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Pharmacology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

incretin effect

A

when food enters GI system, incretin hormones (GLP-1 and GIP) are released which stimulate insulin secretion

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2
Q

function of GLP-1

A

secreted by intestines to suppress glucagon, slow gastric emptying, increase satiety, stimulate insulin secretion

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3
Q

function of DPP-4

A

splits GLP-1 rapidly into inactive metabolite

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4
Q

function of selective sodium-dependent glucose cotransporter-2 (SGLT2)

A

in kidneys; reabsorbs majority of filtered glucose (unless glucose > 180)

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5
Q

AACE and ADA guidelines for tx options based off A1C

A

AACE
2 meds if A1C > 7.5%
metformin & 6 other meds as first-line

ADA
2 meds if A1c > 8.5%
metformin= first line therapy

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6
Q

antidiabetic for HF (esp HFrEF)

A

SGLT2i

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7
Q

if on metformin, no cardiac/renal issues, A1C above target, and need to minimize hypoglycemia, what 4 antidiabetic agents recommended to be added?

A

DPP-4i
GLP-1 RA
SGLT2i
TZD

if still above target, add 3rd agent (usually SGLT2i and GLP-1 RA if already on)
if still above target consider SU or insulin

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8
Q

if on metformin, A1C above target, want to promote weight loss, what meds?

A

GLP-1 RA or SGLT2i

can combine if ineffective
if triple therapy needed, use lowest weight gain risk (DPP-4i** if not on GLP-1 RA)
THEN
SU, TZD, basal insulin

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9
Q

if on metformin, A1C above target, cost is issue, what meds?

A

SU
TZD
then combine if need more
if still need more, consider insulin or other agents based on cost

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10
Q

alternative to mealtime insulin if already on maximum basal regimen as recommended by ADA? AACE?

A

GLP-1 RA

AACE guidelines= GLP-1 RA or SGLT2 or DPP-4 are options as well

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11
Q

when adding basal or NPH insulin, how do you start/titrate?

A

Bedtime
10 IU/day or 0.1-0.2 IU/Kg/day
set FPG target
titrate 2 IU Q3 days to reach FPG
if hypoglycemia, determine cause. If no cause, lower by 10-20%

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12
Q

mechanism, adverse effects/contraindications sulfonylureas

A

enhance insulin secretion blocking K channels= influx Ca; suppresses hepatic glucose production
SE: hypoglycemia & weight gain; hemolytic anemia
contraindication: renal or hepatic impairment, sulfa allergy
***can’t stim insulin at extremely high glucose levels

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13
Q

antidiabetics that end in “-mide” or “-ide”

A

sulfonylureas
DiaBeta, Glynase, or Micronase (glyburide or glibenclamide)
Amaryl (glimepiride)
Diabinese (chlorpropamide)
Glucotrol (glipizide)
Tolinase (tolazamide)
Tolbutamide.

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14
Q

antidiabetics that end in “-nide”

A

nonsulfonylurea secretagogues (glinides)
*meglitinides= epaglinide and nateglinide

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15
Q

nonsulfonylurea secretagogues aka glinides

mechanisms of action, SE, comparison to SUs

A

enhance insulin secretion blocking K channels= influx Ca; suppresses hepatic glucose production
shorter onset/duration compared to SU
*reduce postmeal glucose levels; taken 15-30 min before meals

same SE as SUs= low blood sugars (hypoglycemia) and weight gain

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16
Q

biguanide

A

metformin only approved one
decreases hepatic glucose production, increases insulin sensitivity in hepatic & peripheral muscles
does NOT increase insulin secretion so hypoglycemia not a risk
contraindicated= eGFR < 30, liver disease
avoid excessive alcohol

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17
Q

SE metformin

A

decreased appetite, nausea, diarrhea
B12 malabsorption > neuropathy
lactic acidosis (renal disease or elderly)

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18
Q

thiazolidinediones (TZDs) & SE

A

increase insulin sensitivity
delayed onset for several weeks
***fluid retention, edema, weight gain
contraindicated in HF
limb fx, causes ovulation, bladder cancer, MI with rosiglitazone but reduced cardiac risk w/ pioglitazone

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19
Q

antidiabetics end in “azone”

