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Pharmacology > DM > Flashcards

DM Flashcards

1
Q

What is Type 1 Diabetes?

A
  • Autoimmune Destruction of pancreatic B cells
  • Severe insulin deficiency: needed for survival
  • predisposing pt to ketoacidosis and ketonemia
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2
Q

Which antidiabetic drugs cause weight gain vs wt loss

A

wt gain:
- Thiazolidinediones
- Sulfonylureas

wt loss:
- GLP-1

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3
Q

Onset of Type 1 Diabetes vs type 2 and associations

A

  • associated with ketoacidosis and ketonemia type 2:
  • Onset >30 y/o
  • Associated with obesity
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4
Q

In Type 2 Diabetes hyperglycemia is due to?

A
  • Genetics
  • insulin resistance
  • hepatic glucose production
  • B cell deficiency
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5
Q

Where is insulin normally produced?

A

B cells in Islets of Langerhans in pancreas

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6
Q

What are the functions of insulin

A

-Transport glucose from blood to cell
-glycogenesis: Conversion of glucose to glycogen
-lipogenesis: Conversion of glucose to fatty acids
-Protein synthesis
———- anabolic:
- makes glycogen, fatty acids, proteins

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7
Q

What are long term complications of diabetes? Microvascular? Macrovascular?

A

Macrovascular:
- CVD
- HTN
- Dyslipedemia
- CAD/PVD

Microvascular:
- Nephropathy
- Retinopathy

Neuropathic Complications:
- due to protein synthesis and glucose related demyelination

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8
Q

DM type 2: phase 1 vs phase 2 insulin secretion

A

Phase 1: bolus of insulin secreted minutes after meal
- often diminished in type 2 DM Phase 2: steady insulin secretion
- maintains insulin for several hours after eating
- steady secretion as long as there is glucose stimulation
- can still occur in DM type 2 but is impaired as beta cells dysfunction and insulin resistance increases

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9
Q

Lack of insulin results in what metabolic abnormalities (4)

A
  • ↓ glucose uptake by cells
  • ↑ hepatic output of glucose = HYPERGLYCEMIA
  • ↑ catabolism of protein in muscle = ↑ urea & uric acid
  • ↑ lipolysis & fatty acid levels: body cannot metabolize ketones = Ketoacidosis/ ketonuria
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10
Q

What are some strategies for controlling blood glucose?

A
  • Diet and exercise
  • Increase circulating insulin levels
  • Improve insulin sensitivity
  • Regulate glucose production in the liver
  • Decrease postprandial glucose
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11
Q

Treatment Guidelines ACE/AACE Criteria Screening vs American Diabetes Association screening

A

ACE/AACE Criteria: Begin at 30 y/o for high risk people ADA:
- Begin at 45 y o for all w retesting every 3 years
- Earlier for high risk people

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12
Q

What are treatment goals ACE/AACE Criteria vs ADA

A

ACE/AACE :
- Fasting: under 100
- 2 hr post prandial:
- Before bedtime:NR
- HbA1c: under 6.5

ADA:
- Fasting: 80-120
- 2 hr post prandial: under 180
- Before bedtime: 100-140
- HbA1C: under 7

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13
Q

DM screening: who to screen early/ who is high risk

A
  • obesity
  • 1st degree fam hx
  • high risk ethnic group
  • IGT/IFG
  • hx of gestational DM
  • HTN
  • lipid abnormalities ACE/ACEE: additional risks
  • CVD
  • sedentary lifestyle
  • polycystic ovary ds
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14
Q

Insulin: What are the human derived sources? animal derived

A

Human derived:
- Humulin: genetically engineered E.coli
- Novolin: insertion of human AAs Animal derived:
- pork derived
- do not use bovine!!! mad cow ds

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15
Q

Where should insulin be stored?

A

Fridge until opened

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16
Q

What is the Somogyi effect?

A
  • Nocturnal hypoglycemia
  • compensatory increase in glucagon that causes hyperglycemia in morning
  • pts will complain of nightmares and headaches in the morning
  • Tx: decrease bedtime insulin
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17
Q

Somogyi effect: what will the pt complain of

A

pt will complain of NIGHTMARES or waking up with headaches
- Nocturnal hypoglycemia
- compensatory increase in glucagon that causes hyperglycemia in morning Tx:
- decrease bedtime insulin

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18
Q

What is the Dawn phenomenon?

