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Review Part 2 Flashcards

1
Q

What are the clinical presentations of hyperthyroidism?

A
  • Weight Loss
  • Palpitations
  • Diarrhea
  • Tachycardia
  • A. Fib
  • Bounding Pulse
  • Polyuria
  • Heat Intolerance
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2
Q

What are the labs/lab results used to dx hyperthyroidism?

A
  • TSH: ↓

- TH (T4): ↑

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3
Q

What are the clinical presentations of hypothyroidism?

A
  • Dryness
  • Constipation
  • Bradycardia
  • Dyspnea
  • Peripheral Edema
  • Delayed DTR’s
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4
Q

What are the labs/lab results used to dx primary and secondary/tertiary hypothyroidism?

A 
Primary:
- TSH: ↑
- TH (T4): ↓
Secondary or tertiary: will decrease together
- TSH: Normal to ↓
- TH (T4): ↓
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5
Q

What are the clinical presentations of Myxedema coma crisis?

A
  • Hypotension
  • Reduces LOC
  • Seizures
  • Hypothermia
  • Macroglossia
  • Ptosis
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6
Q

What are the labs/lab results used to dx Myxedema coma crisis?

A
  • TSH:↑

- TH (T4): ↓

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7
Q

What are the clinical presentations of Graves disease?

A
  • Hyperthyroid symptoms
  • Exophthalmos
  • Dermatopathy
  • Onycholysis
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8
Q

What are the labs/lab results used to dx Graves disease?

A
  • TSH: ↓

- TH (T4): ↑

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9
Q

What are the clinical presentations of Subacute thyroiditis?

A
  • Onset acute & severe
  • Sore Throat
  • Exquisitely tender, Enlarged gland (sm goiter)
  • Febrile
  • Signs of: hyper then hypo
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10
Q

What are the labs/lab results used to dx Subacute thyroiditis?

A
  • Thyroid function x 6 mo.
  • WBC: ↑ (left shift)
  • ESR: ↑
  • FNA Bx: if in doubt
  • TPO Ab: Negative
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11
Q

What are the clinical presentations of Thyrotoxicosis/ Thyroid storm?

A
  • Fever
  • Vomiting
  • Delirium
  • Diarrhea
  • Seizures/Coma
  • Jaundice
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12
Q

What are the labs/lab results used to dx Thyrotoxicosis/ Thyroid storm?

A
  • TSH: ↓

- TH (T4): ↑

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13
Q

What is adrenarche?

A

Onset of androgen-dependent body changes such as growth of axillary and pubic hair, body odor, and acne

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14
Q

What is acral?

A

Pertaining to peripheral body parts, such as toes and fingers

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15
Q

What is acanthosis nigricans?

A
  • Common skin pigmentation disorder

- Dark patches of skin with a thick, velvety texture

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16
Q

What is amenorrhea?

A

Absence of menstruation

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17
Q

What is exopthalmosis?

A
  • Prominence of eyes

- “bulging eyes”

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18
Q

What is proptosis?

A

Abnormal protrusion or displacement of an eye or other body due to all other causes

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19
Q

What is hirsutism?

A

Condition of male-pattern hair growth in women

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20
Q

What is menarche?

A

Onset of menstruation

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21
Q

What is precocious puberty?

A

Onset of puberty at an abnormally early age

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22
Q

What is puberty?

A

Appearance of sexual hair

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23
Q

What is striae?

A

Irregular areas of skin that look like bands, stripes or lines

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24
Q

What is thelarche?

A

Onset of female breast development

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25
Q

What is virilization?

A

Biological development of sex differences

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26
Q

What is acromegaly?

A
  • Abnormal growth of hands, feet, jaw and face.
  • D/t overproduction of GH in adulthood
  • Does not grow linear
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27
Q

What is dwarfism?

