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
Q

Oral agent: TZDs
-glitazone

MOA/USES

A

Pioglitazone (Actos), Rosiglitazone (Avandia)

NOT initial therapy
Used in 2-3 drug combo, NEVER monotherapy

MOA: improve insulin sensitivity of cells

26
Q

Oral agent: TZDs

CONTRA/INTERACTION/Monitoring

A

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
Q

Oral agent: Meglitinides MOA/USES

A

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
Q

Oral agent: Meglitinides
CONTRA/AE

A

Contraindications:
CAUTION in renal and hepatic patients
CAUTION Pregnancy

AE: risk for hypoglycemia

29
Q

Oral agent: Meglitinides
INTERACTION/MONITORING

A

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
Q

Oral agent: Glucagon-Like Peptide Agonists (Incretins)

MOA/USES

A

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
Q

Oral agent: Glucagon-Like Peptide Agonists

CONTRA/AE/Monitor

A

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
Q

Oral agent: DDP-4
-gliptins

MOA/USES

A

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
Q

Oral agent: DDP-4
CONTRA/AE

A

Contraindications: impaired renal function = dose adjustment, pancreatitis hx

AE: hypoglycemia may occur in combo w/ sulfonylureas, insulin

34
Q

Oral agent: Amylin Agonist

MOA/USES

A

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
Q

Oral agent: Amylin Agonist

CONTRA/AE/Interactions

A

Contraindications: gastroparesis, drugs stimulate GI motility

AE: hypoglycemia w/ insulin, DEC insulin by 50%

BLACK BOX: hypoblycemia

Interactions: anticholinergics, garlic, chromium, gymnema

36
Q

Oral agent: SGLT-2

MOA/USEs

A

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
Q

Oral agent: SGLT-2

CONTRA/AE/Interactions

A

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
Q

Insulin

A

pancreatic hormone

fosters the influx of glucose out of the bloodstream and into the cell

Only therapy for DM T1

39
Q

DM T1 PATHO

A

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
Q

Actions of Insulin

A

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
Q

Onset, Peak, Duration: RAI

A

Lispro, Aspart

Onset: 15-30 min
Peak: 1-3 hrs
Duration: 3-5 hrs

42
Q

Onset, Peak, Duration: Short-acting insulin

A

Regular

Onset: 30-60 min
Peak: 2-4 hrs
Duration: 3-7 hrs

43
Q

Onset, Peak, Duration: Intermediate-acting

A

NPH

Onset: 1-2 hrs
Peak: 4-12 hrs
Duration: 10-16 hrs

44
Q

Onset, Peak, Duration: Long-acting

A

Detemir,
Glargine (no peak)

Onset: 3-6 hrs
Peak: 3-9 hrs
Duration: 20-24 hrs

45
Q

Insulin Regimens

A

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
Q

Inhaled Insulin

A

Afrezza
inhalation powder
rapid acting insulin
TX T1/T2
preprandial dosing

dispensed in 4-unit and 8-unit cartridges

47
Q

Inhaled insulin: BLACK BOX

A

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
Q

Inhaled insulin: CONTRA/AE

A

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
Q

Insulin AE/INTERACTIONS

A

AE:
hypoglycemia
hypokalemia
lipodystrophy
local reactions
bronchospasm w/ inhaled

Interactions: corticosteroids, thyroid hormone, estrogens, thiazide diuretics, ETOH, BB

50
Q

DM Pediatrics

A

T2 rising
look for acanthosis nigricans, dark pigmentation in skin creases and flexural areas

insulin and metformin only drugs approved for adolescents

51
Q

Gestational DM

A

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
Q

When goal of treatment is NOT MET

A

patient can be at target but remain uncontrolled

metformin + incretin + basal insulin

target = blood glucose level

control = HgbA1C

53
Q

Starting BASAL INSULIN

A

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
Q

Reg + NPH Dosing

A

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
Q

DM T1 DOC

A

ALWAYS INSULIN

patients do NOT make insulin, must be supplied

variety of routes: SubQ, inhaled, pumps

will be started and managed by endocrine

56
Q

DM T2 DOC

A

Managed in primary care

1st Line: Metformin
Add-Ons: GLP-2 or SGLT-2

Alternatives: sulfonylureas, TZDs, DDP-4s

4th step: basal insulin

57
Q

Special cases: BG > 400

A

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