Diabetes Mellitus Flashcards
1
Q
What is the primary function of insulin?
A
Decreases blood glucose concentration
Insulin also decreases blood fatty acid and ketoacid concentration, increases protein synthesis, and promotes K+ uptake by cells.
2
Q
What does glucagon stimulate?
A
Stimulates glycogenolysis and gluconeogenesis
It also increases lipolysis and ketoacid formation.
3
Q
What are the life-threatening complications of Diabetes Mellitus?
A
Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS)
These complications are commonly seen in patients with diabetes.
4
Q
What are the common symptoms of Diabetic Ketoacidosis (DKA)?
A
Confusion, fatigue, increased thirst, frequent urination, abdominal pain, nausea
Physical exam may show thinness, tachycardia, tachypnea, dry skin, and fruity breath odor.
5
Q
What mechanism causes DKA?
A
Insulin deficiency and glucagon (plus other stress hormones) excess causing hyperglycemia
Triggers include stress, infection, new onset DM Type 1, and not taking insulin medication.
6
Q
How does stress trigger DKA?
A
By increasing glycogenolysis and gluconeogenesis
Stress also increases glucagon, epinephrine, and cortisol levels.
7
Q
What is the effect of increased glucagon with insulin deficiency in diabetes?
A
Hyperglycemia and increased lipolysis
Fatty acids are shunted towards ketone synthesis.
8
Q
What is the role of sodium-glucose cotransporters (SGLT2) in DKA?
A
Reabsorb glucose in the proximal tubule
This process is affected by the osmotic diuresis seen in DKA.
9
Q
What electrolyte imbalance is commonly seen in DKA?
A
Hyperkalemia
Caused by extracellular shift of K+ and lack of insulin activation of Na+/K+ ATPase.
10
Q
What acid-base disorder occurs in DKA?
A
Primary anion gap metabolic acidosis
This is characterized by a bicarbonate level reduction and a pH < 7.4.
11
Q
What is the anion gap formula?
A
Na+ – (Cl– + HCO3–)
Anion gap > 12 mEq/L indicates metabolic acidosis.
12
Q
What are the clinical features of DKA summarized in the acronym ‘DKA’?
A
D – Delirium/Psychosis/Coma, K – Kussmaul Respirations, A – Abdominal Pain/Nausea/Vomiting, D – Dehydration, F – Fruity odor in breath
This mnemonic helps remember the key clinical features.
13
Q
True or False: Diabetic Ketoacidosis can occur in patients with Type 2 Diabetes.
A
True
While it is more common in Type 1 Diabetes, it can occur in Type 2 Diabetes under certain conditions.
14
Q
Fill in the blank: The increase in blood glucose with decreased glucose utilization is due to increased _______ and decreased insulin production.
A
glucagon
15
Q
What is the typical age group commonly affected by DKA?
A
Patients with DM Type 1
DKA is most commonly seen in younger individuals with Type 1 Diabetes.
16
Q
What is the age and gender of the patient described in the emergency department?
A
16-year-old female
17
Q
What symptoms has the patient been experiencing since the afternoon?
A
Confusion
18
Q
How long has the patient been feeling fatigued?
A
2 weeks
19
Q
What changes in drinking and urination have been reported for the patient?
A
Drinking more water and urinating more frequently
20
Q
What abdominal symptoms has the patient been complaining of since last night?
A
Abdominal pain and nausea
21
Q
What physical exam findings were noted for the patient?
A
Very thin and pale
22
Q
What was the patient’s heart rate during the examination?
A
Tachycardic at 124 bpm
23
Q
What breathing pattern was observed in the patient?
A
Tachypneic with deep labored breathing
24
Q
What specific signs of dehydration were noted in the patient?
A
Dry skin and dry mucous membranes
25
What unique odor was noted from the patient's breath?
Fruity odor
26
What is the serum glucose level indicative of DKA?
