Week 4: Endocrine System Flashcards

1
Q

Physiological response to high plasma glucose

A
  • Inhbt. alpha cells of the pancreas
  • Stim. beta cells of the pancreas = inc. insulin
    - Liver: Inc. glycolysis, inc. glycogenesis, inc. lipogenesis
    - Cells: Inc. GLUT-4 receptors = inc. glucose transport into cell
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2
Q

Type 1 diabetes

A

Autoimmune attack of beta cells, little to no insulin synthesis/release

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3
Q

Type 2 diabetes

A

Dec. sensitivity to insulin, dec. beta cell function over time

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4
Q

Gestational diabetes

A

From inc. cortisol and placental production of insulin-antagonizing hormones

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5
Q

Diabetic ketoacidosis: Cause, presentation, treatment

A

Cause: High plasma glucose w/ no insulin
Presentation:
- Glucose excreted in urine (glycosuria)
- Water follows glucose out (dehydration, cerebral dehydration, shock)
- Ketoacidosis
Treatment:
- Dec. plasma glucose
- Treat dehydration
- Treat acidosis

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6
Q

Hyperosmolar hyperglycemic state: Cause, presentation, treatment

A

Cause: Gradual rise in plasma glucose
Presentation:
- Glucose excreted in urine (glycosuria)
- Water follows glucose out (dehydration, cerebral dehydration, shock)
Treatment:
- Dec. plasma glucose
- Treat dehydration

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7
Q

Complications of tight glucose control

A

Inc. risk of hypoglycemic episodes

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8
Q

The main difference between types of insulin is (PK/PD)

A

PK

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9
Q

Actions of insulin

A
  • Glycogenesis
  • Cellular uptake of glucose
  • Protein synthesis
  • Triglyceride synthesis
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10
Q

NPH

A
  • Intermediate-acting insulin
  • Can be combined with short-acting insulin
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11
Q

Detemir

A
  • Long-acting insulin
  • Usually wears off during sleep
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12
Q

Glargine

A
  • Longest-acting insulin
  • No peak time of activity
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13
Q

Aspart

A

Short-acting insulin

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14
Q

Lispro

A

Short-acting insulin

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15
Q

Glulisine

A

Short-acting insulin

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16
Q

Blood glucose effectors (5)

A
  1. Stress (inc.)
  2. Ingestion (inc.)
  3. Exercise (dec.)
  4. Alcohol (dec.)
  5. Illness (inc.)
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17
Q

Hypoglycemia: Possible causes

A

Insulin OD, dec. PO intake, nausea/vomiting/diarrhea, excessive alcohol consumption, exercise

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18
Q

Hypoglycemia: Presentations

A

Glucose <70, high HR, sweating, nervousness, severe = confusion, coma, death, hypokalemia

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19
Q

Biguanides: Names, actions, AE

A

Metformin
Actions:
- Inhibits liver glucose production
- Sensitizes insulin receptors
- Reduces gut glucose absorption
AE:
- Dec. B12 and folate absorption
- Lactic acidosis w/ toxicity
- GI upset upon initiation

Drug of choice for initial therapy in type 2

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20
Q

Sulfonylureas: Names, actions, AE

A

Glipizide, Glyburide
Actions: Promotes insulin release
AE:
- Hypoglycemia
- Weight gain
- Disulfiram reaction with alcohol

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21
Q

Meglitinides: Names, actions, AE

A

Nateglinide, Repaglinide
Actions: Promotes insulin release
AE:
- Hypoglycemia
- Weight gain

Shorter acting than Sulfonylureas

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22
Q

Thiazolidinediones: Names, actions, AE

A

Rosiglitazone, Pioglitazone
Actions: Inc. insulin response from cell
AE:
- HF due to fluid retention
- Upper respiratory infections, headaches, sinusitis, myalgia
- Bladder carcinoma from long-term/high dose therapy

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23
Q

Alpha-glucosidase inhibitors: Names, actions, AE

A

Acarbose, Miglitol
Actions: Inhibit brush border enzymes -> delayed carb absorption
AE:
- GI discomfort
- Dec. iron absorption -> anemia risk
- Long term -> liver dysfunction

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24
Q

Dipeptidyl-peptidase-4 inhibitors (DDP-4): Actions, AE

A

Actions: Inc. incretin = inc. insulin secretion response
AE:
- Hypersensitivity reactions
- Rare: Pancreatitis

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25
Q

Sodium-glucose-2 transporter inhibitors (SGLT-2): Actions, AE

A

Actions: Block renal reabsorption of glucose -> glucose excreted in urine
AE:
- Female UTI
- Inc. urination -> dehydration, hypotension

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26
Q

Why do some oral antidiabetics carry a hypoglycemia risk and some don’t?

