndrome
include stress
75
Nonketotic hyperosmolar syndrome has an insidious onset
with progressive glycemic deterioration and lethargy
76
Severe dehydration and altered consciousness
are common findings in nonketotic hyperosmolar syndrome
77
Hyperglycemia above 600 mg/dL and plasma osmolality above 320 mOsm/L
are diagnostic criteria for nonketotic hyperosmolar syndrome
78
Absence of ketonemia and a pH above 7.3
differentiate nonketotic hyperosmolar syndrome from diabetic ketoacidosis
79
Nonketotic hyperosmolar syndrome must be distinguished from
hypoglycemia
80
The first step in treating nonketotic hyperosmolar syndrome
is restoring hemodynamic stability with fluids
81
Patients with nonketotic hyperosmolar syndrome may require
10-12 L of fluid replacement over 24-36 hours
82
Despite normal or high potassium levels
nonketotic hyperosmolar syndrome patients
83
Insulin therapy plays a secondary role in nonketotic hyperosmolar syndrome
with fluid resuscitation being the priority
84
For marked hyperglycemia over 600 mg/dL
regular insulin 5-10 units IV
85
When plasma glucose drops to 250-300 mg/dL
insulin infusion should be reduced
86
Microvascular complications of diabetes
include retinopathy
87
Nonproliferative and proliferative retinopathy
are types of diabetic eye disease
88
Diabetic neuropathy can be
sensory
89
Diabetic nephropathy
is a major cause of chronic kidney disease
90
Macrovascular complications of diabetes
include coronary artery disease
91
Other complications of diabetes
include gastroparesis
92
Hypoglycemia is caused by low glucose levels
triggering sympathoadrenal activation symptoms
93
Symptoms of sympathoadrenal activation
include sweating
94
Neuroglycopenia symptoms include
fatigue
95
Iatrogenic hypoglycemia
is a major limitation of intensive diabetes therapy
96
Risk factors for iatrogenic hypoglycemia
include skipped meals
97
Oral glucose or sugar-containing beverages
are the first-line treatment for conscious hypoglycemic patients
98
IV dextrose is needed for severe hypoglycemia
or if the patient has altered consciousness
99
An initial bolus of 20-50 mL of 50% dextrose
should be given followed by maintenance infusion
100
Glucagon 1 mg IM or SC
is used for severe hypoglycemia when IV access is unavailable
101
Insulin is synthesized in B-cells of the pancreas
and consists of two polypeptide chains linked by bisulfide bridges
102
Amylin is synthesized in B-cells
and decreases insulin release by delaying gastric emptying and increasing glycogenolysis
103
One mg of insulin is equivalent to
22 U
104
The daily insulin output is 30-40 U
and is controlled by food
105
Glucose is the main stimulant of insulin release
along with fatty acids and amino acids
106
GIT hormones such as gastrin and secretin
increase insulin release
107
Glucagon and growth hormone
increase insulin release
108
Somatostatin and PGE-1
decrease insulin release
109
Beta-2 and muscarinic receptor stimulation
increases insulin secretion
110
Alpha-2 receptor stimulation
decreases insulin secretion
111
Hypoglycemia and fasting
decrease insulin secretion by stimulating sympathetic transmitters
112
Sulfonylureas increase insulin release
while phenytoin
113
Exogenous human insulin
is obtained by genetic engineering
114
Insulin is not effective orally
and is usually given subcutaneously or intravenously for soluble insulin
115
Insulin is metabolized in the liver and kidney
by glutathione insulin transhydrogenase and proteolytic enzymes
116
The insulin receptor consists of
two alpha and two beta subunits linked by bisulfide bonds
117
The insulin receptor’s action is mediated
through tyrosine kinase phosphorylation
118
Rapid-acting insulin includes lispro and aspart
with onset within 10-30 minutes and duration of 3-5 hours
119
Short-acting insulin includes regular insulin
with an onset of 30 minutes and duration of 6-8 hours
120
Intermediate-acting insulin includes NPH and lente
with an onset of 2 hours and duration of 18-24 hours
121
Long-acting insulin includes PZI
ultralente
122
Lispro insulin has a shorter duration and faster action
compared to soluble insulin
123
Lente insulin consists of
30% semilente and 70% crystalline zinc insulin
124
Soluble insulin can be acidic or neutral
while PZI is alkaline and should not be mixed with acidic insulin
125
Insulin therapy is usually given as
a mixture of 30% regular insulin and 70% NPH insulin
126
Insulin is administered pre-prandially
with 2/3 before breakfast and 1/3 before dinner
127
Biphasic isophane insulin
is a premixed combination of regular and NPH insulin
128
Insulin is indicated for type 1 diabetes
and type 2 diabetes uncontrolled by diet and oral antidiabetics
129
Insulin is used in critical situations
such as pregnancy
130
Hypoglycemia from insulin therapy
can result from overdose
131
Hypoglycemia causes sympathetic overactivity
leading to tachycardia
132
Severe hypoglycemia can cause
mental confusion
133
Mild hypoglycemia is treated with
a sweet drink or snack
134
Severe hypoglycemia is treated with
IV glucose or IM glucagon
135
Insulin allergy is caused by
IgE-mediated histamine release from mast cells
136
Insulin allergy presents as
localized erythema or systemic anaphylaxis
137
Purified human insulin
reduces the risk of insulin allergy
