Diabetes Mellitus Flashcards

1
Q

Diabetes mellitus (DM) is defined as

A
persistently high fasting glucose levels
greater than 125 on at least 2 separate occasions
(≥ 7.0 mmol/L)
100-125=prediabetes
 (5.6–6.9)
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2
Q

differences Type 1 DM vs 2

  • onset
  • obesity?
  • defined as
A
Type 1 DM
Onset in childhood
Insulin dependent from an early age
Not related to obesity
Defined as insulin deficiency
Type 2 DM
Onset in adulthood
Directly related to obesity
Defined as insulin resistance
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3
Q

Type___ DM is more

resistant to diabetic ketoacidosis (DKA).

A

2

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4
Q

what type presents with decreased wound healing.

A

both

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5
Q

Type _diabetics are much less likely to present with polyphagia

A

1

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6
Q

Diabetes is defined/diagnosed as: Single glucose level above _____ with _____

A

200 mg/dL + above symptoms

≥ 11.1
ojo amboss dice que 200 depués de la carga de glucosa

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7
Q

Hemoglobin A1c >___ is a diagnostic criterion and is the best test to _____ over the last several months.

A

6.5%

follow response to therapy

5.7-6.5=preDBT

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8
Q

DM Tx

A
    • Diet, Exercise, and Weight Loss

2. - Oral Hypoglycemic Medication

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9
Q

Diet, Exercise, and Weight Loss efficacy:

A

can control as much as 25% of cases of Type 2 DM without the need
for medications

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10
Q

The best initial drug therapy is

A

oral metformin

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11
Q

Sulfonylureas SE

A

increase insulin release from the pancreas,

thereby driving the glucose intracellularly and increasing obesity

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12
Q

The goal of therapy is.

A

HgA1c <7%

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13
Q

Metformin works by

A

blocking gluconeogenesis

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14
Q

Metformin is contraindicated in those with___. Because

A

renal dysfunction

because it can accumulate and cause metabolic acidosis.

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15
Q

who are the DPP-IV inhibitors

Dipeptidyl peptidase-4 inhibitors

A

sitagliptin, saxagliptin, linagliptin, alogliptin

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16
Q

DPP-IV inhibitors, how do they work

A

block the metabolism of the incretins, also called glucose insulinotropic peptide (GIP) and glucagon-like peptide (GLP)

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17
Q
The incretins (GIP and GLP) \_\_\_\_ insulin release and \_\_\_\_\_\_glucagon
release from the pancreas.
A

increase

decrease

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18
Q

The incretins normally have a half-life of

A

only 1–2

minutes.

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19
Q

who are the Incretin mimetics

A

(exenatide, liraglutide, albiglutide, dulaglutide)

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20
Q

Incretin mimetics are generally_____ before the DPP-IV inhibitors, because_____

A

not given

they must be administered by injection

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21
Q

Incretin agonists SE

A

markedly slow gastric motility (apparently DPP-IV too) and decrease weight.

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22
Q

Thiazolidinediones use , contraindication and whyyyy

A

provide no clear benefit over the other
hypoglycemic medications. They are relatively contraindicated in CHF because
they increase fluid overload.

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23
Q

who are the Thiazolidinediones

A

glitazones) e.g. pio/rosi

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24
Q

who are the SGLT2 inhibitors

Sodium-glucose Cotransporter-2

A

(empagliflozin, dapagliflozin, canagliflozin, ertugliflozin

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25
Q

SGLT2 inhibitors, when to use

A

added when 2 or 3 other oral hypoglycemic medications have not been effective.

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26
Q

SGLT2 inhibitors inhibit the reabsorption of glucose in the __________ after it has been ______.

A

proximal convoluted tubule

filtered

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27
Q

MOST IMPORTANT SE of SGLT2i glifozins

A

The extra sugar in the urine increases the likelihood of

urinary tract infections and fungal vaginitis. P/E

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28
Q

Metiglinides: Nateglinide and repaglinide pharmacodynamics

A

are stimulators of insulin release in a similar

manner to sulfonylureas, but do not contain sulfa

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29
Q

Nateglinide and repaglinide Importance

A

They do not add any

therapeutic benefit to sulfonylureas.

30
Q

Alpha glucosidase inhibitors who are this pipol

A

(acarbose, miglitol)

31
Q

Alpha glucosidase inhibitors (acarbose, miglitol) pharmacodynamics. Results

A

agents that block glucose

absorption in the bowel. They add about half a point decrease in HgA1c

32
Q

Alpha glucosidase inhibitors (acarbose, miglitol) SE

A

flatus, diarrhea, and abdominal pain

33
Q

Alpha glucosidase inhibitors(acarbose, miglitol) USE

A

They can be used with renal insufficiency.

34
Q

Pramlintide is an analog of a_____ that is secreted normally

with insulin.

A

protein called amylin

35
Q

Pramlintide , how it works

A

like Amylin, decreases gastric emptying, decreases glucagon levels, and decreases appetite

36
Q

while treating with insuline, therapy goal is:

A

HgA1c <7%.

37
Q

Insulin _______gives a steady state of insulin for the entire day

A

glargine

38
Q

glargine vs NPH

A

Glargine provides much more steady blood levels than NPH insulin,
which is dosed twice a day.

