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Pharmacology Flashcards

1
Q

What is the treatment for patients with HYPOthyroidism?

A

Treat with Thyroid hormones

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2
Q

What is the treatment for patients with HYPERthyroidism?

A

Anti-thyroid agents

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3
Q

What are the drugs used for treatment of HYPOthyroidism?

A
  • Levothyroxine – L isomer of T4 – drug of choice
  • Liothyronine (T3) synthetic version of triiodothyronine
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4
Q

In which organ does T4 get deiodinated to T3?

A

In the liver

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5
Q

H absorbed?

A

In the Small intestines

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6
Q

Where is Levothyroxine (T4) metabolized?

A

In the liver

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7
Q

What is the name of the plasma protein to which Levothyroxine (T4) binds extensively to?

A

Thyroxine-binding globulin

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8
Q

What are the clinical uses of Levothyroxine?

A
  • Myxedema coma (medical emergency – hypothermia, respiratory depression, unconsciousness)
  • Thyroid gland suppressive therapy (thyroid cancer, thyroid nodules, diffuse goitre) ;T4 → ↓ TSH → ↓ stimulation of abnormal thyroid tissue → ↓ size of thyroid gland.
  • Prevention of mental retardation in newborns with thyroid deficiency (infantile hypothyroidism)
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9
Q

True or False? Liothyronine (T3) has a Faster onset of action & greater oral bioavailability than T4.

A

TRUE!!

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10
Q

What are the adverse effects of Levothyroxine & Liothyronine (T3) ?

A
  • High T3 & T4 can cause Hyperthyroidism
  • Tachycardia, heat intolerance, tremors, arrhythmias.
  • Increased risk of osteoporosis in women ( T4)
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11
Q

What is a Thyroid storm?

A

Sudden, life-threatening exacerbation of hyperthyroidism which may occur spontaneously, after infection, surgery.

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12
Q

What are the manifestations of a Thyroid storm?

A
  • Nausea, vomiting, diarrhoea
  • Hyperthermia
  • Severe arrhythmias
  • Congestive heart failure
  • Extreme weakness
  • Dehydration
  • Coma
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13
Q

What are the Anti-thyroid agents?

A

Thioamides & Iodides

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14
Q

What are examples of Thioamides?

A
  • Propylthiouracil
  • Methimazole
  • Carbimazole
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15
Q

What are examples of Iodides?

A
  • Lugol’s solution – (mixture of iodine & potassium iodide)
  • Potassium iodide
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16
Q

In the steps of Thyroid synthesis,The Proteolytic release of T3 and T4 from thyroglobulin is inhibited by what drug?

A

Inhibited by high doses of iodide

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17
Q

In the steps of Thyroid synthesis, Conversion of T4 to T3 via 5’ deiodinase in peripheral tissues is ihibited by what drug?

A

Inhibited by propylthiouracil

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18
Q

What are the Therapeutic uses of Thioamides?

A
  • Hyperthyroidism
  • Thyroid storm
  • Preparation for thyroid surgery
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19
Q

What is the mechanism of Action of Propylthiouracil

A

Competitively inhibits thyroid synthesis by inhibiting

  • Iodide organification (inorganic I - → organic I +) by thyroid peroxidase.
  • Iodination (incorporation of iodine into tyrosine residues within the thyroglobulin molecule )
  • Coupling [monoiodotyrosine (MIT ) & diiodotyrosine ( DIT ) → triiodothyronine (T 3) & tetraiodothyronine (T 4 , thyroxine)]
  • Peripheral conversion of T 4 → T 3
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20
Q

True or False? Propylthiouracil (PTU) is the preferred drug to treat Hyperthyroidism in Pregnant women.

A

TRUE!!

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21
Q

Why is Propylthiouracil (PTU) the preferred drug to use in Pregnant women?

A

PTU crosses the placental barrier -It has an increased protein binding compared to methimazole so less free drug is available to cross into the foetus.

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22
Q

True or False? Propylthiouracil (PTU) is more metabolically active than Methimazole.

A

FALSE!! Methimazole is MORE active than PTU

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23
Q

Fill in the blanks. “ Methimazole is a more potent inhibitor of _________ than PTU & DOES NOT inhibit __________.

A

Inhibitor of iodide organification & DOES NOT inhibit the coupling or the peripheral conversion of T 4 → T 3.

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24
Q

Which anti- thyroid drug can cause Aplasia cutis?

