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Endocrine/Thyroid Flashcards

1
Q

Hypothyroidism PATHO/CAUSES

A

HYPO = DEC thyroid hormone = SLOW

Causes:
iodine deficiency
hashimoto thyroiditis
TX hyperthyroidism
Drugs: amiodarone, lithium

Deficit of thyroid hormone

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2
Q

Hypothyroidism SX

A

slow mind, body
weak heartbeat
constipation
slow reflexes
hair thinning
depression
thin skin
dry skin
cold intolerance

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3
Q

Hypothyroidism DIAGNOSTIC CRITERIA

A

TSH - test of choice (elevated)

T4 and T3 - DEC

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4
Q

Hypothyroidism GOALS OF THERAPY

A

return patient to euthyroid state

TREATMENT is LIFELONG

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5
Q

Hypothyroidism MONITOR RESPONSE

A

Serum TSH every 6-8 wks

TSH every 6 months once euthyroid

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6
Q

Hypothyroidism DRUG THERAPY

A

Levothyroxine (T4)
Brand: Synthroid

Do NOT switch b/w brand and generic

Dosage:
START: 1.6mcg/kg/day
Adjust in 25mcg intervals every 4-6 wks
TSH 1-3

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7
Q

Hypothyroidism: DRUG AE/EDUCATION

A

Pregnancy = need INC dosage until delivery

AE: Sx hyperthyroidism

education:
1) should not expect immediate relief in sx: takes 2-4 wks
2) Lifelong therapy
3) periodic lab testing

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8
Q

Hyperthyroidism PATHO/CAUSES

A

HYPER = INC thyroid hormone = FAST

Causes:
Graves disease
toxic nodular goiter
thyrotoxicosis
drug related
pituitary tumor

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9
Q

Hyperthyroidism SX

A

wide pulse pressure
sweating
anxiety
fine tremors
brink reflexes
diarrhea
weight loss
afib

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10
Q

Hyperthyroidism DIAGNOSTIC CRITERIA

A

LOW TSH
HIGH free T4 or T3

Free T4 - most useful and preferred to confirm dx (elevated)

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11
Q

Hyperthyroidism GOALS OF THERAPY

A

return to euthyroid state

therapy usually 1-2 years

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12
Q

Hyperthyroidism TREATMENT OPTIONS

A

1) meds
2) radioactive iodine ablation (NO PREGNANCY)
3) complete or partial thyroidectomy

Screen for hypothyroidism after RAI or surgery

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13
Q

Hyperthyroidism DRUG THERAPY

A

Methimazole (Tapazole)
Propylthoiuracil (PTU)

MOA: inhibit organification, block conversion of T4 to T3

Methimazole longer acting = less frequent dosing

Drugs may be used pre RAI or surgery

AE: minimal, rash, arthralgias, itching

BLACK BOX: Liver injury

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14
Q

Hyperthyroidism ADJUVANT MEDS

A

1) BB - DEC sx of adrenergic stimulation from INC T4

2) Iodine-containing compounds - SSKI, treat thyroid storm

3) Lithium - block release of thyroid hormone

4) Glucocorticoids - reduce conversion of T4 to T3

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15
Q

DM Patho

A

supply and demand
1) beta cell destruction (T1)
2) decreased production (T2)
3) insulin not recognized or resisted
4) altered hepatic metabolism of glucose

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16
Q

DM2 TREATMENT OPTIONS

A

prevent macro and microvascular complications

TLC’s
Education
Glucose monitor, strips, stylets
foot care

GOALS of therapy:
HgbA1C <6.9, preferably <6.5
Preprandial glucose: 90-130
Postprandial glucose: <180

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17
Q

Oral agent: Biguanides
MOA/USES

A

Metformin (Glucophage)
FIRST-LINE TX

MOA:
1) INC peripheral glucose uptake and utilization
2) DEC hepatic glucose production
3) DEC intestinal absorption

Excreted unchanged in urine

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18
Q

Oral agent: Biguanides Benefits/Dosing

A

Bene:
No hypoglycemia
No weight gain
Combines w/ other agents

Dosing: MAX dose is 2,550mg/day, but NO additional benefit when dose exceeds 2000mg

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19
Q

Oral agent: Biguanides
CONTRAINDICATIONS/AE/Monitoring

A

Contraindications:
1)renal dysfunction, metabolic acidosis
2) CAUTION HF, dehydration, resp failure, ETOH, liver damage
3) hold for 48 hrs w/ iodine study

AE: GI disturbance (take w/ food), usually 2 wk limitation, STOP if risk of DEHYDRATION
Lactic acidosis

Monitoring: renal function before tx and annually, HgbA1C q3 months, home glucose monitoring