>250 mg/dL (commonly between 350 to 500 mg/dL)
27
What is a more accurate serum assay for diagnosing DKA?
β-hydroxybutyrate
28
What urine test can be used to detect ketones?
Positive Nitroprusside stick test
29
What is the expected plasma osmolality in DKA?
Hyperosmolality
30
What does anion gap greater than 12 indicate?
Metabolic acidosis
31
What pH level is indicative of acidosis in DKA?
< 7.3
32
What is the treatment for hypovolemia and electrolyte imbalance in DKA?
Normal saline infusion
33
When should insulin be administered in DKA treatment?
Only if K+ ≥ 3.3 mEq/L
34
What should be monitored throughout DKA treatment?
K+ levels and hypoglycemia
35
What is a common complication associated with DKA?
Cerebral edema
36
What fungal species can thrive in acidic and high glucose conditions?
Mucormycosis
37
What is a key feature of Hyperosmolar Hyperglycemic State (HHS)?
Insulin deficiency and inadequate water intake causing hyperglycemia and hyperosmolarity
38
What triggers can lead to HHS?
* Stress
* Myocardial infarction
* Stroke
* Sepsis
* Pneumonia
* Inadequate water intake
39
What is the typical serum glucose range in HHS?
600-1200 mg/dL
40
What is the expected urine ketone level in HHS?
Absent to mild
41
What treatment is carried out until plasma osmolality is < 315 mOsmol/L in HHS?
IV fluids and IV insulin
42
What is the pH level indicative of HHS?
Normal pH (>7.3)
43
Why is Kussmaul breathing not present in HHS?
Kussmaul respiration is absent due to lack of acidemia
44
Define Diabetes Mellitus and its types
Types include Type 1, Type 2, and Gestational diabetes.
45
What is the normal fasting blood glucose range?
80 to 110 mg/dL.
46
What is considered hyperglycemia?
Above 126 mg/dL.
47
What is considered hypoglycemia?
Below 70 mg/dL.
48
List the signs and symptoms of Diabetes Mellitus.
* Polyphagia
* Polydipsia
* Polyuria
* Blurred vision
* Fatigue
* Poor wound healing
* Recurrent infections
49
What are the macrovascular complications of Diabetes Mellitus?
* Coronary Artery Disease (CAD)
* Peripheral Artery Disease (PAD)
* Stroke
50
What are the microvascular complications of Diabetes Mellitus?
* Eye complications
* Neuropathy
* Nephropathy
51
What is the role of glycated hemoglobin (HgA1C) in diabetes control?
It reflects long-term glucose control; lower levels are associated with decreased cardiovascular risk.
52
Describe the insulin action on liver.
* Inhibits glycogenolysis
* Inhibits conversion of amino acids to glucose
* Promotes glucose storage as glycogen
53
Describe the insulin action on muscle.
* Increases glycogen synthesis
* Increases protein synthesis
* Increases glucose transport
54
Describe the insulin action on adipose tissue.
Stores triglycerides.
55
What is the primary focus of treatment in Type 1 diabetes?
Exogenous insulin replacement.
56
What is the primary focus of treatment in Type 2 diabetes?
Overcoming insulin resistance; may involve insulin replacement.
57
What insulin type is most appropriate for diabetic ketoacidosis?
Short-acting insulin (regular insulin).
58
What is the onset and duration of regular insulin?
Onset: 30-60 minutes; Duration: 2-7 hours.
59
What are the advantages of rapid-acting insulins like Lispro, Aspart, and Glulisine?
* Quick onset (5-10 minutes)
* Physiologic coverage of post-prandial glucose rise
* Suitable for insulin pumps
60
What is the onset and duration of Intermediate-acting insulin (NPH)?
Onset: 2-4 hours; Duration: 10-20 hours.
61
What is the onset and duration of Long-acting insulins like Glargine and Detemir?
Onset: 0.5-1 hour; Duration: 24 hours.