A

Methimazole

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25
What are the adverse effects?
* Neutropenia * Agranulocytosis * Hepatotoxicity (hepatitis typically cholestatic in pattern) re propylthiouracil FDA added boxed warning in April 2010 * Vasculitis * Skin rash * Arthralgia * Fever * Hypoprothrombinemia
26
Thioamides taken with which other drug can cause an increase in agranulocytosis ?
Clozapine & carbamazepine
27
What is the treatment for Thyrotoxic crisis?
Potassium iodide/sodium iodide + propylthiouracil + Beta- blocker
28
What is the mechanism of Iodide?
* Inhibit release of thyroid hormones (possible inhibition of thyroglobulin endocytosis) Decrease size and vascularity of hyperplastic gland.
29
What are the adverse effects of Iodides?
* Angioedema * Chronic iodide intoxication (iodism) * Burning in mouth & throat + sore teeth & gums * Irritation of eye, swelling of eyelids * Enlarged parotid & submaxillary glands
30
What is the metabolic effects of cortisol ?
Metabolic effects of cortisol increase nutrient availability by raising blood glucose, amino acid & triglyceride levels
31
How does cortisol increase glucose?
It does this by antagonizing insulin action & by promoting gluconeogenesis in the fasting state.
32
True or False? Cortisol increases muscle protein catabolism .
TRUE!!! The release of amino acids that can be utilized by liver as fuels for gluconeogenesis
33
True or False? Glucocorticoids inhibit Vitamin D- mediated Ca2+ absorption.
TRUE!!
34
What is the result of Cortisol on the bones?
* It inhibit Vitamin D- mediated Ca2+ absorption → hypocalcaemia →Increase secretion of parathyroid hormone (secondary hyperparathyroidism) →bone resorption * Directly suppress osteoBLASTS function
35
Fill in the blanks. "Bone loss due to long term glucocorticoid therapy often results in ________."
Osteoporosis
36
What are the result of High levels of adrenocorticosteroids?
Decrease release of ACTH (via negative feedback control of cortisol levels) → atrophy of adrenal cortex Decrease release of LH →low testosterone in men , ovulation disturbances in women Decrease release of TSH Decrease release of growth hormone
37
True or False? Glucocorticoids used at pharmacologic doses should have minimal mineralocorticoid activity to avoid consequences of mineralocorticoid excess (hypokalemia, volume expansion, HTN).
TRUE!!
38
Which synthetic glucocorticoids helps in lung maturation in foetus which helps increase production of surfactant?
Betamethasone
39
What are the adverse effects of the Corticosteroids?
Hyperlipidemia Hyperglycemia Hypertension CHF (due to fluid retention) CNS effects (mood swings, euphoria, depression, insomnia, psychosis) Growth suppression in children Peptic ulcers Muscle wasting & weakness Oropharyngeal candidiasis Hoarseness Glaucoma Cataract formation
40
What are the adverse effects of Fludrocortisone?
Hypertension Hypokalaemia Congestive heart failure due to volume expansion
41
What is the name of an example of a Synthetic mineralocorticoid?
Fludrocortisone
42
Which drug can be used to try Cushing syndrome?
Ketoconazole
43
What are examples of Antagonists of adrenocortical agents - Synthesis Inhibitors?
Aminoglutethimide Metyrapone Ketoconazole
44
Which Antagonists of adrenocortical agents - Synthesis Inhibitors ,Inhibits CYP P450 which catalyses rate limiting step of conversion of cholesterol →pregnenolone?
Aminoglutethimide
45
Which Antagonists of adrenocortical agents - Synthesis Inhibitors ,Reduces corticosteroid biosynthesis by inhibiting final step in the pathway ( 11- hydroxylation) ?
Metyrapone
46
What is the name of a mineralocorticoid antagonist?
Spironolactone
47
What are the clinical uses for Gluccocorticoids?
Adrenal insufficiency (Addison’s disease) in conjunction with a mineralocorticoid Congenital adrenal hyperplasia Asthma Collagen vascular diseases Ocular disease – uveitis, optic neuritis Lung maturation in foetus (betamethasone) – helps increase production of surfactant Dermatologic conditions – psoriasis, contact dermatitis, eczema Anaphylactic reactions Inflammation reduction Chemotherapy (prednisone esp. for B cell lymphomas) Cerebral oedema (
48
How is Premixed NPH/regular insulin made?
It is made by combining NPH and regular insulin.
49
What is the treatment for Type I diabetes?
* Isophane [NPH]) *
50
What are the adverse effects of Insulin?
* Hypoglycemia – diaphoresis, vertigo, tachycardia (may be treated w glucose, other soluble sugar or glucagon) * Allergic reactions – IgE mediated * Lipodystrophy (rare) * Lipoatrophy - localized atrophy of s.c fat - may be due to immune response. * Lipohypertrophy – enlarged fat deposits – may be due to synthesis of fats by localized action of insulin * Weight gain
51
What are drugs that can DECREASE the effect of Insulin?
Corticosteroids Birth control pills/ patches, estrogens Sympathomimetic amines Thyroid hormones Nicotine Olanzapine Clozapine
52
What are drugs that can INCREASE the effect of Insulin?