A

thiazolidinediones (TZDs)
rosiglitazone, pioglitazone

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20
Q

alpha-glucosidase inhibitors

A

GI SE limit use
acarvose & miglitol
delay absorption of carbs to reduce postprandial BG

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21
Q

DPP-4i aka gliptins and SE

A

-liptin
sitagliptin, saxagliptin, linagliptin, alogliptin
inhibit DPP-4 which degrades GLP-1 so basically more GLP-1 and lower postprandial BG
SE: nasopharyngitis & HA, acute pancreatitis
hypoglycemia NOT risk
No cardiac benefit

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22
Q

SGLT-2i and SE

A

-ozin
canagliflozin, dapagliflozin, empagliflozin, ertugliflozin
reduces reabsorbed glucose in kidneys > increase glucose excretion and lower BG

SE: dehydration, kidney problems, increased cholesterol, and yeast infections

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23
Q

antidiabetics end in -ozin

A

SGLT-2i

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24
Q

Best SGLT-2i for ASCVD risk

A

**empagliflozin (reduce cardiac death)
canagliflozin (reduce cardiac death, MI, stroke; increased risk lower amputation)
dapagliflozin (no effect on ASVD risk but decrease death and HF)

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25
Q

adverse effects SGLT-2i

A

UTI, genital mycotic infections, hypotension, bone fx, fournier gangrene

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26
Q

antidiabetic end in “tide”

A

GLP-1 RA

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27
Q

GLP-1 RA aka incretins and SE contraindications

A

produce glucose-dependent insulin secretion, reduce postmeal glucagon secretion, increase satiety, regulate gastric emptying. WEIGHT LOSS

ex: exenatide, lireaglutide, dulaglutide, semaglutide, lixisenatide

SE: n/v/d, all except lixisenatide have black box warning thyroid c-cell tumor, pancreatitis

contraindication: personal/family hx thyroid tumor, h/o pancreatitis, exenatide & lixisenatide contraindicated in renal disease (the 2 with X)

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28
Q

which GLP-1 RA reduce risk of cardiovascular events

A

liraglutide, dulaglutide, injectable semaglutide

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29
Q

GLP-1 RA that reduce risk or worsening nephropathy

A

liraglutide & semaglutide

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30
Q

last option PO antidiabetic therapy

A

central-acting dopamine agonist
bromocriptine
improves insulin sensitivity

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31
Q

central-acting dopamine agonist

A

bromocriptine
last option antidiabetic therapy
improves insulin sensitivity

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32
Q

bile acid sequestrants and interactions

A

colesevelam
rarely used
drug interactions= levothyroxine, glyburide, OCP, phenytoin, warfarin, digoxin
malabsorption fat-soluble vitamins (A, D, E, K)

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33
Q

regular insulin

A

human insulin
30 min before meal

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34
Q

rapid acting insulin

A

aspart, glulisine, lispro
onset 15-30 min
peak 1-2 hrs

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35
Q

intermediate/NPH insulin

A

covers in between meals and overnight
onset 30 min
unknown peak/duration

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36
Q

rule for mixing insulin

A

NPH insulin > shorter acting drawn into syringe first

Always draw up regular (clear) insulin before NPH (cloudy)

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37
Q

what’s added for ultra rapid acting insulin

A

niacinamide

38
Q

long-acting insulin

A

glargine, detemir, degalude

39
Q

benefits of insulin glargine

A

higher concentration 300 U/mL so more prolonged release
duration 36 hrs
fewer episodes hypoglycemia

40
Q

slowest insulin release

A

degludec
half life 25 hrs, duration 42 hrs
patients can miss/delay dose just keep 8 hr interval between any 2 doses

41
Q

when to consider prandial insulin in T2DM

A

when on basal insulin, FBG at/near goal but A1C remains high

42
Q

what to consider before prandial insulin T2DM

A

GLP-1 RA

43
Q

amylin

A

pramlintide acetate= synthetic amylin
T1DM
slows gastric emptying, suppresses glucagon, increases satiety

SQ before meals

can delay absorption of PO meds
don’t give w/ meds that alter GI motility

44
Q

ex ACEi, ARBs, CCB

A

ACEi = Lisinopril (-pril)
ARBs= Losartan (-sartan)
CCB= Amlodipine (Norvasc) Diltiazem (Cardizem, Tiazac, others) Felodipine