62
What is Insulin Degludec (Tresiba®) and its duration?
Onset: 30-90 minutes; Duration: 42 hours.
63
What factors can influence insulin release?
* Vasodilators (e.g., diazoxide, minoxidil)
* Thiazide diuretics
* Calcium channel blockers
64
Fill in the blank: The _______ is responsible for regulating insulin release in response to blood glucose levels.
pancreatic beta cells
65
True or False: Insulin therapy can lead to weight gain as an adverse effect.
True.
66
What is lipodystrophy in the context of insulin therapy?
A condition where fat distribution changes due to insulin injections.
67
What is the significance of the 120-day life span of red blood cells in diabetes?
It allows for the formation of glycated hemoglobin (HbA1c), which indicates long-term glucose levels.
68
What are the classes of antidiabetics?
1. Sulfonylureas
2. Meglitinides
3. Biguanides
4. Thiazolidinediones (TZD)
5. Alpha-glucosidase inhibitors
6. GLP-1 agonists
7. DPP-4 inhibitors
8. SGLT2 inhibitors
69
What is the mechanism of action (MOA) of Metformin?
Decreased hepatic gluconeogenesis
70
What are common adverse effects of Sulfonylureas?
* Hypoglycemia
* Weight gain
* Rash
* Allergies
71
What is the first line treatment for Type II diabetes?
Metformin
72
What is the mechanism of action of Thiazolidinediones?
Agonist at PPAR-γ, increases glucose uptake into adipose tissues by GLUT-4 transporters
73
What are the adverse effects of Thiazolidinediones?
* Fluid retention
* Weight gain
* CHF
* Bone fractures in women
* Liver toxicity
74
What do Alpha-glucosidase inhibitors do?
Block intestinal brush border enzymes, delaying disaccharide to monosaccharide breakdown
75
Fill in the blank: The drug _______ is a synthetic amylin analog used to modulate postprandial glucose.
Pramlintide
76
What are the adverse effects of GLP-1 agonists?
* Pancreatitis
* Medullary thyroid cancer
77
True or False: DPP-4 inhibitors increase circulating GLP-1.
True
78
What is the impact of SGLT2 inhibitors on glucose?
Promotes glucose excretion by the kidney via proximal tubule
79
What drugs are used to counteract hypoglycemia?
Glucagon and dextrose
80
What is a significant risk associated with Metformin?
Lactic acidosis
81
What is the role of ACE inhibitors in Type II diabetes?
Renal protective
82
What do vasodilators like diazoxide and minoxidil do?
Stop the release of insulin from pancreatic beta cells
83
What is the effect of glucocorticoids on glucose levels?
Causes hyperglycemia
84
What is the mechanism of action of Metoclopramide?
D2 receptor blocker that increases GI motility
85
Fill in the blank: The drug _______ is known for improving triglyceride and HDL values via PPAR-α.
Rosiglitazone
86
What should be used to treat hypoglycemia with Alpha-glucosidase inhibitors?
Dextrose, not sucrose
87
What is the primary action of pramlintide?
Suppresses glucagon release and delays gastric emptying
88
What are the adverse effects of DPP-4 inhibitors?
* Hypersensitivity reactions
* Upper respiratory infection
* Headaches
* Arthralgia
89
What is the preferred sulfonylurea for the elderly?
Glipizide
90
Fill in the blank: The drug _______ is contraindicated in pregnancy and should be replaced with insulin.
Thiazolidinediones
91
What components regulate appetite and body weight?
Both endocrine and neural components
## Footnote
These components interact to maintain energy balance
92
How do you calculate BMI?
BMI = body weight (in kg) ÷ height (in meters) squared
93
What is the BMI classification for overweight?
≥25 and <30
94
What waist circumference suggests increased cardiometabolic risk for men?
≥40 in (102 cm)
95
What waist circumference suggests increased cardiometabolic risk for women?
≥35 in (88 cm)
96
What is the importance of treating obesity and metabolic syndrome?
