drugs and enzyme transporters Flashcards

1
Q

What is an enzyme inhibitor?

A

A molecule that binds to an enzyme and decreases its activity by preventing the substrate from binding or the reaction from occurring.

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2
Q

What are the two types of enzyme inhibitors?

A

Irreversible inhibitors: Bind permanently, often through chemical reactions like covalent bonding.

Reversible inhibitors: Bind non-covalently and can be removed.

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3
Q

How do reversible inhibitors work?

A

They can bind to the enzyme, the enzyme-substrate complex, or both, depending on the type.

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4
Q

Can enzymes themselves be used as drugs?

A

Yes, some enzymes (e.g., clot-busting drugs) are used as therapeutic agents.

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5
Q

What do statins do?

A

Statins block a key step in the cholesterol production pathway to lower cholesterol levels.

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6
Q

What type of medications are statins?

A

Statins are lipid-lowering medications that reduce “bad cholesterol.”

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7
Q

Why are statins used?

A

To prevent cardiovascular disease and reduce the risk of heart-related death in high-risk individuals.

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8
Q

What is the role of the renin-angiotensin-aldosterone system (RAAS)?

A

It regulates blood pressure by increasing salt and water retention, which raises blood pressure.

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9
Q

What does ACE (angiotensin-converting enzyme) do in the RAAS?

A

ACE converts angiotensin I into angiotensin II, which increases blood pressure through vasoconstriction and stimulating aldosterone secretion.

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10
Q

How do ACE inhibitors help control blood pressure?

A

ACE inhibitors block the conversion of angiotensin I to angiotensin II, lowering blood pressure by reducing vasoconstriction and water retention.

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11
Q

How does ACE inhibition affect blood pressure?

A

ACE inhibitors reduce the production of angiotensin II, lowering blood pressure by decreasing vasoconstriction and water retention.

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12
Q

What is the role of angiotensin II in the body?

A

Angiotensin II increases blood pressure by causing blood vessel constriction and stimulating water and salt retention.

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13
Q

What was the improvement introduced with second-generation ACE inhibitors like Enalapril?

A

Enhanced effectiveness and bioavailability, making it a billion-dollar drug.

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14
Q

How does SARS-CoV-2 use ACE2?

A

SARS-CoV-2 binds to ACE2 on cell surfaces to enter and infect human cells.

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15
Q

What is the role of ACE inhibitors in the RAAS system?

A

ACE inhibitors block the production of angiotensin II, reducing blood pressure and preventing organ damage.

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16
Q

What do ARBs (angiotensin receptor blockers) do?

A

ARBs prevent angiotensin II from binding to its receptor, reducing inflammation, lung injury, and blood vessel leakage.

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17
Q

parkinsons signs

A
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18
Q

What causes Parkinson’s disease symptoms?

A

Degeneration of dopaminergic neurons in the nigrostriatal pathway.

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19
Q

Name key symptoms of Parkinson’s disease.

A

Hypokinesia, tremor at rest, muscle rigidity, motor inertia, cognitive impairment, and basal ganglia degeneration.

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20
Q

How does treatment for Parkinson’s disease work?

A

By using enzyme inhibitor drugs to increase dopamine levels in the brain.

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21
Q

Which brain pathway is affected in Parkinson’s disease?

A

The nigrostriatal pathway.

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22
Q

What is L-DOPA?

A

A precursor to dopamine synthesized from L-Tyrosine.

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23
Q

Why is L-DOPA important in Parkinson’s disease treatment?

A

It crosses the blood-brain barrier and is converted into dopamine to improve symptoms.

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24
Q

What enzyme converts L-DOPA into dopamine?

A

DOPA decarboxylase.

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25
Q

What is the blood-brain barrier (BBB)?

A

A selective barrier that separates circulating blood from the brain.

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26
Q

What does a peripheral DDC inhibitor do?

A

It blocks DOPA decarboxylase in the periphery to increase L-DOPA availability for the brain.

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27
Q

Why is Carbidopa used with L-DOPA?

A

To prevent dopamine formation in the periphery, ensuring more L-DOPA crosses the blood-brain barrier

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28
Q

What is the benefit of blocking DDC in the periphery?

A

It reduces peripheral side effects and increases dopamine production in the CNS.

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29
Q

What is the role of peripheral COMT inhibitors?

