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Endocrine System > Pharmacology > Flashcards

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
Q

What are the adverse effects?

A
  • Neutropenia
  • Agranulocytosis
  • Hepatotoxicity (hepatitis typically cholestatic in pattern) re propylthiouracil FDA added boxed warning in April 2010
  • Vasculitis
  • Skin rash
  • Arthralgia
  • Fever
  • Hypoprothrombinemia
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26
Q

Thioamides taken with which other drug can cause an increase in agranulocytosis ?

A

Clozapine & carbamazepine

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27
Q

What is the treatment for Thyrotoxic crisis?

A

Potassium iodide/sodium iodide + propylthiouracil + Beta- blocker

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28
Q

What is the mechanism of Iodide?

A
  • Inhibit release of thyroid hormones (possible inhibition of thyroglobulin endocytosis)

Decrease size and vascularity of hyperplastic gland.

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29
Q

What are the adverse effects of Iodides?

A
  • Angioedema
  • Chronic iodide intoxication (iodism)
  • Burning in mouth & throat + sore teeth & gums
  • Irritation of eye, swelling of eyelids
  • Enlarged parotid & submaxillary glands
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30
Q

What is the metabolic effects of cortisol ?

A

Metabolic effects of cortisol increase nutrient availability by raising blood glucose, amino acid & triglyceride levels

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31
Q

How does cortisol increase glucose?

A

It does this by antagonizing insulin action & by promoting gluconeogenesis in the fasting state.

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32
Q

True or False? Cortisol increases muscle protein catabolism .

A

TRUE!!! The release of amino acids that can be utilized by liver as fuels for gluconeogenesis

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33
Q

True or False? Glucocorticoids inhibit Vitamin D- mediated Ca2+ absorption.

A

TRUE!!

34
Q

What is the result of Cortisol on the bones?

A
  • It inhibit Vitamin D- mediated Ca2+ absorption → hypocalcaemia →Increase secretion of parathyroid hormone (secondary hyperparathyroidism) →bone resorption
  • Directly suppress osteoBLASTS function
35
Q

Fill in the blanks. “Bone loss due to long term glucocorticoid therapy often results in ________.”

A

Osteoporosis

36
Q

What are the result of High levels of adrenocorticosteroids?

A

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
Q

True or False? Glucocorticoids used at pharmacologic doses should have minimal mineralocorticoid activity to avoid consequences of mineralocorticoid excess (hypokalemia, volume expansion, HTN).

A

TRUE!!

38
Q

Which synthetic glucocorticoids helps in lung maturation in foetus which helps increase production of surfactant?

A

Betamethasone

39
Q

What are the adverse effects of the Corticosteroids?

A

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
Q

What are the adverse effects of Fludrocortisone?

A

Hypertension
Hypokalaemia
Congestive heart failure due to volume expansion

41
Q

What is the name of an example of a Synthetic mineralocorticoid?

A

Fludrocortisone

42
Q

Which drug can be used to try Cushing syndrome?

A

Ketoconazole

43
Q

What are examples of Antagonists of adrenocortical agents - Synthesis Inhibitors?

A

Aminoglutethimide
Metyrapone
Ketoconazole

44
Q

Which Antagonists of adrenocortical agents - Synthesis Inhibitors ,Inhibits CYP P450 which catalyses rate limiting step of conversion of cholesterol →pregnenolone?

A

Aminoglutethimide

45
Q

Which Antagonists of adrenocortical agents - Synthesis Inhibitors ,Reduces corticosteroid biosynthesis by inhibiting final step in the pathway ( 11- hydroxylation) ?

A

Metyrapone

46
Q

What is the name of a mineralocorticoid antagonist?

A

Spironolactone

47
Q

What are the clinical uses for Gluccocorticoids?

A

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
Q

How is Premixed NPH/regular insulinmade?

A

It is made by combining NPH and regular insulin.

49
Q

What is the treatment for Type I diabetes?

A
  • Isophane [NPH])
    *
50
Q

What are the adverse effects of Insulin?

A
  • 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
Q

What are drugs that can DECREASE the effect of Insulin?

A

Corticosteroids
Birth control pills/ patches, estrogens
Sympathomimetic amines
Thyroid hormones
Nicotine
Olanzapine
Clozapine

52
Q

What are drugs that can INCREASE the effect of Insulin?