To reduce morbidity and mortality associated with these conditions
97
What are the key hormones involved in energy balance regulation?
* Ghrelin: stimulates hunger
* Leptin: promotes satiety
98
What is the resting metabolic rate's contribution to daily energy expenditure?
Approximately 70%
99
What is the thermic effect of exercise's contribution to daily energy expenditure?
Active physical activity contributes 5-10%
100
What is the definition of obesity?
A state of excess adipose tissue mass, not body weight
101
What factors are associated with obesity screening barriers?
* Stigma associated with a diagnosis of obesity
* Physician bias
102
What is the BMI classification for Class I Obesity?
≥30 and <35
103
How does obesity affect hospitalization risk during COVID-19?
Obese patients have increased risk for hospitalization and death
104
What is functional leptin resistance?
A condition where the body does not respond effectively to leptin
105
What is the role of genetics in obesity?
Identified genetic variants account for <5% of the variance of body weight
106
What is Prader-Willi Syndrome characterized by?
* Hyperphagia and obesity
* Intellectual disability
* Hypogonadism
* Neonatal hypotonia
107
What is Beckwith-Wiedemann Syndrome?
A pediatric overgrowth disorder with a predisposition to tumor development
108
What are common features of Cushing’s Syndrome?
* Weight gain
* Truncal obesity
* Moon facies
* Buffalo hump
109
What is the effect of hypothyroidism on obesity?
Uncommon cause, easily ruled out with TSH measurement
110
What are common drug classes that can induce obesity?
* Antidepressants
* Antipsychotics
* Mood stabilizers
* Glucocorticoids
111
What is the most common cause of Cushing's syndrome?
Exogenous corticosteroids
112
What is metabolic syndrome also known as?
Syndrome X
113
How does obesity impact insulin levels?
Increased food intake along with high insulin levels promotes energy storage in fat
114
What is the significance of waist circumference in obesity screening?
It helps assess abdominal obesity and associated health risks
115
True or False: Muscle weighs more than fat.
True
116
Fill in the blank: Obesity can result from increased energy intake, decreased energy expenditure, or a combination of the two, often related to _______.
[sedentary lifestyle]
117
What is the most common cause of increased facial hair growth in women?
Exogenous corticosteroids
## Footnote
Increased facial hair growth can be a symptom of various conditions, but exogenous corticosteroids are a common cause.
118
What are the key components of Metabolic Syndrome (Syndrome X)?
A constellation of metabolic abnormalities that confer increased risk of cardiovascular disease (CVD) and diabetes mellitus
## Footnote
Metabolic Syndrome includes several risk factors that contribute to serious health conditions.
119
List the risk factors for Metabolic Syndrome.
* Overweight or obese
* Sedentary lifestyle
* Diabetes mellitus
## Footnote
These risk factors can significantly increase the likelihood of developing Metabolic Syndrome.
120
What are the associated diseases with Metabolic Syndrome?
* Cardiovascular disease
* Diabetes Mellitus Type II
* Non-alcoholic Fatty Liver Disease
* Hyperuricemia/Gout
* Polycystic Ovary Syndrome
* Obstructive Sleep Apnea
* Hepatocellular carcinoma and intrahepatic cholangiocarcinoma
* Dementia
## Footnote
These diseases are often linked to the presence of Metabolic Syndrome.
121
What are the five traits used to diagnose Metabolic Syndrome?
* Waist circumference ≥40 in. in men and ≥35 in. in women
* Serum triglycerides ≥150 mg/dL or drug treatment for elevated triglycerides
* Serum HDL cholesterol <40 mg/dL in men and <50 mg/dL in women or drug treatment for low HDL cholesterol
* Blood pressure ≥130 SBP or ≥85 DBP or drug treatment for elevated blood pressure
* Fasting plasma glucose ≥100 mg/dL or drug treatment for elevated blood glucose
## Footnote
Meeting three of these five traits is necessary for a diagnosis of Metabolic Syndrome.