A

They block the enzyme Catechol-O-methyl transferase (COMT) in the periphery to prevent the breakdown of L-DOPA.

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30
Q

How do COMT inhibitors improve L-DOPA therapy?

A

By increasing the amount of L-DOPA available to cross the blood-brain barrier.

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31
Q

Name two peripheral COMT inhibitors.

A

Tolcapone and Entacapone.

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32
Q

What do central COMT inhibitors do?

A

They prevent the breakdown of dopamine in the CNS.

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33
Q

How do central COMT inhibitors benefit Parkinson’s patients?

A

By keeping dopamine levels high in the brain, they help improve motor symptoms.

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34
Q

Name a central COMT inhibitor.

A

Tolcapone

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35
Q

What is the role of MAO-B inhibitors?

A

They prevent the breakdown of dopamine in the CNS.

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36
Q

How do MAO-B inhibitors help in Parkinson’s disease?

A

By increasing dopamine availability, they help alleviate motor symptoms.

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37
Q

Name two examples of MAO-B inhibitors.

A

Selegiline and Rasagiline.

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38
Q

What is the role of central dopamine receptor agonists in Parkinson’s disease?

A

They directly activate dopamine receptors in the brain.

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39
Q

How do dopamine receptor agonists differ from enzyme inhibitors in Parkinson’s treatment?

A

They mimic dopamine by activating its receptors, whereas enzyme inhibitors alter dopamine breakdown or production.

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40
Q

Name examples of dopamine receptor agonists.

A

Bromocriptine, Pergolide, Pramipexole, Ropinirole, and Rotigotine.

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41
Q

What does the diagram illustrate about therapeutic options?

A

It shows that multiple treatments can target different steps in a pathway to achieve the desired outcome.

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42
Q

Why are multiple therapeutic options important in a pathway?

A

They provide flexibility to address different aspects of the disease mechanism, allowing for tailored treatments.

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43
Q

What is the common goal of treatments shown in the diagram?

A

To enhance dopamine activity or mimic its effects in the brain for symptom management.

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44
Q

What is passive transport?

A

Transport that does not require energy, including symporters (e.g., Na/K/2Cl) and ion channels (e.g., Na, Ca, K, Cl).

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45
Q

What is active transport?

A

Transport that requires energy from ATP, facilitated by ATP-ases like Na/K pumps or K/H pumps.

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46
Q

Name examples of passive transport mechanisms.

A

Symporters (e.g., Na/K/2Cl) and ion channels (e.g., Na, Ca, K, Cl).

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47
Q

What are ATP-ases used for?

A

They drive active transport processes such as Na/K and K/H exchanges.

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48
Q

What energy source does active transport use?

A

ATP, which is converted to ADP or AMP during the process.

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49
Q

What does active transport help cells obtain?

A

Ions, glucose, and amino acids.

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50
Q

what are the three main protein ports

A
51
Q

What does the Na-K-Cl co-transporter (NKCC) do?

A

It transports sodium, potassium, and chloride ions into cells in the same direction.

52
Q

Where is the NKCC symporter found?

A

In organs that secrete fluids.

53
Q

What happens when the NKCC is inhibited in the kidney?

A

Sodium, chloride, and potassium ions are lost in the urine.

54
Q

Why is NKCC inhibition important in medicine?

A

It helps manage fluid retention and high blood pressure.

55
Q

ion channel examples

A
56
Q

What does the Epithelial Sodium Channel (ENaC) do?

A

It reabsorbs sodium ions in the kidney’s collecting ducts, colon, lungs, and sweat glands.

57
Q

What blocks ENaC activity?

A

High-affinity diuretics like amiloride.

58
Q

Why is ENaC important in medicine?

A

It plays a role in fluid balance and blood pressure regulation and is targeted by diuretics for hypertension.

59
Q

how do thiazide diuretics work with ENaC inhibitors?

A

Thiazides block the Na-Cl co-transporter, enhancing the effects of ENaC inhibitors in lowering blood pressure.

60
Q

Where are voltage-gated calcium channels (VGCCs) found?

A

In the membranes of excitable cells such as muscles, neurons, and glial cells.

61
Q

What happens to VGCCs at resting membrane potential?

A

They remain closed.

62
Q

What triggers the opening of VGCCs?

A

Depolarization of the membrane potential (action potential).

63
Q

What is the function of calcium ions (Ca²⁺) entering the cell through VGCCs?