* Alcohol * Aspirin * Beta- adrenergic blocker
53
What are First Generation Sulfonylureas ?
Chlorpropamide Tolbutamide " CT come first"
54
What are Second Generation Sulfonylureas ?
* Glyburide / Glibenclamide * Glipizide * Gliclazide * Glimepiride "4 G's came Second"
55
What is the Mechanism of Action for Sulfonylureas?
Enhances insulin release from pancreatic Beta cells
56
What are the clinical uses for Sulfonylureas (orally given)?
Type II diabetes (functional Beta cells required)
57
What are the Adverse effects of Sulonylureas?
* Hypoglycemia (from over-secretion of insulin) * GI disturbances (A,N,V, D) * Hyperinsulinemia * Weight gain (↑ insulin activity in adipose cells) * Hypersensitivity (photosensitivity, skin rash, jaundice) * Agranulocytosis & aplastic anemia (rare) * Fluid retention (chlorp. stimulate ADH release) * Disulfiram-like action (chlorpropamide if taken w alcohol)
58
What are examples of Meglitinides?
Repaglinide Nateglinide "Repa and Nate went to see the Meg"
59
What is the Mechanism of Action for Meglitinides?
Stimulate secretion of insulin from pancreatic beta cells (action similar to sulfonylureas)
60
What are the Adverse effects of Meglitinides?
Hypoglycemia (less than w sulfonylureas) Hypersensitivity reactions (rare) Transient increase in liver enzymes (rare) Upper respiratory tract infection Headache GI effects (diarrhoea, nausea)
61
The main Biganuide is ?
Metformin
62
What is the mechanism of Action for Metformin?
* Decrease hepatic gluconeogenesis through activation of AMP-activated protein kinase (AMPK). * By triggering hepatic AMPK, Metformin also inhibits fatty acid synthesis & cholesterol synthesis * Improves glucose uptake in peripheral muscle * Increases insulin signalling
63
Which drug is used in treatment of polycystic ovarian syndrome (PCOS) - – assoc. insulin resistance & hyperinsulinemia ?
Biguanides ( Metformin)
64
What are the Clinical uses for Biguanides?
* Type II diabetes * Diabetes + hyperlipidemia (→ ↓ LDL, ↓ triglycerides, Increase HDL) * Diabetes + obesity
65
What is the mechanism of action of Thiazolidinediones ?
* Insulin “sensitizers”; enhance action of insulin at target tissues; do not directly affect insulin secretion. * Drug interacts with peroxisome proliferator activated receptor gamma (PPAR gamma) in nucleus * Increase uptake of glucose into adipose tissue & skeletal muscle via increase in number of GLUT 4 glucose transporters.
66
What are the adverse effects Biguanides?
* GI effects (METALLIC TASTE , nausea, diarrhea) * Lactic acidosis especially in pts who have other conditions predisposing to metabolic acidosis (liver disease, renal failure, heart failure, respiratory disease, hypoxemia, severe infection, alcohol abuse) * Decreased absorption of Vitamin B 12 & folate may occur with long term therapy
67
What are adverse affects of Thiazolidinediones ?
* Weight gain * Oedema * Anemia * Increase risk of heart failure & MI * Hypercholesterolemia ( LDLc & HDLc) * Hepatotoxicity? (evidence insufficient however regular monitoring of liver enzymes recommended)
68
What are alpha glucosidase inhibitors?
Acarbose Miglitol
69
What is the MOA of Acarbose?
* Inhibit alpha glucosidase - enzyme localized in intestinal brush border & involved in degradation of starches & disaccharides. * Digestion of complex carbohydrates in small intestine delayed & glucose absorbed more slowly into bloodstream
70
What are the adverse effects of Alpha Glucosidase Inhibitors?
* GI disturbances (unabsorbed carbohydrates can cause bloating, flatulence, diarrhea, abdominal pain, borborygmi due to osmotic effects & bacterial fermentation) * Hypersensitive skin reactions (rare) * Liver dysfunctions (hepatitis) (rare)
71
Which drug is concurrent with Alpha Glucosidase Inhibitors may result in Hypoglycemia?
Sulfonylureas
72
What is the treatment hypoglycemia after giving ( Alpha Glucosidase Inhibitors + sulfonylureas )
Oral glucose (dextrose),
73
GLP-1 is rapidly degraded by what enzyme?
Dipeptidyl peptidase-4 (DPP-4)
74
Which drug mimics the effects of Incretin , GLP-1 ?
Exenatide
75
Sitagliptin ,Saxagliptin ,Linagliptin & Vildagliptin are apart of which group of Drugs?
Dipeptidyl peptidase IV (DPP-4) inhibitors
76
What is the MOA of Sitagliptin?
Selective inhibition of dipeptidyl peptidase (DPP-4) responsible for inactivation of incretins GLP-1 & GIP.
77
What are the adverse effects of Sitagliptin?
* Headaches * Nasopharyngitis * Upper respiratory tract infection * Hypersensitivity reactions * GI – N, V
78
What are examples of Selective sodium-glucose transporter-2 inhibitors (SLGT-2 inhibitors)?
* Canagliflozin * Dapagliflozin * Empagliflozin
79
What are the standard combinations for Diabetic patients?
1. Sulfonylurea + metformin & / or TZD / AGI 2. Metformin + meglitinide / TZD / AGI 3. Dipeptidyl peptidase IV (DPP-4) inhibitor+ Metformin
80
Which diabetic drug Inhibits the metabolism of sucrose?
Alpha Glucosidase Inhibitors
81

Endocrine System (10 decks)

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