122
What initial tests should be performed to assess a patient for Metabolic Syndrome?
Waist circumference, Blood Pressure, HDL Cholesterol, Triglycerides, Fasting Plasma Glucose
## Footnote
These tests help determine if a patient meets the criteria for Metabolic Syndrome.
123
What is the primary goal of obesity treatment?
Lifestyle management
## Footnote
Lifestyle management is the first step in treating obesity, often followed by pharmacotherapy or surgery.
124
What is a realistic initial weight-loss goal for patients?
8–10% over 6 months
## Footnote
Setting achievable weight-loss goals is crucial for patient success.
125
What are the components of lifestyle modifications for obesity treatment?
* Dietary habits
* Physical activity
* Behavior modification
## Footnote
These components are essential for effective weight management.
126
What calorie deficit is recommended for weight loss?
500–750 kcal/d compared with the patient’s usual diet
## Footnote
This calorie deficit can help achieve a weight loss of approximately 1–2 lbs per week.
127
What should be included in a healthy diet according to AHA guidelines?
* A variety of fruits and vegetables
* Whole grains
* Low-fat dairy products
* Skinless poultry and fish
* Nuts and legumes
* Non-tropical vegetable oils
## Footnote
A diverse diet supports overall health and weight management.
128
How much physical activity is recommended for adults to manage obesity?
At least 150 minutes of moderate physical activity or 75 minutes of vigorous physical activity each week
## Footnote
Regular physical activity is vital for weight management and overall health.
129
What are the two major categories of anti-obesity medications?
* Appetite suppressants (anorexiants)
* Gastrointestinal fat blockers
## Footnote
Understanding the types of medications available can help in choosing the right treatment.
130
What is the preferred first-line pharmacotherapy for obesity?
Glucagon-like peptide 1 (GLP-1) agonist (e.g., semaglutide)
## Footnote
This medication is effective for weight loss and managing obesity.
131
What criteria indicate the need for bariatric surgery?
BMI ≥40 kg/m2 or BMI ≥35 kg/m2 with serious medical conditions
## Footnote
Bariatric surgery is considered when lifestyle modifications and pharmacotherapy are not effective.
132
What average total body weight loss can be expected from bariatric surgery?
30–35% weight loss maintained in ~60% of patients at 5 years
## Footnote
Bariatric surgery can lead to significant long-term weight loss.
133
What role do social determinants of health play in obesity?
They impact access to healthy foods, safe physical activity, and overall health equity
## Footnote
Addressing these social determinants is crucial for effective obesity prevention and treatment.
134
What is the role of Leptin and Ghrelin in weight regulation?
* Ghrelin: stimulates hunger
* Leptin: stimulates satiety
## Footnote
These hormones are key regulators of energy balance and appetite.
135
How is obesity defined?
A state of excess adipose tissue mass (body fat)
## Footnote
Obesity is not solely based on body weight.
136
What is the significance of waist circumference in obesity assessment?
≥40 in. for men and ≥35 in. for women suggests increased cardiometabolic risk
## Footnote
Waist circumference is an important measurement in evaluating obesity-related health risks.
137
What waist circumference for men is suggestive of increased cardiometabolic risk?
≥40 in.
138
What waist circumference for women is suggestive of increased cardiometabolic risk?
≥35 in.
139
What is metabolic syndrome?
A constellation of metabolic abnormalities that confer increased risk of cardiovascular disease (CVD) and diabetes mellitus.
140
How is a patient classified as having metabolic syndrome?
By meeting three of the five ATPIII criteria.
141
What should treatment for obesity always begin with?
Lifestyle modifications, including diet and exercise.
142
When should pharmacotherapy be considered for obese patients?
For patients with a BMI ≥30 kg/m² or BMI ≥27 kg/m² with concomitant obesity-related diseases when dietary and physical activity therapy has not been successful.
143
What BMI indicates severe obesity for considering bariatric surgery?
BMI ≥40 kg/m².
144
What BMI indicates moderate obesity associated with a serious medical comorbidity for considering bariatric surgery?
BMI ≥35 kg/m².
145
What are the key references mentioned for obesity management?
* Harrison's Principles of Internal Medicine, 20e and 21e * Can Fam Physician * First Aid for the USMLE Step 1 2018 * UpToDate
146
True or False: Obesity treatment does not require lifestyle modifications.
False.
147
Fill in the blank: Patients are classified as having metabolic syndrome if they meet _______ of the five ATPIII criteria.
three
148
T or F: DM I is a B-cell mediated autoimmune disease.
False
It is T-cell mediated
149
T or F: Countries at higher latitudes, such as Scandinavia, have a higher incidence of DM I compared to countries at lower altitudes
True
Fun Fact:
Possible correlation to sun rays and endogenous production of Vit. D.????
150
T or F: Data has shown a stronger genetic correlation w/ Type 2 DM compared to Type 1 DM
True (according to textbooks at the very least)- many health researchers remain skeptical of the validity of such data
Fun Fact:
In the early 2000s, a multi-million dollar investment to find genetic links to Type II DM in native american populations did not yield enough power to be statistical significance
151
What are the main triggers of DKA?
Infection
MI
Pancreatitis
Trauma
non-compliance w/ Insulin
152
What type of infections increase risk of DKA the most?
RIs and UTIs
153
T or F: a normal pH for suspected DKA increases the likelihood of a different metabolic disorder being the culprit
False
It is important to keep in mind how certain symptoms can influence pH balance
DKA does cause anion gap metabolic acidosis but if the pt. is also vomiting, pH can be normal b/c emesis causes metabolic alkalosis
Pts. can present w/ both acidosis and alkalosis
154
How does hypovolemia affect BP?
It lowers it leading to dangerously low BP
155
What kind of hyponatremia occurs w/ DKA? Explain your reasoning.
Fastidious Hyponatremia
156
What hormone is released in response to decreased ECV? Describe the mechanism
ADH
hypovolemia increases aldosterone secretion leading to potassium wasting
157
What substances can increase anion gap?
glycols
oxoproline (toxic metabolite of acetaminophen)
Alcohols
Aspirin (later effect)
158
An increases in plasma levels of what biomolecules stimulate ketogenesis?
free fatty acids
159
T or F: hyperglycemia causes the increased anion gap in DKA metabolic acidosis
FALSE
Although hyperglycemia does contribute to metabolic acidosis for DKA, blood sugar is not used to measure the anion gap. In DKA, it is the excess ketone bodies that contribute to decreased -charged anions increased anion gap b/c ketone protons are donated to HCO3- to form the neutrally charged compound H2CO3
160
HIgh serum levels of what biomolecules contributes to increased plasma osmolality in DKA
glucose
161
Excess Ketone bodies increase serum levels of what metabolite?
lactic acid
162
T or F: excess ketone bodies causes vomiting
True
hyperglycemia is not the direct contributor of this symptom
163
T or F: Hyperglycemia causes hypovolemia while excess ketones cause metabolic acidosis
True
164
T or F: a negative nitroprusside stick test indicates the absence of ketoacidosis and ketonuria
FALSE
During a Diabetic Ketoacidotic states, the most abundant ketone body is BHA; nitroprusside sticks detect acetoacetate not BHA which yields high sensitivity but very little specificity
165
Fungal species like Mucormycosis can thrive in acidic and high glucose conditions due to what enzyme
ketone reductase
166
how is mucormycosis enter the host
penetrates the cribriform plate to invade the cavity holding the brain parenchyma
167
What is the most common cause of HHS?
INFECTIONS
168
T or F: Cerebral Oedema is more common in DKA than HHS?
