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Pharmacology > Endocrine: pancreas > Flashcards

Endocrine: pancreas Flashcards

1
Q

List the rapid acting insulins

  • what is their:
    1. onset
    2. peak
    3. Duration
    4. coverage–when to give and used with what other insulins
A

Lispro (humalog)
Aspart (novolog)
Glulisine (Aprida)

  • **rapid absoprtion
  • *quicker onset
  • **shorter DOA
  1. 5-15 mins onset
  2. 45-75 minPEAK
  3. duration is 2-4 hours
  4. give this at the same time as a meal… can beused with intermediate or long acting insulin
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2
Q

list the short acting insulin

  1. onset
  2. peak
  3. Duration
  4. coverage–when to give and used with what other insulins
A

Regular Insulin

  1. 30 min onset
  2. 2-4 hour peak
  3. duartion 5-8 hrs
  4. give 30-60 min PIROR to meal… can be used with intermediate or long acting insulin
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3
Q

list the intermediate acting insulin

  1. onset
  2. peak
  3. Duration
  4. coverage–when to give and used with what other insulins
A

NPH

  1. 2 hour onset
  2. 4-12hour peak
  3. 8-18 hour duration
  4. covers insulin for about 1/2 day…. OR over night.
    Can be given in combo with rapid or short acting
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4
Q

list the long acting insulin

  1. onset
  2. peak
  3. Duration
  4. coverage–when to give and used with what other insulins
A

Detemir and Glargine

  1. 2 hours
  2. 3-9 hours (Detemir) and NO PEAK for Glargine
  3. 6-24 hours..dose dependent (Detemir) and 20-24hours for Glargine
  4. Detemir covers insulin for 24 hours—BASAL insulin
    Glargine has fewer hypoglycemic episodes than NPH

do not mix long acting with other insulins*

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5
Q

DOA for Repaglinide

A

2 hours

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6
Q

DOA for Acarbose

A

6 hours

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7
Q

DOA for metformin

A

6 hours

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8
Q

DOA for Glyburide

A

18 hours

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9
Q

DOA for GLipizide

A

20 hrs

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10
Q

DOA for canalilflozin

A

24 hours

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11
Q

DOA for Glimepiride

A

24 hours

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12
Q

DOA for Sitagliptin

A

24 hours

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13
Q

insulin

  • type of hormone
  • pre cursor?
A

polypeptide hormone

pro-insulin—->insulin + c-peptide

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14
Q

how is insulin produced

A

recombinant DNA technology

  • get it from an animal source
  • used to use bovine or equine
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15
Q

factors that affect the duration of various insulins

A
  1. dose
  2. timing of dose
  3. inj site
  4. blood supply
  5. temperature of PT
  6. patients physical activity
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16
Q

why is insulin always SC or IV injection and not PO?

A

polypeptide hormone=degrades in GI tract Rapidly

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17
Q

when is IV insulin indicated?

A

more so for emergent situations

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18
Q

routes of admin for insulin

A

SC–daily basis
IV–emergent settings
inhalation—not as effective tho

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19
Q

adverse effects of insulin

A
  1. hypoglycemia
  2. weight gain
  3. local injection site rxns
  4. lipodystrophy
  5. bronchosapsms (with inhaled use)
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20
Q

s/s of hypoglycemia begin at what serum level?

A

70 or below

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21
Q

do we want patients to adminsiter Insulin in the same site or various ones? why?

A

VARIOUS

so lipodystrophy and site irritation does not occur

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22
Q

what is the general progression of DM2 treatments

A
  1. diet–life style mods
  2. 1+ metformin
  3. combo therapy
  4. multiple injections of insulin—— after 15+ years of DM2… a lot of patients are not producing insulin bc their bodies are sooooooo resistant and need exogenous insulin
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23
Q

Aspart
Onset
Peak action
DOA

  • when do administer
  • combo tx with?
A

Rapid acting
onset: 5-15 mins
peak: 0.5-1.5 hours
DOA: 2-4 hrrs

  • Give this at the same time as a meal… 15 mins B4
  • can be used with NPH or long acting
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24
Q

Glulisine
Onset
Peak action
DOA

A

Rapid acting
onset: 5-15 mins
peak: 0.5-1.5 hrs
DOA: 2-4 hrs

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25
Q 
Lispro 
Onset
Peak action 
DOA
*when do administer 
*combo tx with?
A

Rapid acting
onset: 5-15 mins
peak: 0.5-1.5 hours
DOA: 2-4 hrrs

  • Give this at the same time as a meal… 15 mins B4
  • can be used with NPH or long acting
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26
Q

Regular Insulin
onset
peak hrs
DOA

  • when to give
  • comb tx with?
A

Short acting
onset: 0.5-1.0 hours
peak: 2-3 hours
DOA: 3-6 hours

Give 30-60 mins B4 meals
-used with NPH or long acting insulin

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27
Q

when do you administer regular insulin

-what happens if you wait longer or dont eat the meal?