45
Q

ssx hypoglycemia

A

shaky, sweating, fatigue, hunger, HA, confusion

46
Q

tx hypoglycemia

A

if awake 15g carbs, wait 15 min > retest

47
Q

ex 15g carbs

A

4 oz OJ
box raisins
8 oz skim mimlk
3-4 glucose tabs

48
Q

electrolytes in DKA

A

low NA
high K

49
Q

tx DKA and HHS

A

NS 1-1.5 mL/hr
regular insulin 0.1 U/Kg/hr IV
when < 250 dextrose 5% added to fluids

50
Q

tx neuropathy

A

pregabalin, duloxetine, gabapentin

51
Q

tx PAD

A

aspirin or clopidogrel
cilostazol to improve blood flow/improve sx if needed

52
Q

goal glucose for critically ill diabetic

A

140-180

53
Q

HPT axis

A

hypothalamic-pituitary-thyroid axis
hypothalamus releases TRH which stim. pituitary to release TSH > thyroid release T3 & T4 > back to hypothalamus

54
Q

what meds can inhibit release of TRH & TSH

A

TRH= inhibited by somatostatin & analogs
TSH= inhibited by dopamine, dopamine agonists, high levels glucocorticoids

55
Q

target TSH

A

0.5-4.5

56
Q

TSH compared to T3/T4 in thyroid axis

A

2 fold change in T4 will result in 100 fold change TSH
inverse relationships: high TSH = HYPOthyroid, low TSH= HYPERthyroid

57
Q

target TSH when being treated thyroid disorder

A

mean value= 1.5

58
Q

what other conditions can elevate TSH

A

significant obesity (BMI >40), elderly

59
Q

ssx hypothyroidism

A

myxedema, delayed deep tendon reflexes, fatigue, weight gain, paresthesia, cold intol., dry skin, constipation, decreased appetite, goiter, bradycardia

60
Q

TSH reference ranges for hypothyroidism dx

A

mild/subclinical= 4.5-10
overt= > 10

61
Q

first-line tx hypothyroidism and why

A

synthetic LT4 (levothyroxine/Synthroid)
mimics normal physiology of thyroid; peripheral tissue convert T4 to T3 so if tx with T3 the peripheral tissue lose ability to control local metabolic rates
7-10 day half life so smooth dose-response curve with little peak/trough effect

62
Q

Narrow therapeutic index (NTI)

A

small differences in dose or blood concentration may lead to serious therapeutic failures and/or adverse drug reactions

63
Q

Issue that bioequivalence has on NTI of LT4

A

FDA bioequivalence methods not strict enough
switching LT4 products when stable hypothyroidism has resulted in abnormal TSH levels so not actually therapeutically equivalent
very small changes in LT4 dose changes TSH drastically

64
Q

what to do if LT4 is switched

A

TSH in 6-8 weeks then retitrate PRN

65
Q

LT4 initiation in mild/subclinical hypothyroidism

A

12.5-50mcg/day, titrate Q6-8 weeks
overtime, LT4 dose will need to slowly be increased as thyroid loses function

66
Q

LT4 dose mod-severe ssx overt hypothyroidism

A

(< 65 y/o) 1.6-1.8 mcg/kg/day
( > 75 y/o or ischemic heart disease) 1 mcg/kg/day 12.5-25 mcg/day
change dose by 10-20% Q6-8 weeks

Most adult patients may be started on the full replacement dose of levothyroxine (~75-125 mcg/day) without problems. However, patients with cardiac concerns or elderly patients may benefit from starting on a lower dose (~12.5-50 mcg/day) and titrated as tolerated.

67
Q

Risks of long-term over treatment of hypothyroidism

A

a-fib & other cardiac, anxiety, depression, mental status change, osteoporosis

68
Q

best time to take LT4

A

evening on empty stomach

69
Q

what factors alter LT4 dose requirements

A

increased dose requirements when admin w/ Ca or iron supplements, PPI
should take 2 hours before or 6 hours after Ca or iron

decreased= age

70
Q

how often to monitor thyroid

A

while titrating= 6-8 weeks
stable= 6-12 months, more freq. if status change like pregnancy