A
  • Alcohol
  • Aspirin
  • Beta- adrenergic blocker
53
Q

What are First Generation Sulfonylureas ?

A

Chlorpropamide
Tolbutamide

” CT come first”

54
Q

What are Second Generation Sulfonylureas ?

A
  • Glyburide / Glibenclamide
  • Glipizide
  • Gliclazide
  • Glimepiride

“4 G’s came Second”

55
Q

What is the Mechanism of Action for Sulfonylureas?

A

Enhances insulin release from pancreatic Beta cells

56
Q

What are the clinical uses for Sulfonylureas (orally given)?

A

Type II diabetes (functional Beta cells required)

57
Q

What are the Adverse effects of Sulonylureas?

A
  • 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
Q

What are examples of Meglitinides?

A

Repaglinide
Nateglinide

“Repa and Nate went to see the Meg”

59
Q

What is the Mechanism of Action for Meglitinides?

A

Stimulate secretion of insulin from pancreatic beta cells (action similar to sulfonylureas)

60
Q

What are the Adverse effects of Meglitinides?

A

Hypoglycemia (less than w sulfonylureas)

Hypersensitivity reactions (rare)

Transient increase in liver enzymes (rare)

Upper respiratory tract infection

Headache

GI effects (diarrhoea, nausea)

61
Q

The main Biganuide is ?

A

Metformin

62
Q

What is the mechanism of Action for Metformin?

A
  • 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
Q

Which drug is used in treatment of polycystic ovarian syndrome (PCOS) - – assoc. insulin resistance & hyperinsulinemia ?

A

Biguanides ( Metformin)

64
Q

What are the Clinical uses for Biguanides?

A
  • Type II diabetes
  • Diabetes + hyperlipidemia (→ ↓ LDL, ↓ triglycerides, Increase HDL)
  • Diabetes + obesity
65
Q

What is the mechanism of action of Thiazolidinediones ?

A
  • 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
Q

What are the adverse effects Biguanides?

A
  • 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
Q

What are adverse affects of Thiazolidinediones ?

A
  • Weight gain
  • Oedema
  • Anemia
  • Increase risk of heart failure & MI
  • Hypercholesterolemia ( LDLc & HDLc)
  • Hepatotoxicity? (evidence insufficient however regular monitoring of liver enzymes recommended)
68
Q

What are alpha glucosidase inhibitors?

A

Acarbose
Miglitol

69
Q

What is the MOA of Acarbose?

A
  • 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
Q

What are the adverse effects of Alpha Glucosidase Inhibitors?

A
  • 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
Q

Which drug is concurrent with Alpha Glucosidase Inhibitors may result in Hypoglycemia?

A

Sulfonylureas

72
Q

What is the treatment hypoglycemia after giving ( Alpha Glucosidase Inhibitors + sulfonylureas )

A

Oral glucose (dextrose),

73
Q

GLP-1 is rapidly degraded by what enzyme?

A

Dipeptidyl peptidase-4 (DPP-4)

74
Q

Which drug mimics the effects of Incretin , GLP-1 ?

A

Exenatide

75
Q

Sitagliptin ,Saxagliptin ,Linagliptin & Vildagliptin are apart of which group of Drugs?

A

Dipeptidyl peptidase IV (DPP-4) inhibitors

76
Q

What is the MOA of Sitagliptin?

A

Selective inhibition of dipeptidyl peptidase (DPP-4) responsible for inactivation of incretins GLP-1 & GIP.

77
Q

What are the adverse effects of Sitagliptin?

A
  • Headaches
  • Nasopharyngitis
  • Upper respiratory tract infection
  • Hypersensitivity reactions
  • GI – N, V
78
Q

What are examples of Selective sodium-glucose transporter-2 inhibitors (SLGT-2 inhibitors)?

A
  • Canagliflozin
  • Dapagliflozin
  • Empagliflozin
79
Q

What are the standard combinations for Diabetic patients?

A
  1. Sulfonylurea + metformin & / or TZD / AGI
  2. Metformin + meglitinide / TZD / AGI
  3. Dipeptidyl peptidase IV (DPP-4) inhibitor+ Metformin
80
Q

Which diabetic drug Inhibits the metabolism of sucrose?

A

Alpha Glucosidase Inhibitors

81
Q
A

Endocrine System (10 decks)

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