A
  • GH deficiency
  • Etiology: genetics
  • Common complications: Bowing of legs, hunching of the back, and crowded teeth
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28
Q

What is disproportionate and proportionate dwarfism?

A

Disproportionate:
- Average size torso w/ shorter extremities or vice versa
Proportionate:
- Body parts are proportion but shortened

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29
Q

What is Galactorrhea?

A
  • Discharge of milk-like substance from the breast

- Caused by Hyperprolactinemia

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30
Q

What is an acrochordon and what diseases are these seen in?

A
  • Skin tags
  • Common in DM pts
  • If in younger pts think Cushing’s disease
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31
Q

What is the workup for possible DM?

A
  • Screen all adults over 45 yrs q 3 yrs
  • At least 1 risk factors (obesity, family hx, hx of gestational dm) + BMI >25
  • Early screening for AA and Native Americans
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32
Q

What is the MC cause of SIADH?

A

ADH producing tumors: SCLC

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33
Q

What is the clinical presentation of SIADH?

A
  • Hyponatremia sxs
  • Weakness
  • HA
  • Weight gain
  • N/V
  • Coma
  • Mental status change
  • Seizures
  • Irritability
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34
Q

What are the complications of SIADH?

A
  • Hyponatremia
  • Hypo-osmolality
  • Increase in water retention and impaired water excretion
  • Loss of or dilution of electrolytes or solutes (Na, K, Cl)
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35
Q

What are the dx test for SIADH?

A
  • CBC: H&H ↓
  • CMP: BUN/Cr ↓ and electrolytes (Na, K, Cl): ↓
  • Plasma Cortisol: ↓
  • ADH: ↑
  • CT scan of head and CXR: Meningitis, Tumor mass, Neoplasm, Infectious process
  • Radioimmunoassay of ADH
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36
Q

What is the management of SIADH?

A
  • Treat underlying cause
  • Fluid restriction of 800-1,000 ml/d
  • IV saline for symptomatic pts only (confusion, convulsions, coma)
  • TURF TURF TURF
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37
Q

What is the cause of DI?

A
  • Kidneys are unable to prevent excretion of water
  • ADH deficiency (pituitary and Neurogenic DI)
    OR
  • Unresponsiveness of renal tubules to ADH (Nephrogenic DI)
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38
Q

What are the causes of Neurogenic/pituitary DI?

A
  • Idiopathic
  • Neoplasm of brain of pituitary gland
  • Head trauma: basal skull fx
  • Granulomatous disorders: sarcoidosis or TB
  • Meningitis
  • Post encephalitis
  • MS
  • Guillain barre syndrome
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39
Q

What are the causes of Nephrogenic DI?

A
  • Drugs: Lithium
  • Metabolic: hypercalcemia and hypokalemia
  • Sarcoidosis
  • Sickle Cell disease
  • Low protein diets
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40
Q

What is the presentation of DI?

A
  • Abrupt onset
  • Nocturia
  • Polyuria: 2.5 - 6 L/day
  • Polydipsia
  • Neuro manifestations: Seizures, HA, visual field defects
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41
Q

What is the complication of DI?

A

Inability to concentrate urine

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42
Q

How do you diagnose DI?

A
  • Vasopressin: differentiate between nephro and neuro DI. >50% increase of urine osmolarity = neurogenic
  • Hypernatremia
  • Urine and plasma osmolarity: >295 mOsm/kg
  • MRI of pituitary gland
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43
Q

What is the management of DI?

A

Endocrinology consultation for dx testing, referral and structured tx plan

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44
Q

What are the functions of ADH?

A
  • Regulate water retention in the kidneys

- Vascular constriction

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45
Q

What are ADH deficiencies?

A
  • Cause of DI

- Increased thirst and frequent urination

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46
Q

What are EKG findings of hypocalcemia?

A

Prolonged QT interval

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47
Q

What are EKG findings for hypokalemia?

A
  • Prominent U wave

- T wave flattened

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48
Q

What are EKG findings of hyperkalemia?

A
  • Tall peaked T waves
  • QT interval shortened
  • P wave flattening
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49
Q

What are EKG findings of hypomagnesemia?

A
  • Torsades
  • Prolonged PR and QT interval
  • Afib
  • Vfib
  • Ventricular tachycardia
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50
Q

What are incidentalomas?

A
  • Pituitary lesions that are discovered while investigating other neurological problems
  • Not causing any physiological changes/associated symptoms
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51
Q

What is the cause of gigantism?

A
  • Too much growth hormone as a child

- Epiphyseal growth plates are open

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52
Q

What is the presentation of gigantism?

A
  • Vertical growth
  • Tall stature course facial features
  • Enlarged forehead
  • Large hands and feet
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53
Q

What are S/Sxs of a pituitary adenoma (peds lecture)?

A
  • Vision changes and HA

- Hormones can also be affected, interfering with menstrual cycles and causing sexual dysfunctions

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54
Q

What is the tx of a pituitary adenoma (peds lecture)?

A
  • Surgery and Medication to block excess hormone production or shrink the tumor
  • In some cases: radiation
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55
Q

What is precious puberty? and what age does it typically occur in girls and boys?

A
  • Onset of puberty at an early age
  • Girls: 8 yrs (may be 7 in AA, Mexican and American girls)
  • Boys: 9 yrs
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56
Q

What are the labs/lab results used to dx central (true) precocious puberty?

A
  • LH, FSH, testosterone, estradiol, DHEAS, Androstenedione: all elevated
  • Refer!
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57
Q

What are the labs/lab results used to dx peripheral variety precocious puberty?

A
  • Low gonadotropins and various steroid results

- Refer!

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58
Q

What pubertal changes are present that needs to be evaluated? which hormones are involved in each?

A
  • Breast development: estrogen
  • Body odor, pubic/axillary hair, skin changes (androgens)
  • Boys: if androgen changes w/o testicular growth think exogenous testosterone
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59
Q

What is delayed puberty? and what age does it typically occur in girls and boys?

A
  • Girls: no breast development by age 13 yrs

- Boys: no testicular development (SMR 2) by age 14 yrs

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60
Q

What is the MC delayed puberty?

A 
Constitutional delay 
(more concerning compared to familial short structure)
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61
Q

What is constitutional delay?

A
  • Puberty and height delay
  • Bone age delay
  • Often positive w/family hx
  • Follow longitudinally, occasionally low dose short course testosterone in boys
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62
Q

What are the screening tests for delayed puberty?

A
  • General health: CBC, CMP, thyroid

- Gonadotropins: LH, FSH should be ↓

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63
Q

If levels of gonadotropin are increased what would that mean?

A

Gonad failure

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64
Q

What is Klinefelter syndrome? and what are the clinical presentations?

A
  • Occurs in males (C.47, XXY)
  • Small testes
  • Sparse pubic, armpit, and facial hair
  • Enlarged breast
  • Tall stature
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65
Q

What are the lab findings in a pt w/ Klinefelter syndrome?

A
  • LH and FSH: ↑

- Testosterone: ↓

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66
Q

What is Turner syndrome? and what are the clinical presentations?

A
  • Occurs in Females (C.45, XY)

- webbed neck, lymphedema nevi (brown spots), short stature

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67
Q

What are the lab findings in a pt w/ Turner syndrome?

A
  • LH and FSH: ↑

- Estrogen: ↓

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68
Q

What is tanner staging (I-V)?

A
  • I: flat, alONE –> no pubic hair
  • II: 11 yrs old, 2 breast buds form, pubic hair appear, 2 balls (teste enlargement)
  • III: 13 yrs old, breast mounds form, course, curly pubic hair, penis increases in size and testicular growth
  • IV: 14 yrs old, coarse pubic hair, not on thighs yet, raised alveolar, 2 mounds form
  • V: adult, pubic hair extends onto thighs
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69
Q

When does tanner staging usually start? and what stage is the 1 sign of puberty?

A
  • 10 yrs old

- Tanner stage II is the 1st sign of puberty

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70
Q

What is Prader-Wili syndrome?

A
  • Hypogonadotropic hypogonadism
  • Prenatal hypotonia
  • Postnatal growth delay
  • Development disabilities
  • Obesity after infancy
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71
Q

What are early childhood sings of Prader-Wili syndrome?

A
  • Constantly hungry
  • Hyperphagia
  • Obesity
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72
Q

What does Prader-Wili syndrome cause in adolescent children?

A
  • Premature development and axillary hair w/delay of the other secondary sex characteristics
  • Increased incidence of epilepsy and scoliosis
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73
Q

What are the physical characteristics of Prader-Wili syndrome?

A
  • Almond-shaped eyes
  • High/narrow forehead
  • Thin upper lip w/ small, downturned mouth
  • Prominent nasal bridge
  • Small feet and hands
  • Soft skin
  • Excess fat
74
Q

What is the onset, age, body type in type 1 DM? and is ketosis common or rare?

A
  • Sudden onset
  • Any age, typically young
  • Usually thin
  • Ketosis is common
75
Q

What is the classic triad of DM1?

A
  • Polyuria
  • Polydipsia
  • Weight loss
76
Q

What is the onset, age, body type in type 2 DM? and is ketosis common or rare?

A
  • Gradual onset
  • Onset of age mostly in adults
  • Frequently obese
  • Ketosis is rare
77
Q

Why is there usually no sxs in a pt with congenital hypothyroidism?

A

Usually no sxs at birth d/t having moms TSH level in utero

78
Q

What are early signs of congenital hypothyroidism?

A
  • Decreased activity, tone, and temp
  • Prolonged jaundice
  • Large fontanelles
  • Puffy hands
  • Protuberant abdomen
79
Q

What are late signs of congenital hypothyroidism?

A
  • Poor growth
  • Lethargy
  • Mottling
  • Breathing difficulty
  • Edema
  • Umbilical hernia
  • Developmental delay
80
Q

What lab test should be performed for congenital hypothyroidism? and how do you treat?

A
  • TSH, if elevated get T4 and T3

- Begin Levothyroxine as soon as dx is confirmed (early brain damage is irreversible)

81
Q

Aside from labs what are other workups that can be done for congenital hypothyroidism?

A
  • Radioactive iodine test to look for absent or ectopic thyroid gland
  • May see a goiter: defects in synthesis
  • Check iodine levels (severe iodine deficiency should be seen)
82
Q

What is primary hypogonadism?

A

Ovaries or testes themselves do not function properly

83
Q

What is central hypogonadism?

A

Centers in the brain that control the gonads (hypothalamus and pituitary) do not function properly

84
Q

What can you expect to see in girls (pre-puberty) with hypogonadism?

A
  • Will not begin menstruating

- Will affect breast development and height

85
Q

What can you expect to see in women with hypogonadism?

A
  • Hot flashes
  • Loss of body hair
  • Low libido
  • Menstruation stops
86
Q

What can you expect to see in boys (pre-puberty) with hypogonadism?

A
  • Lack of muscle and beard development

- Growth problems

87
Q

What can you expect to see in men with hypogonadism?

A
  • Breast enlargement
  • Decrease beard and body hair
  • Muscle loss
  • Sexual problems
88
Q

What is the first line oral tx for DM2? (class name and drug name)

A

Bigunaides: Metformin

89
Q

What is the MOA of Metformin?

A
  • Reduces hepatic resistance to insulin and decreases hepatic glucose dumping
  • Insulin sensitizers in the liver
90
Q

What are the ASEs of Metformin?

A

GI distress:

  • Nausea
  • Diarrhea
  • Abdominal pain
91
Q

How do you improve GI distress caused by metformin?

A
  • Slow dose- titration
  • Administration w/after a meal
  • ER formulations
92
Q

Metformin is primarily eliminated by what? and is CI in pts with what?

A
  • The kidneys

- Impaired renal fxn or acute/unstable HF d/t concern of lactic acidosis

93
Q

What eGFR levels do you not want to start Metformin? What eGFR levels do you want to d/c Metformin in a pt whos been taking it for a while?

A
  • Don’t start: <45

- Discontinue: <30

94
Q

What other drug is apart of the Biguanides class? and why was it withdrawn?

A
  • Phenformin

- High rates of mortality and lactic acidosis

95
Q

What line of tx is Sodium-GLucose Transporter-2 (SGLT-2) Inhibitors? and how are they excreted?

A
  • 2nd line tx

- Renal

96
Q

What are the drug names in the SGLT-2 class?

A

“-gliflozin”

  • Canagliflozin
  • Dapagliflozin
  • Empagliflozin
  • Ertugliflozin
97
Q

What is the MOA of SGLT-2?

A
  • Reduce blood sugar by increasing urinary glucose excretion.
  • Reabsorption of glucose (co-transported with sodium) occurs in the proximal tubule via the SGLT.
98
Q

Which SGLT-2 is usually added to monotherapy that shows better lower A1c effect as well as better effects on weight and hypoglycemia?

A

Canagliflozin + Metformin

99
Q

What are the “advantages” of SGLT-2 drugs?

A
  • Reduce CV (HF) and renal events
  • Lower A1c
  • Low risk of hypoglycemia
  • Lower B/P (↓ systolic by 3-5 mmHg)
100
Q

SGLT-2 drugs are eliminated by what? and is CI in pts with what?

A
  • The kidneys

- Severe renal impairment

101
Q

What are the ASEs/Warnings of SGLT-2 drugs?

A
  • GU infxns (UTI and candida)
  • Euglycemia DKA
  • Amputation
  • Fournier gangrene
  • Fracture risk
  • $$$
102
Q

What line of tx are the Thiazolidinediones? are eliminated by what?

A
  • 3rd line

- Hepatic

103
Q

What are the drug names in the Thiazolidinedione class?

A
  • Pioglitazone

- Rosiglitazone

104
Q

What is the MOA of the Thiazolidinedione drugs?

A
  • Agonism of the PPAR-y receptor
  • Insulin sensitizers in the peripheral insulin-responsive tissues
  • Receptor located primarily in adipose tissue
105
Q

What is the rate of glycemic control of the Thiazolidinedione drugs?

A

Slow, occurs over wks to months as tissue insulin-sensitive improves and FFA levels are reduced

106
Q

Why was the drug Troglitazone (Thiazolidinedione) withdrawn from the market?

A

Rare but severe liver toxicity

107
Q

What is the concern of Rosiglitazone?

108
Q

What is the concern of Pioglitazone?

A

Risk for bladder cancer

109
Q

What are the ASEs of the Thiazolidinedione class?

A
  • Water retention and weight gain
  • Macular edema
  • Anemia
  • Bone density loss (osteoporosis)
  • Increase fracture risk
  • Monitor liver enzymes
110
Q

What is the BBW and CI of Thiazolidinediones?

A
  • BBW: may cause of exacerbate CHF

- CI: CHF, hepatocellular disease, and pts with ALT >2.5x the norm

111
Q

What line of tx are the GLP-1 Analogs? are eliminated by what?

A
  • 2nd line

- Renal

112
Q

What are the drugs in the GLP-1 Analog class?

A
  • Exenatide
  • Liraglutide
  • Dulaglutide
  • Semaglutide
113
Q

What is the MOA of GLP-1 Analog class?

A
  • Stimulates insulin synthesis and release
  • Suppress post-prandial glucagon secretion
  • Slows gastric emptying and has an anorectic effect.
114
Q

Are almost all GLP-1 SubQ or oral? What is unique about Semaglutide?

A
  • SubQ ( most often used in addition to oral diabetes meds, but can be added to basal insulin)
  • Semaglutide is the only oral
115
Q

What are common ASEs and the serious ASEs of GLP-1 Analogs?

A 
Common:
- Nausea (MC)
- HA
- Infxn
Serious:
- Pancreatitis
- Immunolocis rxns
- Acute kidney injury
- Angioedema
116
Q

What is the BBW and CI of GLP-1 Analogs?

A
  • BBW: Thyroid c-cell tumor

- CI: Personal and family hx of medullary thyroid carcinoma and in pts w/ MEN 2

117
Q

How often is Liraglutide (Victoza) administered? and when added to Metformin it improves what?

A
  • SubQ once daily

- Improve outcomes in pts w/ established ASCVD

118
Q

Liraglutide (Saxenda) is often used as an adjunct to reduce what?

A

Reduce calorie diet and increase physical activity for chronic weight management in adult pts w/ obesity or overweight + weight-related comorbidity

119
Q

What drug is a new once weakly GLP-1 agonist?

A

Extenatide ER

120
Q

GLP-1 agonist are primarily combined with other medications except for what drug class?

A

DPP-4 inhibitors (d/t MOA)

121
Q

What line of tx are the Dipeptidyl Peptidase-4 (DPP-4) Inhibitors? are eliminated by what?

A
  • 2nd line

- Most are renal excreted but Linagliptin is most excreted by bile

122
Q

What are the drugs in the DPP-4 Inhibitor class?

A

“-liptin” (like Lipton tea)

  • Sitagliptin
  • Saxagliptin
  • Linagliptin
  • Alogliptin
123
Q

What is the MOA of DPP-4 Inhibitors?

A

Increase GLP-1 concentrations by inhibiting the enzyme that metabolizes endogenous GLP-1, dipeptidyl peptidase-4 (DPP-4)

124
Q

What are the advantages of DPP-4 inhibitors? and what med are these usually combined with?

A
  • Oral administration
  • weight neutral
  • combined with metformin (A1c lowering 1.5-2%)
125
Q

What is the increased risk when combining DDP-4 + SU?

A

Hypoglycemia

126
Q

What line of tx are the a-Glucosidase inhibitors? and are eliminated by what?

A
  • 3rd line

- Renal and bile (50%)

127
Q

What are the drugs in the a-Glucosidase inhibitor class?

A
  • Acarbose

- Miglitol

128
Q

What is the MOA of a-Glucosidase inhibitors?

A

Inhibits a-glucosidase and delays/reduces absorption of dietary carbohydrate given before carbohydrate load

129
Q

What are the ASEs of a-Glucosidase inhibitors?

A
  • Flatulence
  • Diarrhea
  • Abdominal pain
130
Q

What line of tx is the bile acid sequestrant? are eliminated by what?

A
  • 3rd line

- Bile

131
Q

What is the only drug in the bile acid sequestrant class?

A

Colesevlam

132
Q

Colesevlam is useful in treating pts with DM type 2 and what?

A

Dyslipidemia.

133
Q

When taking Colesevlam with meals it can cause what?

A
  • Can bind other drugs
  • Increase serum triglycerides
  • Cause constipation or bloating.
134
Q

Why would a pt not want to take Colesevlam?

A
  • Large tablets and need to take many per day.

- Dose = 3 tabs BID or 6 tabs QD with meals

135
Q

What line of tx are Sulfonylureas 2nd gen? are eliminated by what?

A
  • 2nd line

- Hepatic

136
Q

What are the drugs in the Sulfonylureas 2nd gen class?

A
  • Glipizide
  • Glimepiride
  • Glyburide
137
Q

What is the MOA of the Sulfonylureas 2nd gen class?

A

Binds to SUR1, closes the ATP-sensitive K channel and causes B-cell depolarization and insulin exocytosis

138
Q

What are the ASEs and CI of Sulfonylureas 2nd gen class?

A
  • ASEs: hypoglycemia and nocturnal hypoglycemia

- CI: pts w/ sulfa allergies

139
Q

What drug of the Sulfonylureas 2nd gen class is the most potent?

A

Glyburide

-causes 2x more hypoglycemia than Glipizide or Glimepiride

140
Q

What line of tx are the other Secretagogues/Meglitinides? and eliminated by what?

A
  • 2nd line

- Hepatic

141
Q

What are the dugs in the Secretagogues/Meglitinides class?

A
  • Repaglinide

- Nateglinide

142
Q

What is the MOA of the Secretagogues/Meglitinides class?

A

Short-acting, closes ATP-sensitive K channel to stimulate insulin release

143
Q

What is the benefits/indications of drugs in the Secretagogues/Meglitinides class?

A
  • Postprandial glucose excursions
  • No sulfa group
  • Simply hold a dose if missed a meal
144
Q

Why wouldn’t a pt want to take drug from the Secretagogues/Meglitinides class?

A
  • Multiple doses per day; 3-4

- $$$

145
Q

What is good DM control?

A
  • Healthy diet and exercise routine
  • A1c goal <7.0%
  • Fasting glucose: 80 - 130
  • Postprandial glucose: <180
146
Q

What is the setting for use of rapid insulin?

A
  • Post-prandial glucose peaks
  • Usually combined with long acting
  • Preferred for insulin pumps
147
Q

What is the setting for use of short insulin?

A

Covers insulin needs for meals eaten within 30-60 minutes

148
Q

What is the setting for use of intermediate insulin?

A
  • Covers insulin need for about half the day or overnight

- Often combined with a rapid or short-acting insulin

149
Q

What is the setting for use of long insulin?

A
  • Covers insulin needs for about a day

- Often combined when needed with rapid or short-acting insulin

150
Q

What is the typical DM type 1 insulin tx?

A

Long-acting (basal) insulin and rapid/short-acting insulin at mealtimes

151
Q

What is the typical DM type 2 insulin tx?

A

Long-acting (basal) insulin (esp. when adding to oral agents), prandial insulin is optional and often helpful

152
Q

What is the indication for glucagon?

A

SubQ injected glucagon is the preferred tx of hypoglycemia for an unconscious pt

153
Q

When to you use oral glucose?

A
  • Oral glucose dose 15 g is the preferred treatment of conscious hypoglycemic pt
  • Monitor blood glucose to ensure adequate tx
  • Repeat dose if necessary after 15 minutes
154
Q

What is the 1st line tx for Hypothyroidism?

A

Levothyroxine (T4)

155
Q

What is the MOA of Levothyroxine (T4)?

A

A synthetic form of thyroxine (T4), converts to its active metabolite triiodothyronine (T3)

156
Q

What are the other indications of Levothyroxine (T4)?

A
  • Hypothyroidism
  • Postpartum thyroiditis
  • Subacute de Quervain’s Painful Thyroiditis
  • Myxedema Coma
  • TSH Suppression for thyroid cancer
157
Q

What is the dosing adjustment of Levothyroxine (T4) for pregnancy? and in general when should it be taken?

A
  • Frequent increase during pregnancy: increase by 30-50%

- Should be taken first thing in the morning at least 30-60 minutes before breakfast

158
Q

What is the dosing of Levothyroxine (T4) in adults and elderly?

A
  • Adults <60 w/o CAD: 50-100 ug daily

- Elderly or known CAD: 12.5-25 ug daily

159
Q

What are the ASEs and CI of Levothyroxine (T4)?

A
  • ASEs: can alter INR and interact with drugs that bind to the GI (Sucralfate and Bile Acid Sequestrants)
  • CIs: for tx of obesity or weight loss
160
Q

What is the medication for T3 and indication?