False
pts. w/ HHS are at a greater risk for developing cerebral oedema compared to pts. w/ DKA
169
What symptoms of DKA would you expect to be absent for a pt. w/ HHS? Explain your reasoning.
N/V
Kussmaul respirations
abdominal pain
ketone body induced-acidemia causes the above symptoms seen in DKA
170
What symptoms would you expect to be the same for both DKA and HHS? Explain your reasoning.
Polyuria
Polydipsia
dehydration
Hypovolemia
Explanation: both DKA and HHS present with hyperglycemia which contributes to all the symptoms listed above.
171
what is the function of GLUT1 receptors?
expressed in all tissues
assists w/ basal glucose uptake
172
Glut2 receptors are expressed in what cells
pancreatic beta cells
173
GLUT3 transporters can be found in high concentrations of these organs
placenta
brain
kidneys
neurons
allows for uptake of glucose through neural tissues
174
What cell types contain GLUT4 transporters
muscle and adipose tissues
INSULIN MEDIATED
175
What type of hypersensitivity is Type 1 DM?
Type IV hypersensitivity rxn.
176
T or F: insulin can be given to pts. that have CCB-induced hyperglycemia and bradycardia
true
CCBs also block Ca channels on pancreatic beta cells
177
How is insulin released from beta pancreatic cells
Glucose is transported into the cytoplasm of beta pancreatic cells via GLUT2 transporters
Glucose then metabolizes to make ATP which subsequently closes the potassium channels allowing depolarization to occur
Depolarization open the Ca Channels to allow Ca ions into the Intracellular compartment; these ions are required for insulin secretion from the cells
178
T or F: short-acting insulin analogs must be taken at meal time to avoid a hypoglycemic incident
True
w/ short-acting insulin agonists, glucose levels plummet within 4 hrs. of admin.
179
short-acting insulin is generally.........in nature to allow for quick absorption
a monomer
180
What kind of insulin analog would you want to administer via IV for a pt. w/ DKA
a short-acting insulin analog
181
why should you also administer KCl in conjuction w/ IV insulin
Insulin shifts K cation flow into cells decreasing potassium serum concentration and subsequent hypokalemia if not compensated
182
T or F: short-acting insulin has a onset duration of 5-10 minutes.
False
this is the onset duration for rapid-acting insulin
183
the short-acting insulin analogs lack what physiologic coverage provided by the rapid-onset analogs?
postprandial glucose rise:
the effect of rapid-acting insulin is short-lived which allows glucose absorbed from bolus of a recent meal to increase serum glucose levels back to the basal level
with the short-acting insulin analogs, the insulin effect is prolonged inhibiting glucose levels to rise for a longer period of time
184
What component of insulin degludec prolongs its absorption
the insulin molecule is formulated w/ protective multihexamers composed of phenol and zinc
185
how do vasodilators cause hyperglycemia?
vasodilators inhibit the Ca mediated contraction of SM in blood vessels by opening potassium channels to keep cells in a hyperpolarized state
186
how do thiazides cause hyperglycemia?
Recall that thiazides are potassium-wasting diuretic agents
this causes hypokalemia and subsequent hyperglycemia
187
Describe the disulfiram reaction.
excessive consumption of alcohol with chlorpropamide will lead to a blockage of the acetaldehyde dehydrogenase causing a disulfiram rxn: redness, palpitations, nausea
188
chlorpropamide can cause what type of hyponatremia
dilutional hyponatremia and SIADH
189
T or F: ghrelin is produced in the stomach.
True
190
T or F: sleep deprivation decreases daily levels of ghrelin
false
it increases ghrelin
191
what would be the ultimate effect of damage to the lateral nucleus in the hypothalamus
lateral injury makes you lean
192
damage to this hypothalamic nucleus would cause overeating and massive weight gain
ventromedial nucleus
VM injury makes you Very Massive
193
T or F: the BMI of a lean person can be high
True especially if the pt. has pathologic short-stature
194
what are the symptoms of BW syndrome
wilms tumor, macrosomia, hemihyperplasia, macroglossia, versceromegaly
195
how should readiness to change be assessed when taking to obese pts. about weight loss.