A

It activates calcium-sensitive potassium channels, induces muscle contraction, and excites neurons.

64
Q

Define an action potential.

A

A temporary change in electrical potential across a nerve or muscle cell membrane, causing the transmission of an electrical impulse.

65
Q

What type of drug is amlodipine?

A

A calcium channel blocker that is angioselective (targets blood vessels).

66
Q

How does amlodipine work?

A

It inhibits calcium ion influx in vascular smooth muscle cells and cardiac muscle cells, reducing muscle contraction.

67
Q

What are the effects of amlodipine on blood vessels?

A

Causes vasodilation and lowers peripheral vascular resistance, reducing blood pressure.

68
Q

How does amlodipine help the heart?

A

It prevents excessive constriction in coronary arteries, improving blood flow.

69
Q

Why is amlodipine considered angioselective?

A

It has a greater effect on vascular smooth muscle cells than on cardiac muscle cells.

70
Q

What do voltage-gated sodium channels do?

A

They allow Na⁺ ions to pass through cell membranes, enabling the generation and transmission of electrical signals.

71
Q

How are voltage-gated sodium channels activated?

A

By an action potential, which causes Na⁺ ions to flow into the cell and increase the voltage across the membrane.

72
Q

How does lidocaine work?

A

It blocks voltage-gated sodium channels, preventing the transmission of action potentials, which stops pain signals and can reduce heart arrhythmias.

73
Q

What are the two classifications of sodium channels?

A

Voltage-gated and ligand-gated.

74
Q

What do voltage-gated potassium channels do?

A

They allow K⁺ ions to move across cell membranes, helping reset the membrane potential after an action potential.

75
Q

What makes voltage-gated potassium channels selective?

A

They are designed to allow K⁺ ions to pass but exclude other cations like Na⁺.

76
Q

How are voltage-gated potassium channels activated?

A

By an electric current (action potential), which opens the activation gates.

77
Q

How many alpha subunits are there in human voltage-gated potassium channels?

A

There are over 40 known alpha subunits.

78
Q

What role do voltage-gated potassium channels play in insulin regulation?`

A

They regulate insulin in pancreatic β-islets of Langerhans. High glucose blocks ATP-dependent K+ channels, leading to depolarization, Ca²⁺ influx, and insulin secretion.

79
Q

Which drugs block potassium channels to stimulate insulin secretion and lower blood glucose levels?

A

Repaglinide, Nateglinide, and Sulfonylureas.

80
Q

What condition are Repaglinide, Nateglinide, and Sulfonylureas used to treat?

A

Type II Diabetes.

81
Q

What is the endogenous ligand for the GABA-A receptor, and what is its role in the CNS?

A

The endogenous ligand is γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the CNS.

82
Q

What happens when the GABA-A receptor is activated?

A

It opens chloride (Cl⁻) channels, inducing hyperpolarization and inhibition.

83
Q

How do drugs enhance the activation of the GABA-A receptor?

A

Drugs increase the receptor’s sensitivity to GABA, producing greater inhibition.

84
Q

What type of receptor is the GABA-A receptor?

A

A ligand-gated ion channel (ionotropic receptor) that opens to allow ions, like chloride (Cl⁻), to pass through the membrane.

85
Q

What is the function of the GABA-A receptor?

A

It opens Cl⁻ channels upon binding with GABA, causing hyperpolarization and inhibition of neuronal activity.

86
Q

Name the five main drug-binding sites on the GABA-A receptor.

A
87
Q

What is the overall impact of drugs acting on the GABA-A receptor?

A

They can block or modulate receptor activity, altering its inhibitory effects on neuronal activity.

88
Q

What is the function of the Sodium-Potassium (Na/K) Pump?

A

It actively pumps 3 Na⁺ ions out of the cell and 2 K⁺ ions into the cell, against their concentration gradients.

89
Q

Where does the energy for the Na/K pump come from?

A

The energy comes from ATP.

90
Q

What type of activity does the Na/K pump exhibit?

A

It has antiporter-like activity, moving Na⁺ and K⁺ ions against their concentration gradients.

91
Q

How does the Na/K pump contribute to the cell’s environment?

A

It creates an electrochemical gradient between the cell interior and exterior.

92
Q

Is the reverse process of the Na/K pump spontaneous or active?

A

The reverse process is spontaneous, unlike the forward process which requires energy.

