Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Hormonal & Reproductive Week 2 - WLB > Diabetes Mellitus - Christian > Flashcards

Diabetes Mellitus - Christian Flashcards

1
Q

What do alpha cells do?

a. elevate insulin in the blood
b. elevate glucose in the blood
c. secrete glucagon
d. cause liver and kidney to secrete/retain glucose

A

b. elevate glucose in the blood
c. secrete glucagon
d. cause liver and kidney to secrete/retain glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Beta cells secrete which of the following?

a. insulin
b. C-peptide
c. amylin
d. all of the above

A

d. all of the above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the basic pathophysiology of Type 1 Diabetes?

A

Rapid onset of Autoimmune Beta-cell destruction => leading to absolute insulin deficiency (nearly 50-80% of Beta-cell function is lost by the time of Dx)

**Antibodies to glutamic acid decarboxylase (GAD)-65 are frequently present.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the basic pathophysiology of Type 2 Diabetes?

A

Insidious/slow PROGRESSIVE insulin secretory defect on the background of insulin resistance

(more tissue => secrete more insulin => cells stop “listening” to insulin)

***Nearly 50-80% of Beta-cell function is lost by the time of Dx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What therapies can cause Drug Induced Hyperglycemia?

A

***glucocorticoids

oral contraceptives

cyclosporine, tacrolimus, sirolimus

niacin

HIV protease inhibitors

thiazide diuretics

statins

gonadotropin releasing hormone agonists

other — beta blockers, beta agonists, megasterol, alcohol…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What type of diabetes is diagnosed by glucose tolerance test?

A

Gestational diabetes:

(first a one hour challenge – if >140 mg/dL, another 3 hour test will be performed, checking sugar every hour and if 2 reads are high => gestational DM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Who should we screen for diabetes?

A

Screen all overweight adults (BMI >25) with > 1 risk factor:

  • physical inactivity
  • 1st degree relative with DM
  • High risk race/ethnicity
  • Women with a baby >9 lbs or Hx of GDM
  • HTN
  • HDL 250 mg/dL
  • Women with PCOS
  • A1c > 5.7%, IGT or impaired fasting glucose on previous testing
  • Obesity, acanthosis nigricans, and other conditions associated with DM
  • History of CVD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Dx of DM

A

fasting plasma glucose of 126 mg/dL on 2 separate occasions

random plasma glucose of 200 mg/dL with symptoms (polyuria, polydipsia, weight loss)

plasma glucose >200 mg/dL 2 hours after a 75-g oral glucose load (pregnancy)

glycosylated hemoglobin >6.4% (A1c)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the HbA1c for pre-diabetes? Diabetes?

A

Prediabetes = 5.7%-6.4%

Diabetes = >6.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How often do you retest HbA1c?

A

Every 3 months. It takes 3 months to regenerate RBCs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are important areas to focus on when performing a physical exam on pts with DM?

A

Vitals - Height, weight, BP

HEENT - pupillary reaction to light, dilated retinal exam

Neck - thyroid gland

Heart and lung exam, blood flow (pulse) in arms, legs, feet and neck (carotid) arteries

Skin - vitiligo, acanthosis nigricans, ulcers

Feet for sores, injuries, and decreased sensation (monofilament exam annually).

Reflexes and sensation (neuro).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the microvascular complications of DM?

A

retinopathy (annual eye exam)

neuropathy (annual monofilament exam)

nephropathy (annual microalbumin screen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the macrovascular complications of DM?

A

class 1A indication for aspirin daily => both primary and secondary prevention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What laboratory tests are important to check in pts with DM?

A

glucose (fasting or random)

A1c

Lipids

renal panel

microalbumin

TSH

hepatic panel

***Test annually!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the currently incentivized laboratory evaluations and management strategies for patient with DM?

A

measure hemoglobin A1c every 6 months

maintain hemoglobin A12c at individual targets of less than 7%/less than 8%

measure LDL annually => maintain LDL cholesterol to less than 100 mg/dL or at level achieved by high dose statin

BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the recommended treatment strategy for Type 1 DM?

A

Intensive therapy allows the use of insulin in a way that mimics the pancreas (short [prandial] plus long [basal] vs pump)

short (regular, lispro, aspart, glulisine) + long (glargine, detemir)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the list of current drugs used for treatment of Type 2 DM?

A

Biguanides (metformin)

Sulfonylureas (insulin secretagogues)

Alpha-glucosidase inhibitors

Thiazolinediones

Amylinomimetics

Incretin modulators: GLP-1 mimetics (glucagon-like peptide),
DPP-IV inhibitors (dipeptidyl peptidase-IV)

18
Q

What is the 5-part Tx/therapy strategy for Type 2 DM?

A

diet (calorie consumption)

exercise

education

medications

self monitoring

19
Q

What diabetic therapies work by increasing satiety?

A

Amylin Analogs and GLP-1 Agonists

20
Q

What diabetic therapies work by decreasing glucose absorption and decreasing gastric emptying?