First, ideal SH factors-stressful life events, psychiatric status, time availability, occupation, relationship dynamics
Next determine if the pt desires to change or resistant to it
Then achor: use scale of 0-10 to rate level of interest and confidence
196
what is the MOA of orlistat?
inhibits gastric and pancreatic lipase to decrease breakdown and absorption of dietary fats
197
what sulfonylurea is better for pts. w/ renal impairments
glimepiride
198
what sulfonylurea is preferred for the elderly due to its lower potency
glipizide
199
list the meglitinides you need to know
repaglinide
nateglinide
200
waht meglitinide is a D-phenylalanine deriviative
nateglinide
201
T or F: meglitinides are short-acting hypoglycemics
True
202
what are the adverse effects of metformin
lactic acidosis, Vit. B12 deficiency
203
what is the mechanism of metformin-induced lactic acidosis
it inhibits pyruvate carboxylase
204
T or F: metformin can also be used to treat hyperinsulinemia of polycystic ovaries
true
205
what drug class is metaformin
biguanides
206
list the TZDs you need to know
AZONEs
pioglitazone
rosiglitazone
207
what are the AEs of TZDs and their mechanisms
fluid retention and CHF: upregulation of epithelial sodium channels
bone fractures; decreased osteoblast production
208
list the alpha glucosidase inhibitors you need to know
acarbose
miglitol
209
this drug is a synthetic amylin analog
pramlintide
210
This drug is a GLP-1 analog that is commonly used as an adjunct for enhanced glucose control
exenatide
211
describe the mechanism by which GLP-1 analogs induce infammation
increased beta cell production can initiate an inflammatory response
212
This drug is both a GLP1 and GIP agonist
Tirzepatide
213
Describe how tirzepatide GIP component reduces inflammation
increases adiponectin production
adiponectin decreases inflammation thus serves as a cardio-protective factor against atherosclerosis
214
what is the MOA of DPP-4
degrades GLP1
215
list the DPP-4 inhbititors you need to know
LIPTINs
sitagliptin
saxagliptin
linagliptan
alogliptin
216
how does GIP enhance glucose control
increases glucose & fatty acid uptake into adipocytes
regulates glucagon secretion through hyper and hypoglycemic states
stimulates insulin release
suppresses hunger
217
List the roles of GLPs in glucose control
stimulates insulin release
suppresses glucagon secretion during hyperglycemia ONLY
slows gastric emptying
suppresses hunger
218
what drugs have been FDA approved for weight loss
sibutramine
lorcaserin
diethylpropion
orlistat
219
what is the MOA OF sibutramine
NE/5HT reuptake inhibitor
220
what is the MOA of lorcaserin
agonist of 5-HT2C
221
T or F: diethylpropion is a sympathomimetic
true
222
what is the MOA of orlistat
lipase inhibitor
available OTC
223
name the SGLT2 inhibitors you need to know
the FLOZINs
224
what is the ultimate effect of SGLT2 inhibitors
A1c reduction
225
T or F: the symptoms of hypoglycemia mimic parasympathetic stimulation
false
it mimics sympathetic stimulation
226
how should hypoglycemia be managed for the conscious and unconscious pt.
conscious: fast sugar
unconscious: glucagon
227
what drugs can be given for renal protection in Type II DM pts.
ACEIs
ARBs
228
what drug can be given to aid in gastric complications of DM2
metoclopramide: D2 blocker and antiemetic
229
what is the MOA of metoclopramide?
D2 receptor blocker that stops relaxation of GI smooth muscle
increases Ach release to promote gastroparesis relatively quickly so that the feeling of satiety comes on quicker
230
what are the AEs of metoclopramide
prolactinemia
EPS symptoms
Parkinsonism
M1 & H1 blocks as well