A
  • GH hormone decreases tissue sensitivity to insulin early morning
    -Mild hyperglycemia between 5am-8am
  • 75% of pts have it/more common than somogyi effect tx:
  • increase bedtime insulin
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19
Q

What are ADRs of Insulin?

A
  • Hypoglycemia
  • Local allergies
  • systemic allergy (MC animal derived)
  • Immunological resistance, similar to tolerance (increase dose)
  • Local fat atrophy/ hypertrophy: decreased absorption of insulin (with SC injections + injecting in same spot)
    -> rotate the spot where you inject
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20
Q

What are advantages of Insulin?

A
  • No max dose
  • improves cholestrol profile
  • low cost
  • available in variety of dosage forms
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21
Q

Insulin is considered __________ for Type 2 Diabetics. when is it considered first line?

A

SECOND LINE treatment First line DM type 2:
- FPG >250
- HbA1C >10%
- ketouria
- sx of hyperglycemia

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22
Q

What are the rapid acting types of insulin drug names

A

The rapid acting dont LAG
Lisipro
Aspart
Glulisine

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23
Q

What are the rapid acting types of insulin onset, peak, DOA?

A

onset: 10-30 min peak: 1-3 hrs DOA: 3-6.5 hrs

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24
Q

What is the short acting type of insulin?

A

Regular

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25
Q

What is short acting type of insulin , regular onset,peak, DOA?

A

onset: 0.5-1 hr
peak: 1-5 hr
DOA: 6-10 hr

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26
Q

What are the intermediate acting type of insulin? onset, peak, doa

A

NPH onset: 1-2 hr peak: 6-14 hr DOA: 16-24 hr

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27
Q

What are the long acting type of insulin drug names? general onset and DOA?

A

Glargine Degludec Detemir onset: ~1 hr peak: not significant DOA: 24 hrs (determir = shortest)
——- long acting decreases the amount of insulin needed pre-meal

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28
Q

Insulins DOA: rapid, regular, nph, determinr, glargine, degludec

A

rapid acting DOA: 3-6 HOURS
Regular: DOA 6-10 HOURS
NPH: DOA 16-24 HOURS
Detemir DOA: ~12-24 HOURS
Glargine DOA: ~22-24 HOURS
Degludec DOA: >24 HOURS

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29
Q

Most commonly used for patients with unstable and or fluctuating glucose levels?

A

LISPRO (rapid acting)

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30
Q

What is first line therapy for DM type 2?

A

Metformin

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31
Q

What class of drug is metformin? MOA?

A

Biguanides MOA:
- Decrease gluconeogenesis
- increase insulin sensitivity
- increase glucose uptake into muscle note: does not stimulate pancreatic insulin release
-> rarely causes HYPOGLYCEMIA

Formin = no forming glucose
Met = sensitive and brings it into cells

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32
Q

What are contraindications to Biguanides/Metformin

A
  • CR> 1.5 in males >1.4 in females
  • Hold for 48 hr if receiving IV contrast since it can cause Lactic Acidosis
    -> ACUTE RENAL FAILURE
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33
Q

Precautions with Biguanides?

A

Caution with:
- CHF (edema)
- Hepatic Ds
- Pulm Ds
- MI
- ethanol abuse: can increase lactic acidosis risk

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34
Q

What are ADRs with Biguanides?

A
  • LACTIC ACIDOSIS*
  • diarrhea
  • nausea/bloating
  • metallic taste
  • anorexia
    -poor absorption = decreases folate and b12

Prof rec: take your dose early and plan around your bowel movements
- gradually titrate dose due to GI distress
- can give metformin with meals to minimize ADRs

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35
Q

What is an advantage to Biguanides?

A

No weight gain**
+ low risk of hypoglycemia because it doesn’t stimulate insulin release

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36
Q

What are DDIs to Biguanides?

A
  • Sulfonylureas: Exacerbates Hypoglycemia
  • EtOH: Increases risk of lactic acidosis
  • Cimetidine (H2), Nifedipine, Ranitidine, Digoxin, Vancomycin: Increases Metformin levels

“Very Necessary Drugs Raise Metformin”

Very - Vancomycin
Necessary - Nifedipine
Drugs - Digoxin
Raise - Ranitidine
Metformin - Metformin
Concentrations -cimetidine

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37
Q

Biguanides: what can metformin also be indicated for?