39
Q

Long-acting insulin is combined with

A

a short-acting insulin such as lispro, aspart, or glulisine.
Regular insulin is sometimes used as
the short-acting insulin.

40
Q
Order from short acting to long acting:
Detemir
NPH
Glulisine
Degludec
Regular
Lispro
Glargine
Aspart
A
Lispro, aspart, and glulisine
Regular
NPH
Glargine, detemir
Degludec
41
Q

Insulin pump: indication. and what kind of insulin uses

A

Standard of care for type 1 DM

rapid

42
Q

Diabetic Ketoacidosis cxfx

A
Hyperventilation
Possibly altered mental status
Nonspecific abdominal pain
“Acetone” odor on breath
Polydipsia, polyuria
43
Q

Diabetic Ketoacidosis. anion gap

A

increased

44
Q

_____kalemia in blood, but _____ total body potassium because of ______

A

Hyper
decreased
urinary spillage

45
Q

Diabetic Ketoacidosis tx

A

Treat with large-volume saline and insulin replacement

Replace potassium
when the potassium level comes down to a level approaching normal.

Correct the underlying cause: noncompliance with medications, infection,
pregnancy, or any serious illness.

46
Q

best measure of the severity of

DKA.

A

Serum bicarbonate.

If the serum bicarbonate is very low, the patient is at risk of death. If the serum
bicarbonate is high, it does not matter how high the glucose level is, in terms of severity. Serum bicarbonate level is a way of saying “anion gap.” If the bicarbonate level is low, the anion gap is increased.

47
Q

Urine ketones test

A

important, but they are not all detected

48
Q

Nonketotic Hyperosmolar Syndrome (NKHS) VS DKA

  • Glucose level
  • Best initial therapy
  • Hypertonicity alters mental status
  • Hypertonicity causes seizures and brain abnormalities
  • Anion gap
  • Serum bicarbonate
A

NKHS and DKA (BOTH)
-Glucose level: Extremely
elevated
-Best initial therapy: Insulin + Highvolume
fluids
- Hypertonicity alters mental status: YES

NKHS

  • Hypertonicity causes seizures and brain abnormalities: More common
  • Anion gap: Normal
  • Serum bicarbonate:Normal

DKA

  • Hypertonicity causes seizures and brain abnormalities: Less common
  • Anion gap: Elevated
  • Serum bicarbonate:Low
49
Q

All patients with DM should receive: _____ vaccine

A

Pneumococcal

50
Q

All patients with DM should receive: Statin medication if the LDL is above

A

100 mg/dL

51
Q

All patients with DM should receive:ACE inhibitors or ARBs if the blood pressure is

or if

A

greater than 140/90 mm
Hg
OR if urine tests positive for microalbuminuria

52
Q

how frequent you do eye exam to DM

A

yearly

53
Q

goal of blood pressure in DMpatients

A

(below 140/90 mm Hg)

54
Q

Diabetic Nephropathy Dx

A

-microalbuminuria early in the disease.
-The dipstick for urine
becomes trace positive at 300 mg of protein per 24 hours
-Microalbuminuria
means levels of albumin between 30 and 300 mg per 24 hours.

55
Q

Patients with

DM should be screened _____for microalbuminuria

A

annually

56
Q

what to do if microalbuminuria is ppresent

A

start on an ACE inhibitor or ARB

57
Q

Retinopathy: medical tx

A

Vascular endothelial
growth factor (VEGF) inhibitors help.
Aflibercept (eylea)
ranibizumab (lucentis)

58
Q

Gastroparesis initial tx

A

metoclopramide or erythromycin

59
Q

Gastroparesis 2L tx

A

gastric pacemaker.

60
Q

The only management

for nonproliferative retinopathy is

A

tighter control of glucose

Answer is not ASPIRIN

61
Q

proliferative retinopathy. includes

A

neovascularization and vitreous hemorrhages

62
Q

proliferative retinopathy. tx

A

laser photocoagulation, which markedly retards the progression to blindness. VEGF inhibitors treat severe retinopathy

63
Q

When the neuropathy leads to pain, treatment is with

A

pregabalin, gabapentin, or tricyclic antidepressants.

64
Q

who to screen of DBT

A

> =45y
BMI>=25
HTN

65
Q

2 hr OGTT results

A

> =200=DBT
140-200=preDBT
<140= normal

66
Q

DM2 management 1st line

A

metformine+ lifestyle
reasses in 3 months

unless cd,chf. liver dz

67
Q

DM2 management 2nd line

A

if after 1L, not at goal:
Add a secong agent (cualquiera)
Reasses in 3 months

here HGBA1C should lower 3%

68
Q

DM2 management 3rd line

A

if after 2L, not at goal:
Add insuline

here HGBA1C should lower 7%

69
Q

neuropathy screening

A

monofilament

70
Q

hospital setting patient, how to give insulin?

A

Basal-Bolus+ SSI sliding scale insulin (qAcqH5 while eating and q4h while NPO)

Total daily insuln= 50%basa+50%bolus divided into each meal

71
Q

hypoglycemia dx test

A

DG <70 BUT if pt has symptoms already and dg is a bit low consider and treat it as hypoG

72
Q

what tests should you do for a hypog pt + “non DBT”

A

bG, C-peptide, proinsulin, secretagogue screening.