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20
Q

Oral agent: Sulfonylureas
MOA/USES

A

Oldest
2nd gen: more potent, more safe

MOA: stimulates insulin release from beta cells

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21
Q

Oral agent: Sulfonylureas CONTRAINDICATIONS/AE/monitoring

A

Contraindications: SULFA allergy, THIAZIDE diuretic

AE: hypoglycemia, weight gain, hyperinsulinemia, GI disturbances, photosensitivity

Monitoring: HgbA1C, home monitoring

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22
Q

Oral agent: Sulfonylureas INTERACTIONS

A

ETOH produces Antabuse type reaction

NO ETOH

Take same time each day

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23
Q

Oral agent: Alpha-glucosidase inhibitor

MOA/USES

A

Acarbose and Miglitol

MOA: inhibit absorption of complex carbs from small bowel

DEC post-prandial glucose

Uses:
1) post-prandial hyperglycemia
2) High HgbA1C
3) poor dietary adherence
4) High CHO diet ethnicities

24
Q

Oral agent: Alpha-glucosidase inhibitor
CONTRA/AE/Monitoring

A

Must be taken w/ first bite food

Contraindications:
1) bowel disease
2) absorptive disorders
3) cirrhosis

AE: GI effects d/t fermentation: flatulence, bloating, distension, diarrhea (try slow titration of dose to DEC effects)

Monitoring: before tx and annually assess RENAL function, SERUM TRANSAMINASE, FBG, HgbA1C q3 months