A

30 mins before meal

*hypoglycemia

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28
Q

when do you administer rapid acting insulin?

-what happens if you wait longer or dont eat the meal?

A

15 mins before meal

*hypoglycemia

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29
Q

Neutral Protamine Hagedorn (NPH)

  • onset
  • peak
  • DOA

how long does this cover insulin for?
-combo tx with?

A

Intermediate acting

onset: 2-4 hours
peak: 4-12 hours
DOA: 8-18 hours

  • covers insuliin for half the day or over night
  • can be given in combo with rapid (lispro or aspart) or short acting (reg insulin)
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30
Q

what makes regular insulin become NPH

A

+zinc

+protamine–allows for delay in the onset and peak and longer DOA

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31
Q

which insulin preparation do we use in PTs to create “basal rate” of insulin

A

NPH

prevents those peaks and valleys of glucose levels throughout the day

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32
Q

which insulin is indicated for a PT who we want to keep an effective basal rate throughout the day

A

NPH

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33
Q

longer acting insulin preps are meant to control glucseo for greater than _______ hours

A

12

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34
Q

contraindication for long acting insulin preps

A

in treatment of acute “spikes” in glucose

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35
Q

Detemir

  • onset
  • peak
  • DOA

covers insulin for how long
-mix with others?

A

LONG acting

onset: 2 hrs
peak: 3-9hrs
DOA: 6-24 hours

  • cover insulin for 1 full day–>providing basal insulin
  • DO NOT give with other insulins at the same time*
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36
Q

Glargine

  • onset
  • peak
  • DOA

-mix with others?

A

LONG acting

onset: 2-4 hours
Peak: no real peak
DOA: 20-24 hours

  • FEWER hypoglycemic episodes vs NPH**
  • DO NOT give with other insulins at the same time*
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37
Q

which long acting insulin is used for replacement of basal rate insulin>

A

glargine

DOA=20-24 hrs

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38
Q

which insulin prep is similar to NPH

A

Detemir

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39
Q

who is indicated for the combo-preps of insulin

A

WELL controled DM patients

*had DM for a long time, know their diet, know their own peaks and valleys naturally

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40
Q

storage of ALL insulin preps?

A

in the fridge

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41
Q

what is added to insulin preps to make them longer acting?

A

protamine

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42
Q

frequency of the combo preps??

A

usually twice/day BEFORE meals

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43
Q

List the Dual Combo Preps

A

75/25 Proatmine Lispro(75%) and Lispro (25%)

70/30 Protamine aspart (70%) and Aspart (30%)

50/50 Priatmine lispro and lispro

70/30 NPH (70) and Regular insulin (30)

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44
Q 
For all combo preps 
onset
peak
DOA 
*which is MC used?
A

combo prep

Onset: 5-20 mins
Peak: DUAL peaks.. so first is after two hours and then second peak another 2-3 hours
DOA: 10-16 hours

70% NPH and 30% reg insulin MC used

45
Q

which has fewer hypoglycemic episodes–NPH or Glargine

A

Glargine

46
Q

should PTs mix diff insulins in the same bottle?

A

NO

47
Q

when do we generally give the long acting preps?

A

am
or
pm

48
Q

amylin

A

hormone that is co-secreted by B cells of the pancreas in a NORMAL state
-delays gastric emptying,
delays post-prandial glucagon
improves satiety

49
Q 
Pramlinitide 
drug lass 
MOA
INDs
when to take 
Kinetics 
SE 
Contra
A

Synthetic Amylin Analogs

MOA/ind: used as meal-time adjunct to insulin therapy for both DM 1 and DM 2

kinetics: SQ pre-prandial PRIOR to insulin dose. can be given if patient is making their own insulin OR taking exogenous
timing: dose must be RIGHT before meal and before insulin

SE:

  • MUST decrease insulin dose by 50% for meal-time dosing to ensure no hypoglycemia
  • nausea
  • anorexia

contra:
- pre-existing delayed gastric emptying
- do not mix this drug in same syringe as insulin

50
Q

factors that influence the effects of insulin (5)

A
  • stress
  • infection
  • nutrition in the last 12 hours
  • exercise
  • hydration
51
Q

when will insulin work at its best?