138
Insulin resistance is due to
IgG antibodies neutralizing insulin before receptor binding
139
A diabetic needing over 200 U of insulin daily
is considered insulin resistant
140
Insulin lipodystrophy includes
atrophy and hypertrophy at injection sites
141
Lipohypertrophy is caused by
repeated injections at the same site leading to lipogenesis
142
Lipodystrophy can be prevented by
rotating insulin injection sites
143
Insulin therapy can cause
weight gain
144
Sulfonylureas stimulate insulin release
by blocking ATP-sensitive potassium channels in beta cells
145
Sulfonylureas require at least 30% functioning beta cells
to be effective in type 2 diabetes
146
Long-term sulfonylurea therapy
leads to downregulation of sulfonylurea receptors
147
Sulfonylureas increase insulin sensitivity
by upregulating insulin receptors and glucose transporters
148
Sulfonylureas decrease hepatic glucose output
by inhibiting glycogenolysis and gluconeogenesis
149
First-generation sulfonylureas include tolbutamide and chlorpropamide
while second-generation include glibenclamide glipizide and gliclazide
150
Third-generation sulfonylureas
include glimepiride
151
Second-generation sulfonylureas are 100 times more potent
but have the same maximal hypoglycemic effect
152
Sulfonylureas are indicated in
NIDDM not responding to diet and exercise
153
Sulfonylureas can cause severe hypoglycemia
leading to coma
154
Sulfonylureas increase appetite
causing weight gain
155
Sulfonylureas can cause allergic reactions
including rash and photosensitivity
156
Sulfonylureas can cause
bone marrow depression and teratogenic effects
157
Glimepiride is effective in a smaller dose
with less hypoglycemia and no weight gain
158
Biguanides decrease glucose absorption
increase lactate production
159
Biguanides decrease plasma glucagon
and increase insulin sensitivity
160
Biguanides do not increase insulin release
so they do not cause hypoglycemia
161
Biguanides reduce plasma LDL and VLDL
preventing atherosclerosis
162
Metformin is the only biguanide
available for clinical use
163
Metformin is indicated for NIDDM
especially in obese patients due to appetite suppression
164
Metformin is used with sulfonylureas
to reduce hypoglycemia risk in NIDDM
165
Metformin is combined with insulin
to reduce insulin requirements in insulin resistance
166
Metformin can cause lactic acidosis
especially in renal hepatic and cardiopulmonary disease
167
Metformin can cause
anorexia nausea vomiting diarrhea and B12 deficiency
168
Meglitinides are oral insulin secretagogues
that block ATP-dependent K-channels in B-cells
169
Meglitinides include
repaglinide and nateglinide
170
Meglitinides have rapid onset
and are taken 10 minutes before meals to prevent postprandial hyperglycemia
171
Meglitinides are ineffective in
IDDM
172
Meglitinides cause less hypoglycemia
than sulfonylureas
173
Thiazolidinediones include
rosiglitazone and pioglitazone
174
Thiazolidinediones are called insulin sensitizers
and act via PPAR-gamma receptors
175
PPAR-gamma receptors are present in
adipose tissue liver and skeletal muscles
176
Thiazolidinediones increase glucose transport
by increasing GLUT-4 synthesis and translocation
177
Thiazolidinediones require insulin
for their action
178
Thiazolidinediones can cause anemia
weight gain edema and hypervolemia
179
Thiazolidinediones are contraindicated
in hypertension and heart failure
180
Alpha-glucosidase inhibitors include
acarbose and miglitol
181
Alpha-glucosidase inhibitors are poorly absorbed
and competitively inhibit carbohydrate absorption in the gut
182
Alpha-glucosidase inhibitors reduce postprandial hyperglycemia
and promote weight loss
183
Alpha-glucosidase inhibitors can be used alone
or with insulin or sulfonylureas
184
Alpha-glucosidase inhibitors cause
flatulence distension and abdominal pain
185
DPP-4 inhibitors include
alogliptin linagliptin sitagliptin and saxagliptin
186
DPP-4 inhibitors prevent incretin degradation
increasing insulin release and reducing glucagon
187
DPP-4 inhibitors can be used alone
or with sulfonylureas metformin or insulin
188
DPP-4 inhibitors should not be combined
with GLP-1 receptor agonists due to overlapping mechanisms
189
DPP-4 inhibitors are well absorbed orally
and excreted via the renal or enterohepatic system
190
Sitagliptin is mostly excreted unchanged
while saxagliptin is metabolized by CYP450 3A4/5
191
DPP-4 inhibitors can cause
nasopharyngitis headache pancreatitis and joint pain
192
CYP3A4 inhibitors like ketoconazole
can increase saxagliptin levels
193
SGLT2 inhibitors include
canagliflozin and dapagliflozin
194
Empagliflozin reduces cardiovascular mortality
in diabetic patients with heart disease
195
SGLT2 inhibitors reduce glucose reabsorption
increasing urinary glucose excretion
196
SGLT2 inhibitors cause osmotic diuresis
and reduce sodium reabsorption
197
SGLT2 inhibitors can lower systolic blood pressure
but are not used for hypertension treatment
198
SGLT2 inhibitors should be avoided
in renal dysfunction
199
SGLT2 inhibitors can cause
urinary tract infections genital infections and increased urination
200
SGLT2 inhibitors can cause
hypotension in elderly or diuretic users
201
SGLT2 inhibitors can cause
ketoacidosis in high-risk patients