A
  • Gestational Diabetes
  • PCOS
    ——- type 2 DM
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38
Q

What were the first oral agents introduced to market for type 2 DM?

A

Sulfonylureas
- first gen: 1950s
-> not used much anymore use second gen
- 2nd gen: 1980s
-> 2nd line tx for type 2 DM

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39
Q

What are first generation sulfonylureas?

A

Chlorpropamide: ADR
- SIADH and disulfiram-like rxn with alcohol
tolazamide
tolbutamide
(not used much anymore)

-amide

40
Q

What are second generation sulfonylureas?

A

3Gs:
- Glipizide: best for elderly because shorter half life (“zip” = fast half life)
- Glyburide
- Glimeripide

41
Q

Sulfonylureas are considered ______ treatment for Type 2 Diabetics

A

2nd line treatment

42
Q

MOA of sulfonylureas?

A
  • Stimulate insulin release in B cells by binding to sulfonlyurea receptors
  • decrease hepatic clearance of insulin
  • overall: increases circulating insulin levels

note:
- after 1-2 years: patients develop some tolerance over time

43
Q

What is a precaution with sulfonylureas?

A
  • Sulfur containing drugs
  • avoid in Pts with sulfa allergy
  • Renal dysfunction: Need to adjust dosing
44
Q

What are ADRs of sulfonylureas?

A
  • Hypoglycemia**
  • Weight Gain** -> BAD for DM pts
  • Chloropropramide: SIADH and Disulfiram-like rxn with alcohol***
  • CNS effects
  • skin reaction
  • GI effects
  • hematological SEs
45
Q

What is a specific ADR with Chlorproramide?

A

SIADH and disulfiram like rxn with alcohol

46
Q

How long before meals should you take sulfonylureas?

A

30 min

47
Q

sulfonylureas: DDIs

A

Hypoglycemia: Warfarin, Fluconazole, H2 Blockers, Mg Salts, Sulfonamides, TCA,
- also with combo of other oral antidiabetics: hypoglycemia risk

Hyperglycemia: BBs, CCBs, Steroids, Phenytoin, Thiazide diuretics

48
Q

When do sulfonylureas lose effectiveness

A

1-2 years
- patients develop some tolerance over time

49
Q

If sulfonylureas are combined with insulin and other oral antidiabetic agents they can ..

A

increase risk of hypoglycemia

50
Q

Meglitinides: drug names

A

Repaglinide
Nateglinide

51
Q

Melitinides are not useful in what? Meglitinides indication + caution

A

not useful: Type 1 DM Indication: Second line therapy for Type 2 DM
- Not preferred in real life due to SE profile

  • caution: hepatic dysfunction, do not use with insulin or sulfonlyureas

Meg hungover (lots of ADRs) with hepatic dysfunction

52
Q

What are ADRs of Meglitinides?

A
  • Hypoglycemia
  • N/v/d
  • sweating
  • tremor
  • URI
  • arthralgia

Meg got too LIT last night and woke up with hangover and got sick (uri + tremor + sweating)
-n/v/d
-arthralgia
-hypoglycemia

53
Q

Meglitinides: MOA + precaution

A

MOA:
- Stimulates insulin release from β cells by closing K+ channels and opening Ca2+ channels
- take 30 minutes prior to meals

precaution:
- hepatic dysfunction
- do not use with insulin or sulfonlyureas

54
Q

DDIs of Meglitinides?

A

Macrolides and azoles (MA) = ↑ Meglitinide effect

P450 Enzyme inducers (Barbiturates, Carbamazepine, Rifampin) = ↓ Meglitinide effect

Precaution with highly protein bound drugs: NSAIDs, ASA, Sulfonamides, Warfarin

55
Q

When should Meglitinides be taken?

A

30 min prior to meals

56
Q

You can not use Meglitnides with what drugs? what drugs can you use it with

A

DO NOT use with: Insulin or sulfonylureas
can use with: metformin or thiazolidinediones

57
Q

Thiazolidinediones drug names

A

Pioglitazone
Rosiglitazone

-GLITAZONE

58
Q

Thiazolidinediones are considered _______ treatment in Type 2 DM

A

Second line

59
Q

What is Thiazolidinediones unique MOA?

A
  • Reduces insulin resistance by increasing insulin SENSITIVITY in muscle and adipose
  • requires presence of insulin to work
  • also decreases hepatic glucose PRODUCTION
60
Q

Which patients can take Thiazolidinediones?