A

Those that do promote insulin release

Those that do not work via other mechanisms (decreased insulin resistance, decreased glucose absorption or glucose excretion)

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27
Q

When should metformin be held?

A

Hypoperfusion states such as sepsis, cardiac failure, renal failure, etc.

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28
Q

Why do thiazolidinediones not work for type 1 diabetics?

A

Insulin must be present since the drug works by increasing insulin sensitivity

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29
Q

Lugol solution: Class, uses, actions, AE

A

Class: Non-radioactive iodine
Uses: Hyperthyroidism
Actions: Inhibits T4/T3 synthesis and systemic release
AE: High doses can cause paradoxical response → hyperthyroid symptoms

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30
Q

Somatropin: Uses, ROA, adverse effects

A

Uses: Pediatric or adult GH deficiency
ROA: IM or subQ
Adverse effects: Hyperglycemia

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31
Q

Cabergoline, Bromocriptine: Uses and effects

A

Uses: Prolactin excess
Effects: Bind dopamine receptors in pituitary directly

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32
Q

Non-reproductive effects of estrogen (5 ish)

A
  1. Bone: Maintain bone density and mass
  2. CV: Vasodilation, dec. LDL, inc. HDL
  3. Blood: Inc. coagulation and fibrin breakdown
  4. CNS protection
  5. Glucose homeostasis
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33
Q

Exogenous estrogen: AE (4)

A
  • Endometrial hyperplasia -> CA
  • Breast CA
  • CV thromboembolic events
  • Gallbladder disease, jaundice
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34
Q

Exogenous estrogen: Uses (6)

A
  1. Menopausal hormone therapy
  2. Female hypogonadism
  3. Acne
  4. Cancer palliation
  5. Gender affirmation therapy
  6. Contraceptives
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35
Q

Non-reproductive effects of progesterone (3)

A
  • Suppression of GI smooth muscle -> constipation
  • Suppression of maternal immune system
  • Growth/proliferation of breast ducts
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36
Q

Exogenous progesterone: AE (3)

A
  • Breast tenderness
  • Headache
  • Abdominal discomfort
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37
Q

Exogenous progesterone: Uses (6)

A
  1. Menopausal hormone therapy
  2. Dysfunctional uterine bleeding or amenorrhea
  3. Infertility
  4. Premature delivery prevention
  5. Endometrial hyperplasia and carcinoma
  6. Contraceptives
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38
Q

Naturally, what hormone peaks significantly at ovulation?

A

LH

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39
Q

Naturally, what hormone is inc. during the proliferative phase of the menstrual cycle?

A

Estrogen

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40
Q

Menopause: Cause, presentation

A

Cause: Gradual dec. in ovarian estrogens
Presentation:
- Vasomotor symptoms (night sweats, hot flashes)
- Sleep disturbances
- Urogenital atrophy
- Altered lipid metabolism
- Changes in cognition and sexual response

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41
Q

Why is hormone therapy for menopause controversial?

A

Risk of increased thromboembolic events (CV events like blood clots, MI, CVA, etc.)

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42
Q

Hormone therapy: Indications

A
  • Mod-severe vasomotor symptoms
  • Mod-severe vulvar and vaginal atrophy
  • Prevention of osteoporosis
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43
Q

Hormone therapy: ABSOLUTE contraindications (6)

A

1.Pregnancy
2. Breast, endometrial CA
3. Acute liver disease
4. Uncontrolled HTN
5. Thrombosis: DVT, MI, CVA
6. Undiagnosed vaginal bleeding

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44
Q

Hormone therapy: RELATIVE contraindications (7)

A
  1. History of benign breast disease or uterine fibroid
  2. Strong family history of breast CA
  3. Chronic liver disease
  4. Heavy tobacco use
  5. CVD/CAD
  6. DM
  7. Migraine
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45
Q

Why is progesterone added to HT and oral birth control?

A

To prevent endometrial CA

(estrogen only = unopposed proliferation of the endometrium!)
**no uterus, no need to add progesterone!

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46
Q

What does SERM stand for and what does it mean?

A

Selective estrogen receptor modulator

Agonize some estrogen receptors, antagonize others - attempts to provide benefits w/out risks

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47
Q

Tamoxifen: Class, actions, AE, uses

A

Class: SERMs
Actions:
- Inhbts. cell growth in breast tissue
- Protects against osteoporosis
- Improves lipid profile
AE:
- Inc. endometrial cancer risk
- Inc. hot flashes
- Inc. thromboembolism risk
Uses: Breast cancer prevention and treatment

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48
Q

Raloxifene: Class, actions, AE, uses

A

Class: SERMs
Actions:
- Inhbts. cell growth in breast tissue
- Protects against osteoporosis
- Improves lipid profile
AE:
- Inc. hot flashes
- Inc. thromboembolism risk
Uses:
- Osteo prevention
- Breast cancer prevention in high-risk patients

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49
Q

Raloxifene: What’s unique?

A

No risk of endometrial cancer

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50
Q

Which hormones are in oral contraceptives?

A

Estrogen and progesterone
or
just progesterone

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51
Q

Combination oral contraceptives: Mechanism of action

A

Suppression of ovulation: high estrogen provides negative feedback to suppress FSH (follicle cannot mature, no ovulation occurs)

Also alters cervical mucus & endometrium

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52
Q

Progestin-only “minipills”: Mechanism of action

A

Cervical secretion changes

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53
Q

Progestin-only “minipills”: What’s unique?

A
  • Avoids estrogen risks
  • MUCH less effective
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54
Q

Combination oral contraceptives: AE

A
  • Excess estrogen: Nausea, breast tenderness, edema
  • Excess progestin: Inc. appetite, fatigue, depression
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55
Q

Depot medroxyprogesterone acetate (injection) : Actions, AE

A

Actions: Inhibition of FSH/LH secretion
AE: Bone loss risk

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56
Q

Copper IUD: Actions, AE

A

Actions: Local foreign body reaction and chemical changes that are toxic to sperm
AE: Pelvic inflammatory disease if STI is present

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57
Q

Levonorgestrel IUD: Actions, AE

A

Actions: Thickens cervical mucus, inhibits ovulation, alters endometrium
AE: Pelvic inflammatory disease if STI is present

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58
Q

Mifepristone: Class, uses, actions, contraindications/AE

A

Class: Antiprogestin
Uses: Medical abortion
Actions: Blocks progesterone receptors → de-implantation; cervical softening and dilation
AE:
- Abdominal pain
- Vaginal bleeding
- Bacterial infection (give antibiotic)
Contraindications: Ectopic pregnancy, hemorrhagic disorders, anticoagulant use

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59
Q

Misoprostol: Class, uses, actions, contraindications/AE

A

Class: Prostaglandin
Uses: Medical abortion
Actions: Directly stimulates uterine contractions
AE:
- Abdominal pain
- Vaginal bleeding
- Bacterial infection (give antibiotic)
Contraindications: Ectopic pregnancy, hemorrhagic disorders, anticoagulant use

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60
Q

Clomiphene: Uses, actions, AE

A

Uses: Follicular maturation
Actions: Blocks estrogen receptors in the hypothalamus/pituitary
- Causes inc. in LH/FSH
- Blocks negative feedback so that follicular maturation and ovulation can occur
AE:
- Hot flashes
- Bloating
- Breast engorgement
- Ovarian hyperstimulation

61
Q

Menotropin: Uses, actions, AE

A

Uses: Follicular maturation
Actions: 50:50 mix of LH:FSH, direct action on ovary to induce follicular maturation
- If ovaries can respond to LH/FSH, ovulation is ~100%
AE: Ovarian hyperstimulation

62
Q

Follitropin: Uses, actions, AE

A

Uses: Follicular maturation
Actions: FSH that acts on ovary, stimulating follicles
AE: Ovarian hyperstimulation