A

when glycemic control is monitored closely

52
Q

in general: how much insulin will drop BGL by 50 mg/dl?

A

1 unit

53
Q

in general: 1 unit of insulin drops the BGL by?

A

50 mg/dl

54
Q

PT A is 400 pounds and PT B is 100 pounds, one unit of insulin is adminsterd to each–which PT will experience a greater drop in BGL?

A

PT B–100 lb pt

BC fatter patient has more body surface area—more systemic inflammation– more adipose tissue–

55
Q

when treating a PT.. what is the MOST IMP first thing to do before starting tx

A

get their baseline BGL via finger stick
diaries over the course of 1 or 2 wks
knowing peaks and valleys
am, pm, nightime and before bed

56
Q

normal BGL range

A

70-120

57
Q

basal rate is generally calculated how?

A

body wt

58
Q

standard insulin injection involves?

A

two daily injections

59
Q

intensive outPT treatment involves?

A

3+ injections daily

60
Q

ADA recc a target gluclose of______ and a HbA1C below

A

BGL 154 or < which translates to a HbA1c or <7%

61
Q

HbA1c define

A

measurement by which hemoglobin also has glycosylated “sugar” hemoglobin attached to it.

62
Q

The higher above 6.5% for HbA1c means?

A

the poorer control the patient has.

63
Q

standard hospital in-PT treatment has a BGL targget of?

A

<120

64
Q

whcih drug is mainly used inpatient?

A

humalog or Lispro bc its cheap

65
Q

inPT fingerstick scheduling?

what is tighter control scheduling?

A

am and before meals and pm

  • AC
  • HS

tigher control:
q2
q4
q6

66
Q

indications for insulin drips inpatient

  • where is this done?
  • what is the scheudling for finger sticks
A

post-op
HHS
DKA

monitored ward where fingersticks done q1 hr

67
Q

what is an incretin hormone

A

GLP-1 or glucagon like peptide 1
and
Glucose-dependent insulinotropic polypeptide (GIP)

is release in gut
resp for 60-70% of post prandial insulin secretion

68
Q

what is incretin effect

A

-when we take glucose ORALLY, a higher response to it occurs to the body where we secrete MORE insulin than if we were to administer glucose IV
why?
BECAUSE of the incretin hormones released—GLP-1 and GIP

69
Q

when are incretin hormones secreted

A

post-prandially

70
Q

which insulin is adminsited during emergent?

A

REGULAR IV insulin

71
Q

which patients may require decrease in insulin dose?

A

renal insufficicnecy DM

72
Q

what does “basal” insulin levels mean

A

basal=fasting

73
Q

insulins used to acheive basal control

A

NPH

any of the long acting–gargline or detemir

74
Q

variable degrees of insulin resistance, impaired insulin secretion, and excessive hepatic glucose production explains?

A

DM 2

75
Q

when do we start pharmaco-managing DM 2 patietns?

what do we stsrt with

A

not controlled with diet alone

*start with PO

76
Q

PTs who are older than ____ YO are less/more likely to respond well to oral glucose lowering agents and may require____ adjunct

A

40 yo
respond LESS
insulin adjunct

77
Q

list the sulfonylureas.. also called?

  • MOA (3)
  • administered how
  • which generation are these three
  • is there a risk for hypoglycemia with these drugs ?
  • SE?
  • what kind of PT education would you give
  • kinetics
A 
SECOND GEN: 
**insulin secretagogues**
Glybruide 
Glipizide 
Glimepiride

YES risk of hypoglycemia

*PO
MOA
-promotes insulin release from B cells of pancreas
-additionally reduce hepatic glucose production by liver
-increase peripheral insulin sensitivity

SE:

  • hypoglycemia**
  • hyPERinsulinemia
  • Wt gain

PT Education:

  • side effects
  • balance this accordingly with meals
  • need to see nutritionists

Kinetics:

  • heavily met by liver
  • excreted by kidneys in urine/feces
78
Q

hypoglycemia is MC with which class of anti-hyperglycemics used in DM 2

A

sulfonylureas

79
Q

Glyburide

  • class
  • route
  • contraindications
A

Sulfonylureas
PO
contra: patients with CRF

80
Q

list the drugs that reduce effect of sulfonylureas–leading to??? (6)

A

leads to hyperglycemia/loss of glucose control

  1. atypical antipsychotics
  2. corticosteroids
  3. diuretics
  4. Niacin
  5. Phenotihaizdes
  6. Sympathomimetics
81
Q

list the drugs that increase/potentiate effect of sulfonylureas–leading to??? (7)

