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Y2B1 - Endocrine πŸ“• > Pharmacology πŸ’Š > Flashcards

Pharmacology πŸ’Š Flashcards

1
Q

Peripheral metabolism of thyroid hormones

A

The primary pathway is deiodination of T4 to T3, which is 3-4 times more potent than T4

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2
Q

what is the mechanism of action of thyroid hormones?

A
  • Most circulating T3 and T4 is bound to thyroxine-binding globulin in plasma.
  • In the cell : T4 is enzymatically deiodinated to T3, which enters the nucleus and attaches to specific receptors to stimulate transcription followed by translation.
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3
Q

compare between T4 & T3 according to

Scientific name
brand name
advantage
dose
kinetics
uses

A
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4
Q

what is the duration of treatment of patients with hypothyrodism?

A

lifelong levothyroxine therapy and monitoring.

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5
Q

what drugs affect the absorption of levothyroxine?

A

antacids, iron, calcium tablets, and proton pump inhibitors may interfere with absorption of levothyroxine therapy.

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6
Q

Thyroxine replacement therapy in elderly people

A

Thyroxine replacement therapy should be introduced with caution in small doses in the elderly, particularly those with cardiac disease.

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7
Q

weekly administration of Thyroxine replacement therapy

A

Thyroxine replacement therapy can be given weekly in patients who forget their daily doses or who are unable to self-medicate.

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8
Q

what are anti-thyroid drugs?

A
  1. Thioamides.
  2. Radioactive iodine.
  3. Iodides
  4. Beta blocker.
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9
Q

what are examples of thio-amides (thio-uracil)?

A
  • Carbimazole
  • Methimazole
  • Propylthiouracil (PTU)
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10
Q

what is the mechanism of action of (Carbimazole - Methimazole)?

A
  1. Inhibit oxidation of iodide to iodine.
  2. Inhibit iodination of tyrosine = inhibit organification.
  3. Inhibit oxidative coupling.
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11
Q

kinetics of (Carbimazole - Methimazole)

A
  • Half-life: 6h
  • Excretion after: 48h
  • More potent (10 times)
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12
Q

what is the mechanism of action of Propylthiouracil (PTU)?

A
  • Same as carbimazole + Inhibit peripheral conversion of T4 β†’ T3
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13
Q

kinetics of Propylthiouracil (PTU)

A
  • Half-life: 1.5h
  • Excretion after: 24h
  • Safe β†’ highly bound to plasma protein β†’ not cross placenta β†’ used in pregnancy.
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14
Q

what are the adverse effects of thio-amides?

A
  1. Agranylocytosis (Bone marrow depression): rare & fatal.
  2. Hepatitis (hepatotoxicity): more with PTU , cholestatic jaundice with methimazole.
  3. Allergy: rash, vasculitis, lupus like syndrome.
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15
Q

what should pateints treated with thio-amides do to avoid agranulocytosis?

A

Patients treated with thioamide therapy require counseling about symptoms and management of agranulocytosis and should be given written guidance.

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16
Q

preparations of iodine131

A

sodium iodide131

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17
Q

what is the mechanism of action of Iodine131?

A

Trapped within the gland and enter intracellularly and delivers strong beta radiations destroying follicular cells.

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18
Q

penetration range of Iodine131?

A

400 - 2000ΞΌm.

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19
Q

what are the clinical uses of Iodine131?

A
  • Grave’s disease, primary inoperable thyroid CA.
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20
Q

when is Iodine131 contraindicated?

A

pregnancy

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21
Q

what are the advantages of Iodine131?

A
  1. Easy administration.
  2. Effectiveness.
  3. Low expense.
  4. Absence of pain.
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22
Q

what are the adverse effects of Iodine131?

A
  1. Permanent hypothyroidism.
  2. genetic damage.
  3. May precipitate thyroid crisis
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23
Q

thio-amide therapy in relation to iodine131

A
  • Thio-amides should be given initially and stop 5- 7 days before radioactive iodine administration.
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24
Q

dose of Iodine131

A

131I dose generally ranges between 80 120uCi/g of estimated thyroid weight, May be repeated after 6 months.

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25
Q

preparations of inorganic iodine

A
  • Strong iodine solution (Lugol’s)
  • Potassium iodide
  • Iodone
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26
Q

what is the mechanism of action of Inorganic Iodines?

A
  • Acutely blocks release of thyroid hormone from the gland by inhibiting thyroglobulin proteolysis.
  • Inhibit iodide organification
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27
Q

what are the uses of Inorganic Iodines?

A
  • Useful in thyroid storms: 2-7 days
  • Preoperatively: iodides decrease vascularity, size and fragility of hyperplastic gland
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28
Q

precautions of usage of Inorganic Iodines

A
  • It may delay onset of thioamide effects; should be given after initiation of thioamides
  • The gland will escape from inhibition after 2-8 weeks.
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29
Q

what are examples of beta blockers used in hyperthyrodism?

A
  • Propranolol.
  • Metoprolol.
  • Atenolol.
30
Q

what is the mechanism of action of beta blockers in hyperthyodism case?

A
  • Membrane-stabilizing action: inhibits conversion of T4 to T3
  • Decrease many disturbing symptoms of hyperthyroidism secondary to increased circulating catecholamines by blocking beta receptors
31
Q

when are beta blockers indicated? (concerning hyperthyrodism)

A
  • Grave’s disease
  • Thyroid storm.
32
Q

when are corticosteroids like predinosone indicated? (concerning hyperthyrodism)

A

given for patients with Grave’s ophthalmopathy

33
Q

dose of corticosteroids (predinosone) in cases of grave’s ophthalmopathy

A
  • 1mg/kg/day (60mg/day 3 divided doses).
  • If it should be given for more than 4 weeks, taper it gradually to decrease risk of adrenal crisis.
34
Q

what are the options available for treatment of thyrotoxicosis? (in general)

A

thionamide therapy, radioiodine, or surgery.