63
Q

Ovarian hyperstimulation syndrome (OHSS): Cause, presentation, prevention

A

Cause: Exogenous hormone administration for infertility leads to exaggerated response -> ovaries swell, leak fluid, and are painful
Presentation:
- Abdominal pain
- Severe: Fluid accumulation in abdomen/chest, electrolyte disturbances, blood clots, renal failure
Prevention: Ultrasound monitoring

64
Q

hCG and choriogonadotropin alpha (recombinant hCG): Uses, actions, AE

A

Uses: Ovulation
Actions: Acts on ovary to induce ovulation by stimulating LH surge
- IM
- Administered AFTER clomiphene or menotropin/follitropins
AE: Ovarian hyperstimulation or rupture of ovarian cysts

65
Q

Cabergoline, Bromocriptine: Class, uses, actions, AE

A

Class: Ergot alkaloid derivatives
- Dopamine agonists
Uses: Corrects amenorrhea and infertility
Actions: Activates dopamine receptors in anterior pituitary
- Inhibits prolactin secretion
AE: Headache, nausea, dizziness

66
Q

Cabergoline: What’s unique?

A

Preferred, better tolerated, easier dosing

67
Q

What do tocolytics do?

A

Suppress uterine contractions

68
Q

4 classes of tocolytics

A
  1. Beta 2 agonists
  2. Ca2+ channel blockers
  3. COX inhibitors
  4. Oxytocin receptor blockers
69
Q

Terbutaline: Class, actions, AE

A

Class: B2 agonist
Actions: Agonizes B2 on uterine smooth muscle, dec. contractions
AE:
- Pulmonary edema
- HypoTN
- Hyperglycemia
- Tachycardia

70
Q

Nifedipine: Class, actions, AE

A

Class: Ca2+ channel blocker
Actions: Blocks Ca2+ from sarcoplasmic reticulum, dec. contractions
AE:
- Tachycardia
- Facial flushing
- Headache
- Dizziness
- Nausea

71
Q

Indomethacin: Class, actions, AE

A

Class: COX inhibitor
Actions: Inhibits PG synthesis, dec. contractions and cervical ripening
AE:
- Nausea
- Gastric irritation
- Inc. postpartum bleeding

72
Q

Oxytocin receptor blockers: Actions

A

Block uterine contractions by preventing initiation

73
Q

Magnesium sulfate: Class, uses, actions, AE

A

Class: ACh inhibitor
Uses: NOT A TOCOLYTIC
- Neuroprotective effects to fetus
Actions: Inhibits ACh at NMJ
AE:
- Adverse: HypoTN, flushing, headache, dizziness
- Severe: Hypothermia, paralytic ileus, pulmonary edema

74
Q

Hydroxyprogesterase caproate: Uses, AE

A

Uses: Prevention of preterm labor for singleton pregnancy/history of preterm labor
AE:
- Injection site reactivity
- Hives
- Nausea/diarrhea

75
Q

Magnesium sulfate: Fetal effects

A

Hypotonia
Sleepiness
Associated with inc. infant mortality

76
Q

Contraindications of induction of labor (5)

A
  1. Umbilical cord prolapse
  2. Transverse fetal position
  3. Active genital herpes
  4. History of c-section or myomectomy
  5. Placenta previa
77
Q

Indications for induction of labor

A
  • Post-term(>40 weeks)
  • Placental abruption
  • Premature
78
Q

Dinoprostone: Class, actions, AE, ROA

A

Class: Prostaglandin (PGE2)
Actions: Cervical ripening via breakdown of collagenase
AE:
- Fetal distress
- Tachysystole
- Systemic absorption -> nausea/vomiting, diarrhea, fever
ROA: Vaginal gel or pouches

79
Q

Clinical considerations when administering prostaglandin for induction of labor

A

Monitor fetal heart rate & contractions

fetal distress can occur, tachysystole (rapid contractions) can occur

80
Q

Misoprostol: Class, uses, AE

A

Class: Prostaglandin (PGE2)
Uses: Cervical ripening
AE: Higher tachysystole

81
Q

Misoprostol: What’s unique?

A

Not technically approved for cervical ripening, but more effective and cheaper

82
Q

Clinical considerations when using oxytocin/Pitocin to stimulate uterine contractions

A

Only use if fetal lungs are mature and cervix is ripe

83
Q

Pitocin: Effects, AE

A

Effects:
- Uterine stimulation: Inc. force, frequency and duration of contractions -> number of receptors inc. as labor progresses
- Milk ejection
- Water retention
AE:
- Shivering
- Temp elevation

84
Q

Pitocin: What’s unique?