A

↓ Glucose absorption
Alpha-glucosidase inhibitors

↓Gastric Emptying
GLP-1 Agonists
DPP-IV Inhibitors
Amylin Anologs

21
Q

What diabetic therapies work by decreasing glucose production?

A

Metformin and TZDs

22
Q

What diabetic therapies work by increasing insulin secretion and decreasing glucagon?

A 
↑ Insulin Secretion
Sulfonylureas
GLP-1 Agonists
DPP-IV Inhibitors
Meglitinides

↓ Glucagon Secretion
GLP-1 Agonists
DPP-IV Inhibitors
Amylin Analogs

23
Q

What diabetic therapies work by increasing peripheral glucose uptake?

A

Metformin and TZDs

24
Q

What diabetic therapies work by decreasing glucose reabsorption?

A

SGLT2 Inhibitors

25
Q

Why is Metformin a good/bad initial drug monotherapy for treatment of DMII?

A

high efficacy => decreases HbA1c

lipid lowering, decreases macrovascular complications

low risk for hypoglycemia

weight neutral (maybe loss)

side effects of GI upset and ***lactic acidosis

low cost!

26
Q

Which patients can you allow to have a HbA1c of 7?

A

older than 70

problems with hypoglycemia

may not live for another 10 years

27
Q

Who should not take Metformin?

A

renal impairment (Cr >1.5 men, >1.4 women)

cardiac, resp insuf, sepsis leading to hypoxia or reduced tissue perfusion (cellular strain, possibly metabolic acidosis, might lead to lactic acidosis)

lactic acidosis

liver disease, alcohol abuse

radiographic contrast agents

28
Q

What are the pros/cons of using Sulfonylureas for DMII Tx?

A

bind to sulfonylurea receptor on beta cells, stimulate insulin release

hypoglycemia, weight gain, potential impairment of cardiac ischemic preconditioning

29
Q

What are the pros/cons of using Thiazolidinediones (TZDs) for DMII Tx?

A

Increases the amount of glucose taken up by muscle cells and keeps the liver from overproducing glucose

addresses primary defect of T2D, no hypoglycemia, lipid lowering, decreased macrovascular complications

SE - edema, could precipitate CHF, increased fx risk in women, increased? MI with rosiglitazone (Avandia – now off market)

$$expensive$$

30
Q

What are the pros/cons of using GLP-1 agonists (incretin mimetics) and DPP-IV inhibitors for DMII Tx?

A

activate GLP-1 receptors, increase glucose-dependent insulin secretion, decrease glucagon secretion, delay gastric emptying

DPP-IV inhibits degradation of GLP-1 and GIP (gastric inhibitory peptide)

no hypoglycemia, potential weight loss

SE - nausea, vomiting, pancreatitis (rare), no long term studies

expensive

Don’t decrease HbA1c THAT much… not worth cost!

31
Q

What is the role of Incretins (GLP-1 Receptor Agonist)?

A
  1. Increase insulin production
  2. Speeds insulin release
  3. Decreases glucagon production
  4. Slows gastric emptying
  5. Promotes satiety
32
Q

What is the MOA of GLP-1 Receptor Agonists?

A

MOA: incretin (GLP-1) analog => increased insulin synthesis and release (β cells), decreased glucagon secretion (α cells), and decreased hepatic glucose production

Additional benefit of satiety promotion

33
Q

What is the MOA of DPP-IV Inhibitors?

A

MOA: blocks the degradation of incretin by inhibiting the DPP-IV enzyme => increased insulin synthesis and release (β cells), decreased glucagon secretion (α cells), and decreased hepatic glucose production

34
Q

What patients should avoid GLP-1 Receptors Agonists?

A

Use is contraindicated in patients with or a family history of medullary thyroid cancer and in patients with multiple endocrine neoplasia syndrome type 2 (MEN2).

35
Q

What are the 3 rapid acting human insulins?

A

Lispro (Humalog)

Aspart (Novolog)

Glulisine (Apidra)

36
Q

What are the 3 short acting human insulins?

A

Human Regular (Humulin-R or Novolin-R)

37
Q

What are the 2 long acting human insulins?

A

Insulin Detemir (Levemir)

Insulin Glargine (Lantus)

38
Q

ADA’s Glycemic targets

A

Most patients: HbA1c

39
Q

AACE/ACE’s glycemic targets

A

HbA1c

40
Q

AACE/ACE’s diabetes algorithm

A

If A1c 7.6%-9% => Dual therapy (Metformin + GLP-1/DPP4/TZD/ SU/Glinide) for 2-3 months

Then, if A1c is not at goal => triple therapy for 2-3 months

Then, if A1c is STILL not at goal => insulin +/- other agents

41
Q

What are four of the associated metabolic abnormalities in patients with DMII?

A

steatohepatitis

elevated triglycerides/low HDL

hyperuricemia

acanthosis nigricans

42
Q

How many times higher is the risk for heart disease death and stroke in patients with DM compared to patients without DM?

A

2-4x higher

Hormonal & Reproductive Week 2 - WLB (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions