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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
preparations of inorganic iodine
- Strong iodine solution (Lugol’s) - Potassium iodide - Iodone
26
what is the mechanism of action of Inorganic Iodines?
- Acutely blocks release of thyroid hormone from the gland by inhibiting thyroglobulin proteolysis. - Inhibit iodide organification
27
what are the uses of Inorganic Iodines?
- Useful in thyroid storms: 2-7 days - Preoperatively: iodides decrease vascularity, size and fragility of hyperplastic gland
28
precautions of usage of Inorganic Iodines
- It may delay onset of thioamide effects; should be given after initiation of thioamides - The gland will escape from inhibition after 2-8 weeks.
29
what are examples of beta blockers used in hyperthyrodism?
- Propranolol. - Metoprolol. - Atenolol.
30
what is the mechanism of action of beta blockers in hyperthyodism case?
- 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
when are beta blockers indicated? **(concerning hyperthyrodism)**
- Grave’s disease - Thyroid storm.
32
when are corticosteroids like predinosone indicated? **(concerning hyperthyrodism)**
given for patients with Grave’s ophthalmopathy
33
dose of corticosteroids **(predinosone)** in cases of grave's ophthalmopathy
- 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
what are the options available for treatment of thyrotoxicosis? (in general)
thionamide therapy, radioiodine, or surgery.
35
what determines the way of treatment of thyrotoxicosis?
1. Patient age. 2. Cause and severity of thyrotoxicosis. 3. Comorbidity & Patient preference.
36
what is the definition of DM?
Metabolic disorder caused by insulin deficiency or resistance
37
what is the Hallmark clinical features of DM?
1. hyperglycemia 2. Alterations in lipid and protein metabolism.
38
what are the types of DM?
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
what is the mechanism of action of insulin?
40
what are the effects of insulin?
## Footnote or as mentioned in L4 physiology
41
insulin preparations
42
what are the clinical uses of insulin?
- 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
what are the methods of adminstration of insulin?
1) insulin Syringes 2) External insulin pump. 3) Pre-filled insulin pens.
44
what are the methods of administration of insulin under clinical trial?
1. Oral tablets. 2. Intranasal. 3. Insulin Jet injectors. 4. Inhaled aerosol. 5. Transdermal. 6. Ultrasound pulses.
45
what are the adverse effects of insulin?
**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
how is DKA treated?
1. Fluid 2. Insulin 3. Potassium 4. Identify and correct precipitating factors
47
what are anti-hyperglycemic drugs?
48
what are examples of insulin secretagogues?
- Glipizide - Repoglinide - Nateglinide
49
what is the mechanism of action of insulin secretagogues?
Increases insulin secretion from pancreatic beta cells by closing ATP-sensitive K- channels
50
toxicities of insulin secretagogues
- Hypoglycemia - Weight gain
51
what are examples of biguanides?
metformin
52
what is the mechanism of action of biguanides?
- 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
toxicities of biguanides
1. GIT disturbances 2. Lactic acidosis
54
what are examples of alpha-glucosidase inhibitors?
- acarbose - miglitol
55
what is the mechanism of action of alpha-glucosidase inhibitors?
- Inhibit intestinal alpha-glucosidase - reduce absorption of corbohydrates.
56
toxicities of alpha-glucosidase inhibitors
GI disturbances
57
what is the mechanism of action of exenatide?
- Analog of glucagon-like peptide-1 (GLP-1) leads to activation of GLP-1 receptors
58
toxicities of exenatide
1. GIT disturbances 2. headache 3. Pancreatitis
59
what are examples of thiazolidinediones?
Rosiglitazone Pioglitazone
60
what is the mechanism of action of thiazolidinediones?
- Regulates gene expression by binding to PRAR-gama that regulates cellular glucose transporters
61
toxicities of thiazolidinediones
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
what are examples of DDP-4 inhibitors?
sitagliptin
63
what is the mechanism of action of DDP-4 inhibitors?
Inhibitor of the dipeptidyl peptidase-4 (DPP-4) ---->degrades GLP-1 and other incretins.
64
toxicities of DDP-4 inhibitors
1) Rhinitis 2) Upper respiratory infections 3) Rare allergic reactions
65
what is an example of amylin analogue
pramlinitide
66
what is the mechanism of action of amylin analogues?
Analog of amylin activates amylin receptors in the brain causing: - decreased glucagon release - delayed gastric emptying - satiety
67
toxicities of amylin analogues
- GIT disturbances - Hypoglycemia - Headache
68
what are examples of SGLT2 inhibitors?
- canagliflozin - dapagliflozin
69
what is the mechanism of action of SGLT2 inhibitors?
they inhibit renal glucose absorption via sodium glucose transporter SGLT2
70
toxicities of SGLT2 inhibitors
- Osmotic diuresis - genital & urinary tract infections

Y2B1 - Endocrine πŸ“• (7 decks)

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