A

Drug of choice for postpartum hemorrhage due to uterine atony

85
Q

Most common cause for postpartum hemorrhage

A

Uterine atony (80%)
Uterine muscles don’t contract enough to clamp the placental blood vessels shut after childbirth.

86
Q

Misoprostol (Cytotec): Class, uses, actions, AE

A

Class: Prostaglandin
Uses: Postpartum hemorrhage
Actions: Stimulates uterine contractions
AE:
- Nausea/vomiting, diarrhea (rare)
- Shivering
- Temp elevation

87
Q

Caboprost tromethamine (Hemabate): Class, uses, actions, contraindications/AE

A

Class: Prostaglandin
Uses: Postpartum hemorrhage
Actions: Stimulates uterine contractions and INTENSE vasoconstriction
Contraindications:
- Pelvic inflammatory disease
- Cardiac/pulmonary/renal disease
- Caution in asthma, HTN, diabetes
AE:
- GI issues
- HTN
- Bronchoconstriction

88
Q

Methylergonovine (Methergine): Uses, actions, contraindications/AE

A

Uses: Postpartum hemorrhage
- Only in emergencies
Actions: Stimulates uterine contractions and arteriole/venous constriction
Contraindications/AE:
- HTN
- Nausea, vomiting
- Headache

89
Q

Tranexamic acid (TXA): Class, uses, actions, contraindications/AE

A

Class: Fibrinolysis inhibitor
Uses: Menorrhagia
Actions: Inhibits plasmin
- Dec. fibrin mesh dissolving
- Keeps clots in the body
Contraindications/AE:
- History of thrombosis

90
Q

Thyroid-stimulating hormone (TSH): Function, stimulation, inhibition

A

Function: Stimulates synthesis and release of T3/T4
Stimulation: TRH from hypothalamus
Inhibition: T3 + T4

91
Q

Differences between T3 and T4

A

T3: More potent, shorter half-life, less made
T4: Acts as a supply of T3, longer half-life, more made

92
Q

Actions of thyroid hormone (3)

A
  1. Inc. metabolic rate -> inc. O2 consumption and heat production
  2. Inc. HR and contractility -> inc. CO and myocardial O2 demand
  3. Promotion of growth and development
93
Q

Adult hypothyroidism: Causes, presentation (6), treatment

A

Causes:
- Thyroid gland malfunction, often chronic autoimmune thyroiditis (Hashimoto’s)
- Iodine insufficiency
- Surgical resection or destruction due to radioactive iodine
Presentation:
- Pale/puffy/expressionless face
- Cold/dry skin
- Brittle hair w/ hair loss
- Dec. HR and temp
- Lethargy/fatigue
- +/- goiter
Treatment: T4 replacement therapy

94
Q

Congenital hypothyroidism: Causes, presentation (4), treatment

A

Causes:
- Failure in thyroid development
- Autoimmune disease
- Iodine or TSH deficiency
- Exposure to radioactive iodine in utero
Presentation:
- Large, protruding tounge
- Potbelly
- Dwarfish stature
- Impaired development of nervous system, bones, teeth, muscle
Treatment: T4 replacement therapy ASAP

95
Q

Levothyroxine: Class, uses, contraindications/AE (7), ROA

A

Class: T4 replacement
Uses: Hypothyroidism
- Takes 1 month to take full effect
Contraindications/AE:
- Hyperthyroidism
~Affected by~
- Food (dec. absorption)
- CYP450 inducers induce metabolism
- Dec. T4 -> T3 metabolism
- Inc. thyroglobulin binding (binds T3 and T4 together)
- Warfarin: Inc. blood-thinning effects
- Catecholamines: Inc. sensitization of heart
ROA: PO (on empty stomach) and IV

96
Q

Liothyronine: Class, uses

A

Class: T3 replacement
Uses: Hypothyroidism
- Only when T4 can’t convert to T3 or myxedema coma

