Brainscape's Knowledge GenomeTM

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


See full index

ICM Exam 4 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Diagnostic criteria for diabetic ketoacidosis

A

Glu>250; pH

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

Whats up with K in diabetic ketoacidosis?

A

Pt is probably hypokalemic, even if their serum K is WNL. When pt is acidotic, K enters blood from cellular compartment (via H+-K+ antiporter) making serum K relatively high compared to status. Insulin will push K into the cellular compartment, as will treating volume status. Be sure to check serum K continuously when treating pt and supplement if low.

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

How do you correct measured Na in a hyperglycemic patient?

A

true Na= Na + 0.016*(Glc-100)

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

Diabetic ketoacidosis: treatment approach

A

1- fluids to correct acidosis- give 1L NS (0.9%) then switch to 0.45% once Na is corrected. Add D5 once glucose >200.
2- Insulin 1-2 hours after fluids (beware, this could push hypokalemia further)- 0.1 units/kg bolus then 0.1u/kg/hr infusion (make sure they arent hypokalemic first).
3- Treat for K depletion (if K

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

Anion gap calculation:

A

AG= Na-(Cl + HCO3)

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

Diagnostic criteria for DM:

A

HgA1c>=6.5% OR FPG>=126 OR Sx + rPG>=200 OR 2 hr PG>=200 after OGTT

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

Diabetic ketoacidosis: treatment approach

A

1- fluids to correct acidosis- give 1L NS (0.9%) then switch to 0.45% once Na is corrected. Add D5 once glucose >200.
2- Insulin 1-2 hours after fluids (beware, this could push hypokalemia further)- 0.1 units/kg bolus then 0.1u/kg/hr infusion
3- Treat for K depletion (if K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diagnostic criteria for DM:

A

HgA1c>=6.5% OR FPG>=126 OR Sx + rPG>=200 OR 2 hr PG>=200 after OGTT

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

Definition of pre-diabetes/impaired glucose tolerance. What does this mean for patient?

A

FBG 100-125 OR 2hrPG of 140-199 after OGTT OR A1c 5.7-6.4

pt. has 5% annual risk for DM.

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

Who should be screened for DM and pre-DM (kids)?

A

Begin at age 10 or onset of puberty (whichever is first). Retest every 3 yrs.

Kids>85 percentile WFA OR >85th percentile WFH OR weight >120% ideal for height
PLUS two or more of the following:
1. Family Hx of type 2 DM,
2. high-risk ethnicity,
3. signs or conditions associated with insulin resistance (hypertension, dyslipidemia, polycystic ovaries, small for gestational age),
4. maternal history of GDM or DM during pregnancy.

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

Who should be screened for DM or pre-DM (Adults)?

A
  1. All adults >45, esp BMI>=25 (23 if asian)
  2. All adults with BMI>=25 with additional risk factors: physical inactivity, 1st degree relative with DM, high-risk ethnicity (american indian, AA, Latino, asian), women who had GDM or delivered baby > 9lbs, HDL250, women with polycystic ovaries, Hx of CVD

If results normal- then repeat every 3 years.
If pre DM- repeat every year
If 1 test is DM range and another isn’t, then repeat the test that was ABOVE the DM cut point to confirm diagnosis.

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

What is the dawn phenomenon? Somogyi effect? Why does it happen? How do you confirm?

A

Morning hyperglycemia. Occurs due to nocturnal GH secretion (opposes effect of insulin).
Somogyi effect is a rebound to nocturnal hypoglycemia.
Both give morning hyperglycemia.

A: Test glucose at 3AM. If it’s elevated= dawn phenomenon. If it’s low= Somogyi effect (decrease evening insulin).

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

What mean blood glucose levels do the following A1c levels correspond to:
6,7,9,10,11,12?

A 
6- 126
7- 154
8- 183
9- 212
10- 240
11- 269
12- 298
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which physiologic states stimulate insulin release?

A

Glucose (or any food) PO, GI hormones: Secretin, Incretins (GLP-1, GIP); parasympathetic stimulation.

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

Which physiologic states inhibit insulin release?