A

Can be used in Type 1 & Type 2 DM WITH INSULIN USE
- Effective in controlling A1C levels

MOA:
- Reduces insulin resistance by increasing insulin SENSITIVITY in muscle and adipose
- requires presence of insulin to work
- also decreases hepatic glucose production

61
Q

What are precautions with Thiazolidinediones? ***

A

Liver dysfunction**: monitor LFTs every 2 months for first year

CHF pts: Black box warning****
- avoid in class 3 and 4 HF due to increased edema

ROSIGLITAZONE + MI = Black box warning
- do not use if pt has underlying cardiac ds: can increase risk of MI BY UP TO 40%

62
Q

Which thiazolidinedione has the black box warning for MI ?

A

Rosiglitazone

63
Q

What are advantages of Thiazolidinediones?

A
  • Good reduction in HbA1C
  • beneficial on lipid profile
64
Q

What are ADRs to Thiazolidinediones

A
  • Weight gain**
  • edema/ fluid retention**
  • Hypoglycemia
  • Pioglitazone: Risk of Bladder cancer
  • Rosiglitazone: Black Box Warning for CHF and MI. No longer recommended unless absolutely needed
65
Q

Which thiazolidinedione can cause bladder cancer?

A

Pioglitazone

66
Q

DDIs for Thiazolidinediones? Decreased effectiveness of….

A

Decreased effectiveness with oral contraceptives Pioglitazone will have an increased effectiveness with P450 Enzyme Inhibitors

67
Q

when should you take Thiazolidinediones in respect to meals?

A

can be taken without regard to meals due to unique MOA

68
Q

Alpha Glucosidase Inhibitors include

A

Acarbose and miglitol

69
Q

What is the MOA of alpha-glucosidase inhibitors? Drug names ?

A

Reversible inhibitor of alpha glucosidase in small intestine = Decreased hydrolysis of complex carbohydrates in GI tract = ↓ GI Absorption of carbohydrates
- overall: lowers postprandial glucose (by 50-60 mg/DL)

  • not much effect on fasting blood glucuse
  • less effect on HbA1C

Drugs: Acarbose and miglitol

70
Q

What are contraindications to alpha glucosidse inhibitors?

A

IBD
colonic ulceration
intestinal obstruction

CI: gi tract things because the drug slows down GI motility

71
Q

ADRs to alpha glucosidase inhibitors?

A

Flatulence diarrhea abdominal pain

72
Q

When must alpha-glucosidase Inhibitors be taken in respect to meals?

A

With the first bite of a meal
- or else it wont work

73
Q

What kind of agent are Glucagon -like peptide 1 receptor agonist?

A

Incretin Mimetic Agents
- SC injections

74
Q

Glucagon-like Peptide-1 Receptor MOA and indication

A

MOA: Incretin mimetic agent incretin: released In Gi TRACT in response to food
- promotes insulin release
- inhibits glucagon
- Overall: lowers post prandial glucose

Indication:
- adjunct tx with other antidiabetic meds in pts that are not at optimal glycemic control
- not for use with insulin

75
Q

What are examples of GLP-1 Agonists? And description

A

-glutides; “LEAD”

Liraglutide:
- CI: in Medullary Thyroid Carcinoma & MEN2
- QD
- made by recombinant DNA technology; human peptide hormone

Exenatide:
- Do not use if CrCl <30 ml/min
- saliva of gila monster lizard
- BID or once weekly

Albiglutide

Dulaglutide:
- once weekly

76
Q

Do not use Exenatide when

A

CrCL<30 ml/min

77
Q

Do not use Liraglutide in

A

Medullary Thyroid Carcinoma (MTC) + Multiple Endocrine Neoplasia Syndrome type 2 (MEN2)

78
Q

What is an advantage of GLP-1 agonist?

A

Used for weight loss!!!!!
- does NOT cause weight gain

79
Q

What are the ADRs of GLP-1 agonists?

A

GLP

GI effects
PANCREATITIS
Hypoglycemia

80
Q

GLP-1: when do you administer it in respect to meals?

A

give within 60 minutes of a meal

81
Q

GLP-1: advantage and disadvantage

A

advantage: NO WT GAIN and can cause wt LOSS disadvantage: COST

82
Q

Pramlintide: MOA, indication, when to administer it in respect to meals?