97
Q

Graves disease: Cause, presentation (5), treatment

A

Cause: Autoimmune disease. Overproduction of thyroid-simulating immunoglobulins (TSIs), antibodies that stimulate TSH receptors on thyroid gland
Presentation:
- CV: Tachycardia, dysrhythmias, angina
- CNS: Anxiety, insomnia
- High metabolic rate -> inc. heat production
- Weight loss despite appetite
- Exophthalmos
Treatment: Dec. thyroid hormone production
- Thyroid resection
- Radiation
- Suppression of synthesis with antithyroid drug
- Supportive care: Beta blockers

98
Q

Toxic nodular goiter: Cause, presentation (4), treatment

A

Cause: Thyroid adenoma
Presentation:
- CV: Tachycardia, dysrhythmias, angina
- CNS: Anxiety, insomnia
- High metabolic rate -> inc. heat production
- Weight loss despite appetite
Treatment: Dec. thyroid hormone production
- Thyroid resection
- Radiation
- Suppression of synthesis with antithyroid drug
- Supportive care: Beta blockers

99
Q

Thyrotoxic crisis (thyroid storm): Cause, presentation, treatment (6)

A

Cause: Can occur in those with severe
hyperthyroidism under severe stress
- Major surgery
- Severe illness
Presentation:
- Profound hyperthermia
- Tachycardia,
- Restlessness
- Agitation
- Tremor
- If severe: Unconsciousness, coma,
hypotension, HF
Treatment: Immediate treatment is required
1. Suppress T4/T3 synthesis
2. Suppress T4/T3 release
3. Beta blockers (tachycardia)
4. Sedation
5. Cooling
6. IV fluids

100
Q

3 types of drugs for hyperthyroidism

A

Antithyroid drugs, radioactive iodine, and nonradioactive iodine

101
Q

Methimazole: Class, uses, actions, AE

A

Class: Thionamides
Uses: Hyperthyroidism
Actions: Inhibits peroxidase to inhibit T4/T3 synthesis
AE:
- Cannot be used in 1st trimester pregnancy, crosses too much into placenta
- Rare: agranulocytosis, hepatotoxicity, vasculitis
- Overdose: hypothyroidism
- Goiter bc no negative feedback to TSH → release more so enlarge gland

102
Q

Methimazole: What’s unique?

A
  • Longer half-life
  • More potent
  • Less serious adverse effects
103
Q

Propylthiouracil (PTU): Class, uses, actions, AE

A

Class: Thionamides
Uses: Hyperthyroidism and thyrotoxic crisis
Actions: Inhibits peroxidase to inhibit T4/T3 synthesis peripherally
AE:
- Rare: agranulocytosis, hepatotoxicity, vasculitis
- Overdose: hypothyroidism
- Goiter bc no negative feedback to TSH → release more so enlarge gland

104
Q

Propylthiouracil (PTU): What’s unique?

A
  • Shorter half-life
  • Can be used in 1st trimester
105
Q

Adrenocorticotropic-stimulating hormone (ACTH): Function, stimulation, inhibition

A

Function: Stimulates synthesis & release of glucocorticoids & androgens from adrenal cortex
Stimulation: Corticotropin-releasing hormone (CRH) which is released following circadian rhythm and in times of stress
Inhibition: CORT from cortisol negative feedback

106
Q

Cortisol deficiency: Presentation

A

Hypotension, hypoglycemia, cachexia,
depression/lethargy

107
Q

Cortisol excess: Presentation (8)

A

HPA axis suppression, HTN, hyperglycemia,
fat redistribution, CNS excitation, osteoporosis, menstrual irregularities, infection risk

108
Q

Aldosterone deficiency: Presentation

A

Hyponatremia (hypoNa+), hyperkalemia (hyperK+), acidosis, cellular dehydration

Late and untreated: Dec. plasma volume -> renal failure, CV collapse, death

109
Q

Aldosterone excess: Presentation (8)

A

myocardial/vascular remodeling &
fibrosis, SNS activation, baroreceptor reflex
disruption -> decreased contractility, dysrhythmias,
HTN -> HF, MI

110
Q

Androstenedione excess: Presentation

A

In females = virilization

111
Q

Androstenedione deficiency: Presentation

A

Failure to develop secondary sexual characteristics in males and females of pubescent age