combo w/ sulfonylureas = RISK HYPOGLYCEMIA

25
Oral agent: TZDs -glitazone MOA/USES
Pioglitazone (Actos), Rosiglitazone (Avandia) NOT initial therapy Used in 2-3 drug combo, NEVER monotherapy MOA: improve insulin sensitivity of cells
26
Oral agent: TZDs CONTRA/INTERACTION/Monitoring
Contraindications: 1) liver disease 2) HF (fluid retention) 3) BLACK BOX: cardiotoxicity Interactions: DEC oral contraceptive concentration Monitoring: ALT before and q2 months D/C if ALT levels are x3 upper limit of normal MONITOR LIVER FUNCTION
27
Oral agent: Meglitinides MOA/USES
Short-acting insulin secretagogues used to lower post-prandial BG levels works similar to sliding scale insulin used as adjunct therapy MOA: 1) INC secretion of insulin by beta cells 2) Rapid acting: take 20 mins before meals, peaks in 1 hr
28
Oral agent: Meglitinides CONTRA/AE
Contraindications: CAUTION in renal and hepatic patients CAUTION Pregnancy AE: risk for hypoglycemia
29
Oral agent: Meglitinides INTERACTION/MONITORING
Interactions: 1) CYP inducers: INC metabolism 2) CYP inhibitors: DEC metabolism = hypoglycemia Monitoring: FBG, HgbA1C q3 months Do NOT take if meal is skipped
30
Oral agent: Glucagon-Like Peptide Agonists (Incretins) MOA/USES
MOA: Bind to GLP-1 receptors on beta cells to imitate an incretin to potentiate glucose-stimulated insulin secretion SLOW gastric emptying INC satiety Injectable only
31
Oral agent: Glucagon-Like Peptide Agonists CONTRA/AE/Monitor
Contraindications: pancreatitis, severe renal impairment, severe GI disease AE: N/V/D, may subside over time Interactions: warfarin, serum level of OC's DEC Monitor for PANCREATITIS Separate from other meds that rely on rapid absorption from GI
32
Oral agent: DDP-4 -gliptins MOA/USES
Sitagliptin, Saxagliptin, Linagliptin, Alogliptin MOA: blocks the enzyme used to breakdown the body's own GLP-1 well tolerated Can be used as MONOTHERAPY Oral administration, expensive
33
Oral agent: DDP-4 CONTRA/AE
Contraindications: impaired renal function = dose adjustment, pancreatitis hx AE: hypoglycemia may occur in combo w/ sulfonylureas, insulin
34
Oral agent: Amylin Agonist MOA/USES
Pramlintide (Symlin) Injectable: subq MOA: works like GLP-1 agonists: DEC glucagon secretion, SLOW gastric emptying, suppresses appetite DEC caloric intake = INC satiety = weight loss 2nd LINE for those using INSULIN at mealtimes USES: tx DM T1/T2
35
Oral agent: Amylin Agonist CONTRA/AE/Interactions
Contraindications: gastroparesis, drugs stimulate GI motility AE: hypoglycemia w/ insulin, DEC insulin by 50% BLACK BOX: hypoblycemia Interactions: anticholinergics, garlic, chromium, gymnema
36
Oral agent: SGLT-2 MOA/USEs
newest class Canagliflozin (Invokana), Dapglifozin (Farxiga), Pagliflozin (Jardiance) 1st CHOICE after Metformin MOA: lowers reabsorption of plasma glucose concentration in the kidneys = INC glucose excretion possible renal protective role Adjunct to diet/exercise Administer same time everyday, before first meal
37
Oral agent: SGLT-2 CONTRA/AE/Interactions
Contraindications: 1) severe renal impairment or ESRD 2) Allergy 3) TX of DKA or DM T1 AE: genital fungal infections, UTI, hypotension, INC LDL, bladder cancer Interactions: 1) monitor digoxin 2) may INC effect of ACE/ARB
38
Insulin
pancreatic hormone fosters the influx of glucose out of the bloodstream and into the cell Only therapy for DM T1
39
DM T1 PATHO
autoimmune process destroys beta cells No insulin produced = No glucose into cells Demand > Supply DM T2 eventually progresses to beta cell failure = insulin required
40
Actions of Insulin
1) INC storage of glucose in the liver 2) Promotes TG synthesis 3) INC uptake K+ and phosphate in the liver 4) Promote glycogen synthesis in muscles 5) DEC protein catabolism and ketosis 6) DEC circulation of free fatty acids and INC storage of TGs
41
Onset, Peak, Duration: RAI
Lispro, Aspart Onset: 15-30 min Peak: 1-3 hrs Duration: 3-5 hrs
42
Onset, Peak, Duration: Short-acting insulin
Regular Onset: 30-60 min Peak: 2-4 hrs Duration: 3-7 hrs
43
Onset, Peak, Duration: Intermediate-acting
NPH Onset: 1-2 hrs Peak: 4-12 hrs Duration: 10-16 hrs
44
Onset, Peak, Duration: Long-acting
Detemir, Glargine (no peak) Onset: 3-6 hrs Peak: 3-9 hrs Duration: 20-24 hrs
45
Insulin Regimens
GOAL: mimic endogenous insulin Basal insulin: 1) for maintenance (chronic/prophylaxis) 2) NPH, Lente, Glargine, Detemir 3) provides constant multi-hour coverage Bolus insulin: 1) for quick actions (acute/abortive) 2) aspart, lispro, regular 3) RAI, SAI
46
Inhaled Insulin
Afrezza inhalation powder rapid acting insulin TX T1/T2 preprandial dosing dispensed in 4-unit and 8-unit cartridges
47
Inhaled insulin: BLACK BOX
1) asthma and COPD = acute bronchospasm CONTRAINDICATED: chronic lung disease before starting, detailed medical hx, physical exam, spirometry (FEV1) must be done to ID potential lung disease
48
Inhaled insulin: CONTRA/AE
NOT recommended for tx DKA NOT recommended in smokers or who have quit for less than 6 months CONTRAINDICATIONS: hypoglycemia, COPD, hypersensitivity AE: hypoglycemia, cough, throat pain or irritation, HA
49
Insulin AE/INTERACTIONS
AE: hypoglycemia hypokalemia lipodystrophy local reactions bronchospasm w/ inhaled Interactions: corticosteroids, thyroid hormone, estrogens, thiazide diuretics, ETOH, BB
50
DM Pediatrics
T2 rising look for acanthosis nigricans, dark pigmentation in skin creases and flexural areas insulin and metformin only drugs approved for adolescents
51
Gestational DM
screen between 24-28 wks control w/ diet and exercise if not controlled, insulin (ADA standards) Metformin and Glyburide: 1) trials support short-term safety and efficacy 2) crosses placenta 3) metformin slightly INC risk prematurity
52
When goal of treatment is NOT MET
patient can be at target but remain uncontrolled metformin + incretin + basal insulin target = blood glucose level control = HgbA1C
53
Starting BASAL INSULIN
continue Metformin + noninsulin agent START: 10U/day or 0.1-0.2U/kg/day Adjust every 1-2 wks: 10-15% or 2-4 units If becomes hypoglycemic, DEC by 4 units
54
Reg + NPH Dosing
Starting two insulins BID (NPH + reg) 1) AM: give 2/3 total dose w/ 2:1 ratio NPH: reg 2) PM: give 1/3 total dose in 1:1 ratio adjust response in 1-2 unit increments Which one to adjust: look at peak and duration times AM dose given at breakfast 1) reaction within 1st 4 hours: REG 2) reaction within 5-8 hrs: NPH
55
DM T1 DOC
ALWAYS INSULIN patients do NOT make insulin, must be supplied variety of routes: SubQ, inhaled, pumps will be started and managed by endocrine
56
DM T2 DOC
Managed in primary care 1st Line: Metformin Add-Ons: GLP-2 or SGLT-2 Alternatives: sulfonylureas, TZDs, DDP-4s 4th step: basal insulin
57
Special cases: BG > 400
1) go to insulin 2) do not pass metformin 3) do not forget to collect HgbA1C Once glucose is under control, then attempt to titrate back to oral agents alone

Pharmacology (12 decks)

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