A

MOA:
- human amylin analog; this is co-secreted with insulin in response to food intake
- enhances SNS satiety: inhibits food intake
- delays gastric emptying
- decreases blood glucose levels

Indication:
- used for adjunct tx in type 1 and 2 DM who use insulin at mealtimes that have failed to achieve glucose control
- Give immediately before high cal/carb meals
- give to highly motivated and compliant pt (+ rich $$$$)

83
Q

Benefit of pramlintide? disadvantage

A

benefit: No weight gain

con: cost, need motivated and compliant pt

84
Q

What are Oral Dipeptidyl Peptidase IV inhibitors (DPP-4 Inhibitors) drug names

A

-GLIPTIN (4)

Sitagliptan
Saxagliptin
Linagliptin
Alogliptin

85
Q

What is a precaution for DPP-4 Inhibitors?

A

Renal Disease: reduce dose in pts w CrCl < 50 mL/min

86
Q

Oral Dipeptidyl Peptidase IV Inhibitors MOA and indication/precaution

A

MOA: Enhance incretin system in body by blocking DPP-4 Enzyme which degrades GLP1 receptor

Indications:
- Adjunct with diet/exercise in Type 2 DM
- Not as effective in reducing HbA1C levels as other drugs

Precaution:
-CrCl <50: reduce dose

87
Q

Oral Dipeptidyl Peptidase IV Inhibitors ADRs and DDIs

A

ADRs: URI Headache

DDIs: May increase Digoxin levels

88
Q

What is the newest adjunct agent/newest class in adults with type 2 diabetes?** MOA

A

SGLT2 Inhibitors
-Work on PCT, diuresis effect
- blocks sodium glucose transporters in PCT = reduces reabsorption of glucose + increases excretion in the urine
-osmotic diuresis effect: pulls water with it too

89
Q

What are Sodium Glucose Cotransporter Type 2 inhibitors (SGLT-2 inhibitors)

A

-FLOZIN
Dapagliflozin
canagliflozin
empagliflozin

90
Q

What can SGLT2 inhibitors also be used for

A

Cardiovascular Disease**
- Diuretic effect for CVD

91
Q

Sodium Glucose Cotransporter Type 2 inhibitor : MOA and indication

A

MOA:
- SGLT2 in proximal renal tubular reabsorbs filtered glucose from tubular lumen
- By inhibiting SGLT2 = ↑ Urinary Glucose Excretion & ↓ Glucose Reabsorption
-osmotic diuresis: sugar draws water into the tubule and more water excreted

Indications:
- Adjunct treatment with diet/exercise in Type 2 DM
- Is also beneficial in the field of cardiology = Diuretic effect for CVD

-FLOZIN
Dapagliflozin
canagliflozin
empagliflozin

92
Q

ADRs of SGLT2 inhibitors

A
  • ketoacidosis
  • femal genital mycotic infections
  • UTIs
  • increased urination
93
Q

What are some combo products?

A

Janumet: Januvia + Metformin

Kombiglyze: Onglyza + Metformin
Glucovance: Glyburide +Metformin

Jentadueto: linagliptin + metformin hydrochloride

these exist for pts that need multiple meds

94
Q

Drugs can affect blood glucose: What drugs can cause Hyperglycemia?

A

“TTONICS”
- Thiazide diuretics
- Thyroid hormones
- Oral contraceptives
- Niacin
- INH
- Corticosteroids
- Sympathomimetics

“TTONICS taking too much alc can cause hyperglymia.. PARS = hypoglycemia”

95
Q

What drugs can cause hypoglycemia?

A
  • Probenecid
  • ASA
  • Rifampin
  • Sulfonamides

” working so hard for my PARS score i got hypoglycemic”

96
Q

when to take drugs relative to meals: sulfonylureas GLP-1 agonist meglitinides pramlintide alpha-glocosidase inhibitors Thiazolidiones

A

30 minutes before meal:
- sulfonylureas
- meglitinides

Give within 60 minutes of meal:
- GLP-1 agonist

Give immediately before high calorie meal:
- pramlintide

Take with FIRST bite of meal:
- alpha-glocosidase inhibitors

Take REGARDLESS to meal time
- Thiazolidiones (unique MOA)

SM (30)
G (60)
P (immediate before)
A (with first bite)
T (whenever)

97
Q

Which one are good for type 1 and type 2:

A

Insulin
Pramusilide
Thiazido

Pharmacology (15 decks)

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