112
Q

Primary endogenous androgen

A

Androstenedione

113
Q

Primary endogenous glucocorticoid

114
Q

Primary endogenous mineralcorticoid

A

Aldosterone

115
Q

Cushing syndrome: Definition, possible causes, presentation

A

Definition: High glucocorticoid levels
Possible causes:
- ACTH hypersecretion (usually pituitary adenoma)
- Glucocorticoid hypersecretion (usually adrenal adenomas/carcinomas)
- High doses of exogenous glucocorticoids
Presentation:
- Hyperglycemia with glucosuria
- HTN & fluid/electrolyte disturbances
- Osteoporosis, muscle wasting, fat redistribution
- Menstrual irregularities
- Infection risk

116
Q

Describe the approach to treatment for Cushing syndrome

A

Drugs are only used as adjuncts or if surgery isn’t appropriate/successful

117
Q

Spironolactone: Class, actions, AE

A

Class:
- K+ sparing diuretic
- Aldosterone antagonist
Actions:
- Corrects HTN -> allows Na and water excretion
- Conserves K+ because hyper-aldosterone caused hypokalemia
AE:
- Hyperkalemia
- Gynecomastia
- Menstrual irregularities

118
Q

What time of day should adrenal hormone replacement therapy be administered?

A

Morning
(mimics endogenous secretion)

119
Q

Primary adrenocortical insufficiency (Addison Disease): Possible causes, presentation, treatments

A

Possible causes:
- Autoimmune (most)
- TB/other infections
- Adrenal hemorrhage
- Cardiac arrest
- Medications
Presentation: Anorexia, nausea, weight loss, low BP, hyperK+, hypoNa+
- Severe = hypotensive crisis
Treatments: Replacement therapy
- Glucocorticoid
- Mineralcorticoid

120
Q

Secondary and tertiary adrenocortical insufficiency: Possible causes, presentation, treatments

A

Possible causes:
- Secondary = dec. ACTH
- Tertiary = dec. CRH
Presentation: Hypoglycemia, malaise, loss of appetite, reduced stress response
Treatments: Glucocorticoid replacement therapy

121
Q

Acute adrenal insufficiency (Adrenal crisis): Possible causes, presentation, treatments

A

Possible causes:
- Adrenal or pituitary failure
- Insufficient glucocorticoid replacement, especially after abrupt discontinuation of chronic therapy
Presentation: Hypotension, dehydration, weakness, lethargy
- Severe = shock, death
Treatments: Replacement therapy
- Glucocorticoid
- Supportive treatment (fluids, sodium, +/- glucose)

122
Q

Congenital adrenal hyperplasia: Possible causes, presentation, treatments

A

Possible causes: Enzyme deficiency that’s needed for glucocorticoid synthesis
Presentation:
- Increased height but premature epiphyseal closure = short adult stature
- Masculinization of external
genitalia in girls
- Penile enlargement in boys
Treatments: Lifelong glucocorticoid

123
Q

Hydrocortisone: Class, uses, actions, AE, ROA

A

Identical to cortisol

Class: Glucocorticoid drug
Uses: Primary adrenal insufficiency (Addison’s disease)
Actions: Glucocorticoid and mineralcorticoid actions
AE: None at physiologic dose
ROA: PO, IV for stress dose

124
Q

Dexmethasone: Class, uses, actions

A

Class: Glucocorticoid drug
Uses: Secondary and tertiary adrenal insufficiency
Actions:
- High glucocorticoid activity
- Very little mineralocorticoid actions

125
Q

Oxytocin: Function, stimulation, inhibition

A

Function:
Stimulation:
Inhibition:

126
Q

Antidiuretic hormone (ADH): Function, stimulation, inhibition

A

Function: Acts on collecting ducts of kidney -> inc. H2O permeability -> concentrates urine
Stimulation: High blood osmolality
Inhibition: Low blood osmolality

127
Q

Diabetes insipidus: Definition, causes, presentation

A

Definition: Complete or partial deficiency in ADH
Causes: Inherited, TBI, neurosurgery, other various causes
Presentation: Excessive thirst and excessive dilute urine

128
Q

Vasopressin: Uses, effects, AE

A

Uses: Diabetes insipidus and post-op abdominal distension
Effects: Vasoconstriction, identical to ADH
AE: All due to water intoxication/dec. osmolality
- Early signs: Drowsiness, confusion, headache
- Late signs: Seizures, coma

  • High vasopressin doses -> hypertension, angina, MI
129
Q

Desmopressin (DDAVP): Uses, effects, AE, ROA

A

Uses: Diabetes insipidus
Effects: Structurally analogous to ADH
AE: All due to water intoxication/dec. osmolality
- Early signs: Drowsiness, confusion, headache
- Late signs: Seizures, coma
ROA: PO, intranasal

  • No vasoconstriciton
  • Long duration
130
Q

Is the dose of gluco/mineralocorticoid HIGHER for replacement therapy or for anti-inflammation?