A

Sympathetic stimulation; somatostatin (released by Delta cells in pancreas); glucocorticoids (cortisol); beta blockes.
Sympathetic stimulation is biphasic, initially inhibiting, then stimulating via b2 while inhibiting via a2

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

GLUT2 and GLUT4 transporters: role

A

GLUT2- located in Beta cells of pancreas. High Km- respond to high plasma glucose.

GLUT4- located in muscle and adipose. Glucose uptake stimulated by insulin.

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

Lispro

A

ultra short acting insulin formulation- useful t bring down glucose immediately (not crystaline). 10-30 mins onset, peaks in 30-60;; total duration 3-5 hrs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Aspart

A

ultra short acting insulin formulation. 10-30 mins onset, peaks in 30-60;; total duration 3-5 hrs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Glulisine

A

ultra short acting insulin formulation. 10-30 mins onset, peaks in 30-60;; total duration 3-5 hrs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

NPH

A

Intermediate-acting insulin- (AKA isophane).

Onset: 1-2 hrs; peak 4-8hrs; duration: 10-20 hrs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Detemer

A

Long-acting insulin (not as long as glargine)- fatty acid attached increases albumin binding
Onset: 1-2 hrs; peak: 2-4 hrs; duration 12-20 hrs

22
Q

Glargine

A

Lantus- Longest acting insulin. Inject sc at bedtime. No peak.
Onset: 2-6 hrs; Duration: 22-24hrs

23
Q

Insulin: safety

A

Preg cat B; hypoglycemia is largest risk

24
Q

Metformin

A

1st line for type 2 DM (after diet and exercise). “Sensitizer” enhancing insulin effect by activating AMP-dependent protein kinase in muscle and liver (encourages FA oxidation, less fat in liver, inc. insulin sensitivity).
Largest effect is blocking GNG and increasing glucose uptake.
Inhibits microvascular complicatoins.

25
Q

Metformin: safety

A

Side-effects: NV transient, dose-dependent. EtOH can cause lactic acidosis.
half-life is 1.5-3h; CI in renal OR liver disease. Not metabolized, but renal clearance.
Preg: B

26
Q

Metformin (biguanides)

A

1st line for type 2 DM (after diet and exercise). “Sensitizer” enhancing insulin effect by activating AMP-dependent protein kinase in muscle and liver (encourages FA oxidation, less fat in liver, inc. insulin sensitivity).
Largest effect is blocking GNG and increasing glucose uptake.
Inhibits microvascular complicatoins.

27
Q

Sulfonylureas- Glipizide

A

Stimulates insulin release in pancreas by binding to ATP-sensitive K channel (SU subunit)- closing it, causing depolarization, Ca influx, and exocytosis of insulin. Inexpensive!

28
Q

Glipizide (sulfonylurea): safety

A

Can cause weight gain, hypoglycemia. CI in hepatic or renal disease.
Preg: C

NSAIDs exacerbate hypoglycemia induced by glipizide.

29
Q

Meglitinides: Repaglinide

A

Same target as glipizide (ATP-sensitive K channel, SU subunit), same effect- enhanced insulin release.
Vs Glipizide: Shorter-acting, faster response.
Liver metabolism (CI in liver but NOT renal disease)
Preg: C
Same interaction profile, weight GAIN, hypoglycemia risk.

30
Q

Pioglitazone (Thazolidinedione)

A

This is the only med that increases insulin sensitivity at target cells. Target is PPAR-gamma (peroxisome proliferator-activated gamma receptor) located in nucleus in adipose and muscle. Adipose: Modifies gene expression with effect of:
Decreasing lypolysis and FFAs; reducing TNF-alpha, Leptin excretion; increasing adiponectin secretion (increases insulin activity)
Muscle: increases glucose utilization.

31
Q

Pioglitazone: safety

A

Increased risk of heart failure, fluid retention, weight GAIN; CI in liver disease, CVD. Black box warning for CVD. NOT hypoglycemic.

32
Q

Exenatide: GLP-1 mimetics

A

GLP-1 (endogenous insulin stimulator) agonist- causes glucose-dependent increase in insulin secretion, better kinetic profile than endogenous GLP.
Injectable route.