A

leads to HYPOglycemia

  1. azoles
  2. BBs
  3. Chloramphenicol
  4. Clarithromycin
  5. MOAIs
  6. Salicylates
  7. Sulfonamides
82
Q

Metaglitinides–list the drugs

  • MOA
  • administered how
  • when to use?
  • is there a risk for hypoglycemia with these drugs ?
  • SE?
  • what kind of PT education would you give
  • kinetics
A

Repaglinide and Nateglinide
MOA: similar to the sulfonlyureas except these drugs are FASTER onset of action and SHORTER DOA
*insulin secregogues

Admin: PO
IND: monotherapy in PTs with contraindications to metformin or in combo with metformin

SE:

  • some hypoglycemia,
  • LOTS of drug-drug interactions since heavily hepatically metabolized
  • wt. gain

education: HAS to be given with food

83
Q

Repaglinide contraindicated ?? Who can get it

A

hepatic impairment–contra

CAN give to renal failure PTs and sulfa allergies

84
Q

Biguanides

list the drugs

A

metformin

insulin sensitizer

85
Q

Metformin

  • MOA
  • Kinetics/dynamics
  • SE
  • Indications
  • contraindications
A

MOA: increases glucose uptake and use by the target tissues—decreasing insulin resistance (drives glucose INTO cells essentially).
**reduces hepatic gluconeogenesis*

kinetics/dynamics

  • PO
  • very well absorbed
  • NOT bound to proteins
  • excreted urine

SE

  • little effects with hypoglycemia
  • N/V/D
  • Wt loss (which is good for DM2)
  • renal dysfunction
  • macrocytic anemia–B12 deficiency
  • sometimes severe N/V/D
  • metabolic acidosis (esp in PTs who are renal failure)

CONTR:

  • Acute MI
  • sepsis
  • CHF
  • acute or chronic renal failure

Indicactions:

  • first line PO agent for DM 2
  • can be used alone or in adjunct with insulin or insulin secretagogues (incrs risk of hypoglycemia)
86
Q

does metformin promote insulin secretion?

A

NO!!

it is an insulin senitizer— it increases glucose uptake

87
Q

long term use of metformin is assoc with what diseases

A

B12 deficiency and lactic acidosis prodcution

*why we always get CBC and CMP on PTs for check-ups to make sure no anion-gap acidosis

88
Q

what is the BBW for Metformin XR?

A

traces of NDMA in the make up of the pill. N-nitrosodiumethylamine–carcinogenic

89
Q

Thiazolidinediones

  • drug class
  • MOA
  • list the drugs
  • indications
  • SE
  • Contras
A

Pioglitazone and Rosiglitazone

Insulin Sensitizers

MOA: increases insulin sensitivity at the peripheral receptor sites at skel muslces, adipose tissue and liver. Does not promote B islet cell insulin release
no risk of hypoglycemia or hyperinsulinemia
basically, increases insuin receptor sensitivity at the adipose skel muscles and liver rec sites–increased utilization of glucose and decrease glucose production

  • indications:
  • adjunct therapy ONLY ( not monotherapy)
  • second line drug for DM 2

SE

  • hepatoxicity
  • periph edema
  • chf exacerbations
  • incr rates of fx in females
90
Q

SE for Pioglitazone

A

peripheral edema
CHF exacerbations
liver toxicity (ETOH, hepatitis, etc)

91
Q

SE for Rosiglitazone

A

Cardiovascular events

92
Q

DM 2 treatments PO
1st line
2nd line

A 
1st Metformin 
2nd Pioglitazone (only if PT does not have HF)
93
Q

what needs to be done before putitng a PT on Rosiglitazone or Pioglitazone

A

get LFTs

94
Q

which drugs are effective in highly insulin-resistant patients?

A

Thiazolindiinediones—– Pioglitazone and Rosiglitazone

95
Q 
Alpha-GLucosidase Inhibitors 
-what is alpha-glucosidase? 
name the drug 
-MOA 
-when to administer 
-what is the effect on insulin secretion 
-kinetics 
-indications (what is impotant for the PT to have) 
-Contras 
-SE 
-complications
A

Acarbose and Miglitol

alpha-glucosidase–>enzyme found in brush border of intestinal mucosa–resp for b/d of CHOs into glucose

MOA: delays intestinal glucose absoprtion by inhibitng pancreatic alpha amylase–esentially delays digestion of CHOs

Administration: after FIRST bite of EACH meal

NO effect on insulin secretion: NOT a sensitizer or stimulator

kinetics:
- poor absorbed

INDS:

  • pt needs to be able to make their own insulin (see above for reasoning)
  • good to use in PTs with renal insufff

SE

  • GI cramping
  • diarrhea

compications:
- -non-infectious hepatitis

Contras:
-IBS/IBD, bowel obstrucion, colonic dz or ischemic bowel

96
Q

DPP-4

functin?