A

Anti-inflammation

for replacement therapy, we just give the dose that results in the patient having normal hormone levels (not suppressing inflammation). Only higher doses (i.e. putting the patient in “excess”) result in decreased inflammation & infection risk

131
Q

Prednisone: Class, uses, actions

A

Class: Glucocorticoid drug
Uses: General adrenocortical insufficiency
Actions:
- Glucocorticoid activity
- Less mineralocorticoid activity
- Longest acting (more potent)

132
Q

Lugol solution: What’s unique?

A

Immediate effect but temporary

133
Q

Male hypogonadism: Definition and drug options

A

Definition: Testes fail to produce adequate testosterone
Drug options:
- Testosterone enanthate
- Testosterone cypionate

134
Q

Testosterone preparations: PO

A
  • Erratic effects.
  • Both options are 17-alpha-alkylated androgens = hepatoxicity (thus not preferred)
135
Q

Testosterone preparations: Transdermal

A
  • Patches, gels, liquids.
  • Can be transferred w/ skin-skin contact.
  • More consistent
    testosterone levels than PO
136
Q

Testosterone preparations: Nasal gel

A

May interact w/ other nasal sprays

137
Q

Testosterone preparations: Implantable pellets

A
  • 3-6 months.
  • For hypogonadism or delayed puberty (long acting)
138
Q

Testosterone preparations: Buccal tablets

A
  • Have to stay in place until removed (can still eat/brush teeth/etc).
  • May transfer drug
    through saliva with kissing
139
Q

Testosterone preparations: IM

A
  • T cypionate & T enanthate: long acting.
  • High [T] with initial injection, decreases over time
140
Q

Testosterone therapy: AE

A
  • Virilization (most common) – in females,
    fetuses & boys
  • Premature epiphyseal closure
  • Hepatotoxicity
  • Increased LDL/decreased HDL: atherosclerosis risk
  • Edema: due androgen-induced Na+/H2O
    retention
  • Abuse potential
141
Q

Adverse effects of androgen abuse

A
  • Na+/H2O retention = HTN
  • High doses suppress LH & FSH = testicular shrinkage, sterility, gynecomastia
  • CAD/MI risk
  • Hepatotoxicity
  • Psychologic effects: depression, mania, aggressiveness
142
Q

Oral phosphodiesterase (PDE5) inhibitors: Uses, actions, contraindications/AE

A

Uses: Erectile dysfunction
Actions: Inhibits PDE5 so that cGMP accumulates -> erection
Contraindications:
- MI
- Angina
- HypoTN
- HF
- Can’t be taken with alpha blockers or nitroglycerin
AE:
- HypoTN

143
Q

What are 4 types of oral phosphodiesterase (PDE5) inhibitors and what is unique about each of them?

A

Sildenafil: preferred
Vardenafil: prolonged QT
Tadalafil: long-acting
Avanafil: short-acting, fastest onset

144
Q

How do the injectable ED (erectile dysfunction) drugs work?

A

Vasodilation that allows rapid inflow of arterial blood

145
Q

List two main pharmacologic interventions for premature ejaculation

A

Selective serotonin reuptake inhibitors (SSRIs)
Local anesthetics

146
Q

Benign prostatic hyperplasia: Presentation

A
  • Urinary hesitancy, frequency, urgency
  • Nocturia
  • Straining to void
  • Long term, can lead to obstructive nephropathy, bladder stones, recurrent UTIs
147
Q

Finasteride, Dutasteride: Class, actions, AE

A

Class: 5 alpha reductase inhibitors
Actions: Inhibits T → DHT conversion, promotes regression of tissue
AE:
- Decreased libido
- Gynecomastia
- Decreases PSA → evaluate for prostate cancer