33
Q

Exantide (GLP-1 agonist): safety

A

Inc. risk of hypoglycemia when combined with secretagogues. GI side effects, weight LOSS/neutral.
Preg: C

34
Q

Sitagliptin (DPP-4 inhibitor)

A

Inhibits DPP-4, increasing the activity of endogenous GLP-1 (from GI tract) after meals. Increases glucose-mediated insulin secretion.

35
Q

Sitagliptin (DPP-4 inhibitor): safety

A

Increased risk of hypoglycemia when combined with secretagogue. Long term safety unknown. No CIs, but can cause hepatic failure. Weight neutral.
Preg: B

36
Q

Acarbose (alpha-glucosidase inhibitor)

A

Acts in GI tract slowing digestion/absorption of carbohydrates. V. effective at reducing postprandial hypoglycemia.

37
Q

Acarbose (alpha-glucosidase): safety

A

Side effects are GI. CI in chronic GI disease. Increased risk of hypoglycemia with insulin and sulfonylureas (Glipizide) (tx is oral glucose).
Preg: B

38
Q

Which agents are CI in renal disease?

A

Metformin, Glipizide

OK: Repaglimide, Pioglitazone, exantide, sitagliptan, acarbose, canagliflozin
*- CI in liver disease, but ok in kidney disease.

39
Q

Canagliflozin (SGLT-2 inhibitor)

A

Inhibits SGLT-2 in prox renal tubule, inhibiting glucose reabsorption in kidney.

40
Q

Which agents are CI in hepatic impairment? Which are ok?

A

Metformin, Glipizide, Repaglinide, Pioglitazone

OK: Exantide (GLP-1 mimetic), sitagliptin, acarbose, canagliflozin, insulin

41
Q

Which agents are safest in pregnancy?

A

Insulin, metformin, acarbose, sitagliptin are all B

Rest are cat C.

42
Q

Best way to initiate therapy in type II DM (how do you assess)?

A

Start with lifestyle change, then add metformin. F/U in 3 months- if A1c is not at target (7 for most people), then add a second oral agent.

43
Q

You have a pt. on two oral drugs for DM, how do you assess?

A

F/u in 3 months. If A1c target not met, add a 3rd agent that isn’t CI

44
Q

You have a pt on 3 oral drugs for DM, how do you assess?

A

F/u in 3 months. If A1c target not met, consider injectible agents (GLP-1 agonist- exantide, insulin). Ideally, give Metformin+ basal insulin + exantide OR mealtime insulin.

45
Q

Pt is on basal insulin plus exantide for DM, but its still refractory. What now?

A

Add pioglitizone OR canagliflozin to existing regimen.

46
Q

What are the target lipid and BP levels for patients with DM:

A

BP 130/85 = HTN threshold. LDL>100 is hyperlipidemia. If microalbuminurea (30-300 mg/24 hours) is present, treat with ACEi or ARB starting now.

47
Q

What labs do you get for your DM patients?

A

FBG, HgA1c; Urine Albumin! Urine albumin is the most important for identifying early signs of diabetic nephropathy when it’s still reversible.

48
Q

WTF is HHNS?

A 
Hyperosmolar hyperglyucemic nonketotic syndrome. Pt will have seizures, focal neuro defects, lethargy, confusion, polyuria/dipsia
Profound hyperglycemia (>900), hyperosmolarity, 
pH>7.3 NO ACIDOSIS!!! HCO3>15
49
Q

How do you treat HHNS?

A

FLUIDS 1L in fisrt hour, then another in nest 2 hours. Switch to 0.45% saline once pt is stabilized. Switch to D51/2NS once glucose reaches 250.

  1. Insulin- 5-10 units bolus, followed by low-dose infusion.
50
Q

What is the danger of reducing blood glucose too fast?

A

Cerebral edema, in both HHNS and DKA.

51
Q

Canagliflozin: safety

A

Long term safety unknown. Increased risk of UTI, mycotic infections. Weight LOSS.
Preg: C

ICM Exam 4 (2 decks)

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