A

Dipeptidyl peptidase-4

-resp for inactivation of incretin hormones–such as GLP-1

97
Q

GIP

A

glucose dependent insulinotropic peptide

*incretin hormone

98
Q

GLP-1

A

glucagon like peptide 1

*incretin homrone

99
Q
  1. -Glinides
  2. -Liptin
  3. -azone
  4. -liflozin
  5. -tide
A
  1. Metaglitinides
  2. DDP-4 inhibitors
    3 Thiazolidinediones
  3. Sodium-glucose cotranspoter 2 inhibitors
  4. GLP-1 receptor agonists (SCs)
100
Q

DPP-4 inhibitors

  • drug names
  • MOA
  • kinetics
  • SE
  • indications
  • administration
A

-liptin
Alogliptin, Linagliptin, Saxagliptin, Sitagliptin (januvia)

MOA: block DDP-4–>prolonging the acitivty of incretin homrones to increase release of insulin in response to meals—also reduced inapp secretion of glucagon.

Kinetics: PO, well abosrbed, can be combined with any other of the DM2 PO drugs and insulin

SE:

  • HA
  • Nasopharyngitits
  • Acute pancreatitis
  • severe joint point
  • skin changes

INDS:
-monotherapy or adjunctive

ADMIN:

  • take w. or w.o food
  • once/day
101
Q 
Sodium-glucose cotransporter 2 inhibitors 
drug names 
MOA 
SE 
Indications 
contras
A

-liflozin
Canagliflozin, Dapagliflozin, Ertugliflozin, Empaglifozin

MOA: increases urinary glucose excretion by lowering renal glucose threshold—–reabsorbtion of filtered glucose in the tubular lumen of kidney

SE:

  • decrease the sodium reasborption causing—OSMOTIC DIURESIS—– causing HYPOTENSION
  • genitourinary infections-frequent UTIs and yeast infections
  • transient n/v

Indications:
-can be given with metformin

contra:
- renal impairment

102
Q

which drug is approved to reduce cardiovascular events in PTS with DM 2

A

Empagliflozin—– NA-glucose cotransporter 2 inhibitor

103
Q

whats the advantage to first line PO agents?

A

better overall HgA1C reduction over time

104
Q

List the SQ injectables for DM 2
what is their drug class
MOA
general BBW for all

A

-tide
GLP-1 rec agonists

Dulaglutide (truicity)
Liraglutide
Semaglutide
Exenatide

MOA: long acting GLP-1 receptor agonists–they increase glucose dependent insulin release, decreases secretion of glucagon, slows gastric empty and increases satiety

BBW: can cause medulary thyroid CA
CONTRA IN MEN 2 PT

105
Q

Dulaglutide (truicity)
drug class
scheduling for dosing
SE

A

GLP-1 rec agonists
Kinetics: SC
WEEKLY dosing

SE: 
BBW: for medullary thyroid CA 
hypersensitivty GI 
gallbladder dz 
actue pancreatitis
106
Q 
Liraglutide 
drug class 
MOA 
Kinetics 
Admin scheduling 
SE
A

GLP-1 agonist
kintetics: can be in combo with metformin or other POs or with basal insulin

Dosing: 1x/day

SE: injection site rxn, NV/D
BBW: medullary thyroid CA

107
Q

Semaglutide

  • kinetics
  • SE
  • dosing scheudle
A

GLP-1 agonist

kinetics: yes in combo with other oral agents.. not for DM1 PT tho

Dose: once weekly

SE:
injection site rxn, NV/D
BBW: medullary thyroid CA

108
Q 
Exenatide 
kinetics 
dosing schedyle 
SE 
INds 
how much can this reduce HbA1C
A

GLP-1 agonist

kintics:
SC
-can work in combo with basal insulin.

Inds
-for PT who failed metformin

SE:
injection site rxn, NV/D
BBW: medullary thyroid CA

Can reduce HbA1c by 1.5-2 points

109
Q

Other non-hyperglycemic agents to give
Indications?
MOA

A

Bromocriptine–dopamine agonist

Colvestram–bile sequestrant

  • not really used due to high SE profile
  • would be given to pre-DM

MOA: somehow lowr HbA1C

Pharmacology (28 decks)

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