35
Q

what determines the way of treatment of thyrotoxicosis?

A
  1. Patient age.
  2. Cause and severity of thyrotoxicosis.
  3. Comorbidity & Patient preference.
36
Q

what is the definition of DM?

A

Metabolic disorder caused by insulin deficiency or resistance

37
Q

what is the Hallmark clinical features of DM?

A
  1. hyperglycemia
  2. Alterations in lipid and protein metabolism.
38
Q

what are the types of DM?

A
  1. Type 1 diabetes Insulin-dependent diabetes mellitus (IDDM)
  2. Type 2 diabetes Non-insulin-dependent diabetes mellitus (NIDDM)
  3. Other specific types (includes Secondary Diabetes)
  4. Gestational diabetes mellitus (GDM)
39
Q

what is the mechanism of action of insulin?

A
40
Q

what are the effects of insulin?

A

or as mentioned in L4 physiology

41
Q

insulin preparations

A
42
Q

what are the clinical uses of insulin?

A
  • Type 1 diabetes mellitus
  • Type 2 diabetes mellitus uncontrolled on maximal combination therapy with oral agents
  • Gestational diabetes
  • Hyperglycemic emergencies
  • Acute or chronic hyperglycemia provoked by infection or trauma
43
Q

what are the methods of adminstration of insulin?

A

1) insulin Syringes
2) External insulin pump.
3) Pre-filled insulin pens.

44
Q

what are the methods of administration of insulin under clinical trial?

A
  1. Oral tablets.
  2. Intranasal.
  3. Insulin Jet injectors.
  4. Inhaled aerosol.
  5. Transdermal.
  6. Ultrasound pulses.
45
Q

what are the adverse effects of insulin?

A

Hypoglycemia

  • Especially dangerous in Type 1 diabetics
  • Glucose or glucagon treatment

Allergy and resistance to insulin

Lipo-hypertrophy:

  • Due to lipogenic effect of insulin when small area used for frequent injections.

Lipo-atrophy

Insulin edema
- transient, rare

46
Q

how is DKA treated?

A
  1. Fluid
  2. Insulin
  3. Potassium
  4. Identify and correct precipitating factors
47
Q

what are anti-hyperglycemic drugs?

A
48
Q

what are examples of insulin secretagogues?

A
  • Glipizide
  • Repoglinide
  • Nateglinide
49
Q

what is the mechanism of action of insulin secretagogues?

A

Increases insulin secretion from pancreatic beta cells by closing ATP-sensitive K- channels

50
Q

toxicities of insulin secretagogues

A
  • Hypoglycemia
  • Weight gain
51
Q

what are examples of biguanides?

A

metformin

52
Q

what is the mechanism of action of biguanides?

A
  • Increases activity of AMP dependent protein kinase (AMPK), —–> this stimulates fatty acid oxidation, glucose uptake and non-oxidative metabolism & reduces lipogenesis & inhibits gluconeogenesis.
  • It increases glycogen storoge in skeletal muscle, lower rates of hepatic glucose production,
  • Increases insulin sensitivity and reduces blood glucose level.
53
Q

toxicities of biguanides

A
  1. GIT disturbances
  2. Lactic acidosis
54
Q

what are examples of alpha-glucosidase inhibitors?

A
  • acarbose
  • miglitol
55
Q

what is the mechanism of action of alpha-glucosidase inhibitors?

A
  • Inhibit intestinal alpha-glucosidase
  • reduce absorption of corbohydrates.
56
Q

toxicities of alpha-glucosidase inhibitors

A

GI disturbances

57
Q

what is the mechanism of action of exenatide?

A
  • Analog of glucagon-like peptide-1 (GLP-1) leads to activation of GLP-1 receptors
58
Q

toxicities of exenatide

A
  1. GIT disturbances
  2. headache
  3. Pancreatitis
59
Q

what are examples of thiazolidinediones?

A

Rosiglitazone
Pioglitazone

60
Q

what is the mechanism of action of thiazolidinediones?

A
  • Regulates gene expression by binding to PRAR-gama that regulates cellular glucose transporters
61
Q

toxicities of thiazolidinediones

A
  1. fluid retention
  2. edema
  3. anemia
  4. weight gain
  5. bone fractures in women
  6. may worsen heart diseases
  7. increased risk of myocardial infarction
62
Q

what are examples of DDP-4 inhibitors?

A

sitagliptin

63
Q

what is the mechanism of action of DDP-4 inhibitors?

A

Inhibitor of the dipeptidyl peptidase-4 (DPP-4) β€”->degrades GLP-1 and other incretins.

64
Q

toxicities of DDP-4 inhibitors

A

1) Rhinitis
2) Upper respiratory infections
3) Rare allergic reactions

65
Q

what is an example of amylin analogue

A

pramlinitide

66
Q

what is the mechanism of action of amylin analogues?

A

Analog of amylin activates amylin receptors in the brain causing:

  • decreased glucagon release
  • delayed gastric emptying
  • satiety
67
Q

toxicities of amylin analogues

A
  • GIT disturbances
  • Hypoglycemia
  • Headache
68
Q

what are examples of SGLT2 inhibitors?

A
  • canagliflozin
  • dapagliflozin
69
Q

what is the mechanism of action of SGLT2 inhibitors?

A

they inhibit renal glucose absorption via sodium glucose transporter SGLT2

70
Q

toxicities of SGLT2 inhibitors

A
  • Osmotic diuresis
  • genital & urinary tract infections

Y2B1 - Endocrine πŸ“• (7 decks)

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