71
Q

hypothyroidism & pregnancy

A

TSH immediately
will need higher dose LT4 (20-30% or 2 tabs more)
monthly TSH monitoring for mid-low normal range
don’t take w/ prenatal (contain Ca & iron)

72
Q

Tx Myxedema coma

A

200-400mcg LT4 IV
glucocorticoids (hydrocortisone 50mg-100mg Q6h)

73
Q

In what situations do you consider insulin

A

Insulin in conjunction with Metformin should be considered as initial therapy for patients with very high HgbA1C values (> 9%) at diagnosis (usually basal insulin is the first insulin added), especially if the patient is symptomatic. Other dual or triple therapy may also be considered with high initial HgbA1C

If oral agents aren’t working

74
Q

thyrotoxicosis

A

clinical manifestations of high T3 or T4 that are excessive for the individual (hyperthyroidism)

75
Q

tx for thyrotoxicosis

A

Methimazole or PTU is generally used for young adults or patients with mild thyrotoxicosis, small goiters, or fear of isotopes. The drugs do not permanently damage the thyroid and are associated with a lower chance of posttreatment hypothyroidism (compared with RAI or surgery). There is a 50% chance of remission of hyperthyroidism with long-term thiourea therapy.

76
Q

most common cause hyperthyroidism in elderly

A

toxic thyroid nodules or multinodular goiter NOT Graves
over tx of hypothyroidism

77
Q

what can cause false elevated FT4 & false +TSHR-SAb/misdiagnosed Graves

A

high levels biotin

78
Q

dangers of subclinical/mild hyperthyroidism

A

increased cardiovascular morbidity/mortality risk
increase fx rates
cognitive impairment/dementia

tx is controversial and dependent

79
Q

common tx regimens for hyperthyroidism

A

beta blockers (propranolol, nadolol IF needed metoprolol, atenolol)
potassium iodide (SSKI or Lugol solution)
antithyroid drugs (propylthiouracil [PTU] or methimazole [MMI])

80
Q

beta blockers for hyperthyroidism- why? contraindication?

A

manifestations mediated by beta adrenergic system, BB relieve palpitations, tremor, anxiety, heat intolerance

propranolol and nadolol preferred bc don’t affect T4 conversion to T3

propranolol 10mg-40mg QID (HR goal 90bpm)

contraindicated in decompensated HF & athma

81
Q

what to use hyperthyroidism if beta blockers contraindicated

A

clonidine, verapamil, diltiazem
to control HR

82
Q

why iodide for hyperthyroidism?

A

large doses inhibit synthesis/release thyroid hormones
30-100mg of iodide
T4 reduced in 24 hrs, last 2-3 weeks
usually used before surgery or thyroid storm

83
Q

toxic affects of iodide

A

hypersensitivity rxn
iodism= palpitations, depression, wt loss, pustular skin eruptions
gynecomastia

84
Q

Antithyroid durgs/thionamide agents

A

propylthiouracil (PTU) and methimazole (MMI)
inhibit thyroid hormone synthesis by interfering w/ thyroid peroxidase-mediated iodination of tyrosine residues
immunosuppressive effects
PTU also inhibits conversion T4 to T3

85
Q

propylthiouracil (PTU) or methimazole (MMI) for hyperthyroidism?

A

MMI 10-20mg/day
can be given single daily dose, better overall safety, less hepatotoxic

86
Q

how long on antithyroid drugs for graves?

A

tapered after 12-24 months, remission of Graves after 1-2 years of therapy

87
Q

SE antithyroid drug

A

skin rash, arthralgias (joint stiffness), GI upset
hepatotoxicity
*agranulocytosis most serious (fever, malaise, ST, low neutrophil) > d/c immediately, ABX

88
Q

tx of choice w pregnancy & Graves

A

PTU in first trimester, lowest possible dose
switch to MMI 2nd/3rd trimesters

89
Q

nonthyroidal illness/euthyroid sick syndrome

A

dopamine, octreotide, high dose glucocorticoids can reduce TSH

90
Q

most common drug induced thyroid abnormalities

A

amiodarone- blocks T4 > T3 = hypothyroid (usually resolves after 3 months); thyroid must be monitored Q3-6 months

lithium- hypothyroidism after years; inhibits thyroid hormone synthesis/secretion

interforon-alpha for hep C- hypothyroid

Pharmacology (12 decks)

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