A
  • Liothyronine
  • Used in combination w/ levothyroxine for pts who don’t get adequate T4 to T3 conversion
  • Antidepressant augmentation (rarely)
161
Q

What are ASEs and CIs of Liothyronine?

A

ASEs:
- Tachycardia
- Angina
- Tremors
- Can alter INR and interact with drugs that bind to the GI
CIs:
- should not be used on its own for thyroid supplementation and do not use for weight loss

162
Q

What is the thyroid medication that has both T3 and T4?

A

Desiccated Porcine Thyroid

163
Q

What is the MOA of Desiccated Porcine Thyroid? and indication?

A
  • MOA: T3 converted to T4

- Indication: Hypothyroidism

164
Q

What is the ASEs of Desiccated Porcine Thyroid?

A

ASEs:

  • Tachycardia
  • Angina
  • Tremors
  • Can alter INR and interact with drugs that bind to the GI
165
Q

What is the drug class and drugs used for hyperthyroidism?

A
  • Thyroid Synthesis Inhibitors

- Propylthiouracil (PTU) and Methimazole

166
Q

What is the MOA of PTU?

A

inhibits the synthesis of TH by interfering w/ thyroid peroxidase TPO

167
Q

What are the indications of PTU?

A
  • Hyperthyroidism

- Thyroid storm in pregnant women

168
Q

What is the dosing of PTU? and how long does it take to reach full benefit?

A
  • TID dosing

- Full benefit may take 6-12 mos

169
Q

What are the ASEs and CIs of PTU?

A

ASES:

  • Agranulocytosis
  • Not always able to establish a euthyroid state: may lead to hypothyroidism
  • Concerns in pregnancy and lactation (Cat. D)
  • Can cause severe liver damage
170
Q

What is the BBW of PTU?

A
  • Only use during or just prior to the first trimester

- Impaired liver dz

171
Q

What is the MOA of Methimazole?

A

Inhibits the synthesis of thyroid hormones by blocking the oxidation of iodine in the thyroid gland

172
Q

What are the indications of Methimazole?

A
  • Hyperthyroidism
  • May be used as adjunct therapy to thyroid irradiation
  • Used in place of PTU in impaired liver dz
173
Q

What is the dosing of Methimazole? and how long does it take to reach full benefit?

A
  • Once daily dosing

- May take 3-12 weeks for euthyroid state

174
Q

What are the ASEs and CI of Methimazole?

A

ASEs:

  • More dangerous than PTU during 1st trimester of pregnancy and lactation. (Cat. D)
  • Agranulocytosis
175
Q

What is the BBW of Methimazole?

A

Only use Methimazole for 2nd and 3rd trimesters.

176
Q

What is the clinical use of BBs in a pt with thyroid dz? and which BB is used?

A
  • Propanolol

- Used for symptomatic relied not for tx of hyperthyroidism

177
Q

What symptoms does Propanolol help suppress?

A
  • Tachycardia
  • Tremor
  • Anxiety
  • Other sxs of hyperthyroidism
178
Q

What is the low, moderate, and high potency glucocorticoid therapy?

A
  • Low: Hydrocortisone
  • Moderate: Prednisone
  • High: Dexamethasone
179
Q

What are the indications of Fludrocortisone?

A
  • Provides additional mineralocorticoid support
  • Prevents/treats: sodium loss, vascular volume depletion and hyperkalemia

(ie. blood pressure and electrolyte support in adrenal insufficiency)

180
Q

What are the diseases that Fludrocortison is used to treat?

A
  • Addison’s disease
  • Primary hypoaldosteronism
  • Congenital adrenal hyperplasia
181
Q

What are the ASEs of Fludrocortison?

A
  • HTN
  • Edema
  • Cardiac enlargement
  • Hypokalemia

Endocrinology (18 decks)

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