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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
adverse effects SGLT-2i
UTI, genital mycotic infections, hypotension, bone fx, fournier gangrene
26
antidiabetic end in "tide"
GLP-1 RA
27
GLP-1 RA aka incretins and SE contraindications
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)
28
which GLP-1 RA reduce risk of cardiovascular events
liraglutide, dulaglutide, injectable semaglutide
29
GLP-1 RA that reduce risk or worsening nephropathy
liraglutide & semaglutide
30
last option PO antidiabetic therapy
central-acting dopamine agonist bromocriptine improves insulin sensitivity
31
central-acting dopamine agonist
bromocriptine last option antidiabetic therapy improves insulin sensitivity
32
bile acid sequestrants and interactions
colesevelam rarely used drug interactions= levothyroxine, glyburide, OCP, phenytoin, warfarin, digoxin malabsorption fat-soluble vitamins (A, D, E, K)
33
regular insulin
human insulin 30 min before meal
34
rapid acting insulin
aspart, glulisine, lispro onset 15-30 min peak 1-2 hrs
35
intermediate/NPH insulin
covers in between meals and overnight onset 30 min unknown peak/duration
36
rule for mixing insulin
NPH insulin > shorter acting drawn into syringe first Always draw up regular (clear) insulin before NPH (cloudy)
37
what's added for ultra rapid acting insulin
niacinamide
38
long-acting insulin
glargine, detemir, degalude
39
benefits of insulin glargine
higher concentration 300 U/mL so more prolonged release duration 36 hrs fewer episodes hypoglycemia
40
slowest insulin release
degludec half life 25 hrs, duration 42 hrs patients can miss/delay dose just keep 8 hr interval between any 2 doses
41
when to consider prandial insulin in T2DM
when on basal insulin, FBG at/near goal but A1C remains high
42
what to consider before prandial insulin T2DM
GLP-1 RA
43
amylin
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
ex ACEi, ARBs, CCB
ACEi = Lisinopril (-pril) ARBs= Losartan (-sartan) CCB= Amlodipine (Norvasc) Diltiazem (Cardizem, Tiazac, others) Felodipine
45
ssx hypoglycemia
shaky, sweating, fatigue, hunger, HA, confusion
46
tx hypoglycemia
if awake 15g carbs, wait 15 min > retest
47
ex 15g carbs
4 oz OJ box raisins 8 oz skim mimlk 3-4 glucose tabs
48
electrolytes in DKA
low NA high K
49
tx DKA and HHS
NS 1-1.5 mL/hr regular insulin 0.1 U/Kg/hr IV when < 250 dextrose 5% added to fluids
50
tx neuropathy
pregabalin, duloxetine, gabapentin
51
tx PAD
aspirin or clopidogrel cilostazol to improve blood flow/improve sx if needed
52
goal glucose for critically ill diabetic
140-180
53
HPT axis
hypothalamic-pituitary-thyroid axis hypothalamus releases TRH which stim. pituitary to release TSH > thyroid release T3 & T4 > back to hypothalamus
54
what meds can inhibit release of TRH & TSH
TRH= inhibited by somatostatin & analogs TSH= inhibited by dopamine, dopamine agonists, high levels glucocorticoids
55
target TSH
0.5-4.5
56
TSH compared to T3/T4 in thyroid axis
2 fold change in T4 will result in 100 fold change TSH inverse relationships: high TSH = HYPOthyroid, low TSH= HYPERthyroid
57
target TSH when being treated thyroid disorder
mean value= 1.5
58
what other conditions can elevate TSH
significant obesity (BMI >40), elderly
59
ssx hypothyroidism
myxedema, delayed deep tendon reflexes, fatigue, weight gain, paresthesia, cold intol., dry skin, constipation, decreased appetite, goiter, bradycardia
60
TSH reference ranges for hypothyroidism dx
mild/subclinical= 4.5-10 overt= > 10
61
first-line tx hypothyroidism and why
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
Narrow therapeutic index (NTI)
small differences in dose or blood concentration may lead to serious therapeutic failures and/or adverse drug reactions
63
Issue that bioequivalence has on NTI of LT4
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
what to do if LT4 is switched
TSH in 6-8 weeks then retitrate PRN
65
LT4 initiation in mild/subclinical hypothyroidism
12.5-50mcg/day, titrate Q6-8 weeks overtime, LT4 dose will need to slowly be increased as thyroid loses function
66
LT4 dose mod-severe ssx overt hypothyroidism
(< 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
Risks of long-term over treatment of hypothyroidism
a-fib & other cardiac, anxiety, depression, mental status change, osteoporosis
68
best time to take LT4
evening on empty stomach
69
what factors alter LT4 dose requirements
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
how often to monitor thyroid
while titrating= 6-8 weeks stable= 6-12 months, more freq. if status change like pregnancy
71
hypothyroidism & pregnancy
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
Tx Myxedema coma
200-400mcg LT4 IV glucocorticoids (hydrocortisone 50mg-100mg Q6h)
73
In what situations do you consider insulin
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
thyrotoxicosis
clinical manifestations of high T3 or T4 that are excessive for the individual (hyperthyroidism)
75
tx for thyrotoxicosis
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
most common cause hyperthyroidism in elderly
toxic thyroid nodules or multinodular goiter NOT Graves over tx of hypothyroidism
77
what can cause false elevated FT4 & false +TSHR-SAb/misdiagnosed Graves
high levels biotin
78
dangers of subclinical/mild hyperthyroidism
increased cardiovascular morbidity/mortality risk increase fx rates cognitive impairment/dementia tx is controversial and dependent
79
common tx regimens for hyperthyroidism
beta blockers (propranolol, nadolol IF needed metoprolol, atenolol) potassium iodide (SSKI or Lugol solution) antithyroid drugs (propylthiouracil [PTU] or methimazole [MMI])
80
beta blockers for hyperthyroidism- why? contraindication?
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
what to use hyperthyroidism if beta blockers contraindicated
clonidine, verapamil, diltiazem to control HR
82
why iodide for hyperthyroidism?
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
toxic affects of iodide
hypersensitivity rxn iodism= palpitations, depression, wt loss, pustular skin eruptions gynecomastia
84
Antithyroid durgs/thionamide agents
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
propylthiouracil (PTU) or methimazole (MMI) for hyperthyroidism?
MMI 10-20mg/day can be given single daily dose, better overall safety, less hepatotoxic
86
how long on antithyroid drugs for graves?
tapered after 12-24 months, remission of Graves after 1-2 years of therapy
87
SE antithyroid drug
skin rash, arthralgias (joint stiffness), GI upset hepatotoxicity *agranulocytosis most serious (fever, malaise, ST, low neutrophil) > d/c immediately, ABX
88
tx of choice w pregnancy & Graves
PTU in first trimester, lowest possible dose switch to MMI 2nd/3rd trimesters
89
nonthyroidal illness/euthyroid sick syndrome
dopamine, octreotide, high dose glucocorticoids can reduce TSH
90
most common drug induced thyroid abnormalities
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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