93
Q

What is the primary mechanism of action of Digoxin?

A

It inhibits the Na⁺/K⁺ ATPase pump, primarily in the myocardium.

94
Q

What conditions is Digoxin used to treat?

A

Atrial fibrillation, atrial flutter, and heart failure.

95
Q

How does Digoxin affect intracellular ion levels?

A

It increases intracellular Na⁺, decreases Na⁺-Ca²⁺ exchanger activity, and raises intracellular Ca²⁺ levels.

96
Q

What is the effect of Digoxin on the heart’s electrical activity?

A

It lengthens the cardiac action potential, leading to a decrease in heart rate.

97
Q

What is the gastric hydrogen potassium ATPase also known as?

A

The proton pump of the stomach.

98
Q

What type of protein is the H⁺/K⁺ ATPase?

A

A heterodimeric protein (produced by two genes).

99
Q

What does the H⁺/K⁺ ATPase exchange?

A

It exchanges potassium from the intestinal lumen with cytoplasmic hydronium (H⁺).

100
Q

What is the function of the H⁺/K⁺ ATPase in the stomach?

A

It is responsible for the acidification of the stomach and the activation of the digestive enzyme pepsin.

101
Q

What is the proton pump’s role in gastric acid secretion?

A

It is the terminal stage in gastric acid secretion and an ideal target for inhibition.

102
Q

Which class of drugs blocks the proton pump?

A

Proton-pump inhibitors (PPIs).

103
Q

What is Omeprazole, and how does it work?

A

Omeprazole is the first in its class of PPIs; it irreversibly inhibits the H⁺/K⁺ ATPase, reducing acid secretion.

104
Q

How long does Omeprazole act despite its short half-life?

A

It works for 2–3 days.

105
Q

How is Omeprazole metabolized, and what affects its bioavailability?

A

It is metabolized at acidic pH and uses enteric-coated granules to protect and alter bioavailability.

106
Q

What drug class has largely superseded proton-pump inhibitors?

A

H2-receptor antagonists.

107
Q

What are organophosphates, and what do they inhibit?

A

Organophosphates are irreversible inhibitors of cholinesterase.

108
Q

Give examples of organophosphates.

A

Insecticides (e.g., Diazinon) and nerve gases (e.g., Sarin).

109
Q

What are the muscarinic effects of organophosphate poisoning?

A

Salivation, defecation, urination, bradycardia, and hypotension.

110
Q

What are the nicotinic effects of organophosphate poisoning?

A

Twitching, severe weakness, paralysis, and diaphragm failure.

111
Q

What are the central nervous system (CNS) effects of organophosphate poisoning?

A

Confusion, loss of reflexes, convulsions, and coma.

112
Q

What drug group does Omeprazole belong to, and what does it target?

A

Omeprazole is a proton pump inhibitor that targets enzymes.

113
Q

What type of inhibitor is Aspirin, and what protein does it target?

A

Aspirin is a COX inhibitor that targets enzymes.

114
Q

To which drug group does Simvastatin belong, and what is its protein target?

A

Simvastatin belongs to the statin group and targets enzymes.

115
Q

What is Ramipril’s drug group, and what protein does it inhibit?

A

Ramipril is an ACE inhibitor that targets enzymes.

116
Q

Paracetamol belongs to which drug group and targets what type of protein?

A

Paracetamol is a COX inhibitor and targets enzymes.

117
Q

Which drugs in the table are irreversible enzyme inhibitors?

A

Omeprazole and Aspirin are irreversible enzyme inhibitors.

118
Q

What is drug metabolism and what does it involve?

A

Drug metabolism is the metabolic breakdown of drugs through specialized enzymatic systems.

119
Q

What is biotransformation in drug metabolism?

A

Biotransformation is the process by which drugs are metabolized, often making them inactive and easier to excrete.

120
Q

What is the study of drug metabolism called?

A

The study of drug metabolism is called pharmacokinetics.

121
Q

Why is drug metabolism important in pharmacology and medicine?

A

Drug metabolism determines the duration and intensity of a drug’s pharmacologic action.

122
Q

What role do the liver and kidneys play in drug metabolism?

A

The liver and kidneys help metabolize drugs into compounds that are more easily excreted.

123
Q

What are xenobiotics?

A

Xenobiotics are compounds foreign to an organism’s normal biochemistry, such as drugs or poisons.