Pharm to know Flashcards
(106 cards)
1
Q
What is the Tmax of a drug?
A
Tmax is the time it takes for a drug to reach its maximum plasma concentration after administration.
It reflects the rate of absorption
A shorter Tmax means faster absorption
2
Q
What is the mechanism, use, and key adverse effects of phenytoin?
A
Na⁺ channel inactivation; used for focal/tonic-clonic seizures; SE: gingival hyperplasia, hirsutism, teratogen, SJS.
3
Q
What are the main indications and toxicities of valproic acid?
A
Increases GABA and Na⁺ channel inactivation; used for epilepsy, bipolar, migraine; SE: hepatotoxicity, neural tube defects.
4
Q
What is the MOA and major side effect of SSRIs like fluoxetine?
A
Inhibit serotonin reuptake; used in depression/anxiety; SE: sexual dysfunction, serotonin syndrome.
5
Q
What are beta blockers used for and what side effects should be monitored?
A
Block β1; used in HTN, CHF, MI; SE: bradycardia, AV block, masks hypoglycemia.
6
Q
How do ACE inhibitors like lisinopril work and what are their major risks?
A
Block Ang I → Ang II; used in HTN, CHF; SE: cough, angioedema, hyperkalemia, teratogen.
7
Q
What is the MOA and key adverse effect of verapamil and amlodipine?
A
CCBs inhibit L-type Ca²⁺ channels; used for HTN, arrhythmia, angina; SE: edema, constipation, bradycardia.
8
Q
What is albuterol’s mechanism and when is it used?
A
β2 agonist → bronchodilation; used in acute asthma; SE: tremor, tachycardia.
9
Q
Why is fluticasone prescribed in asthma and what side effect should be prevented?
A
Corticosteroid with anti-inflammatory effect; SE: oral thrush → rinse mouth after use.
10
Q
What are the differences between rapid-acting and long-acting insulins?
A
Lispro (rapid), glargine (long); both activate insulin receptor; SE: hypoglycemia.
11
Q
What is the first-line oral agent for T2DM and its main risk?
A
Metformin; decreases hepatic glucose production; SE: lactic acidosis (avoid in renal failure).
12
Q
What are the mechanisms and uses of PTU and methimazole?
A
Inhibit thyroid peroxidase; PTU also inhibits peripheral T4→T3 conversion; SE: agranulocytosis, teratogen (esp. methimazole).
13
Q
How does furosemide work and what are its side effects?
A
Inhibits Na⁺-K⁺-2Cl⁻ in thick ascending loop; SE: hypokalemia, ototoxicity, gout.
14
Q
What electrolyte effects are seen with hydrochlorothiazide?
A
HyperGLUC: glucose, lipids, uric acid, calcium; inhibits Na⁺/Cl⁻ in DCT.
15
Q
What is penicillin’s target and common side effect?
A
Inhibits transpeptidase in cell wall; SE: allergy, hemolysis (Coombs⁺).
16
Q
What is vancomycin’s target and key toxicity profile?
A
Binds D-Ala-D-Ala; SE: nephrotoxicity, ototoxicity, Red Man Syndrome.
17
Q
How do aminoglycosides work and what are their toxicities?
A
Inhibit 30S; used for Gram -; SE: nephrotoxicity, ototoxicity, neuromuscular block.
18
Q
What is the mechanism and reversal agent for heparin?
A
Activates antithrombin (inhibits IIa/Xa); reversed with protamine; SE: HIT.
19
Q
What is warfarin’s mechanism and toxicity?
A
Inhibits vitamin K epoxide reductase; SE: bleeding, skin necrosis, teratogen; reversed with vitamin K.
20
Q
What is methotrexate used for and how is its myelosuppression reversed?
A
Inhibits DHFR; used in cancer, RA, ectopic pregnancy; reversed with leucovorin.
21
Q
How does leuprolide differ with pulsatile vs continuous administration?
A
Pulsatile: GnRH agonist → ↑ LH/FSH; Continuous: antagonist effect → ↓ sex hormones.
22
Q
What does finasteride do and what are its side effects?
A
5α-reductase inhibitor; treats BPH and hair loss; SE: gynecomastia, ↓ libido.
23
Q
What enzyme do corticosteroids inhibit and what are the systemic effects?
A
Inhibit phospholipase A2 → ↓ PGs/LTs; SE: hyperglycemia, osteoporosis, immunosuppression.
24
Q
What is a major risk of TNF-α inhibitors like etanercept?
A
Risk of latent TB reactivation → screen with PPD before starting.
25
What factors affect the Tmax (time to peak concentration) of a drug?
Tmax is primarily affected by the rate of absorption.
* Route of administration (e.g., IV = instant, oral = slower)
26
What kind of drug delivery has the fastest Tmax?
Inhalation
27
True or False: The area under the curve (AUC) is the same for all drug delivery routes, but Tmax and Cmax vary.
True
28
Draw out the curves of solute flux against concentration for facilitated diffusion vs passive diffusion
29
What is the volume of distribution (Vd) of a drug?
Volume of distribution (Vd) is a theoretical volume that relates the amount of drug in the body to the concentration in the plasma.
Vd = Amount of drug in body / Plasma concentration
Low Vd (e.g., 4–8 L): Drug stays in the plasma; often large, hydrophilic, or protein-bound
High Vd (e.g., >40 L): Drug distributes widely into tissues; often lipophilic or tissue-bound
30
Characteristics of a drug which would have low volume of distribution
= remains mostly in the plasma compartment (no diffusion)
* positive charge
* protein-bound
* high molecular weight
* lipophobic
31
What is the formula for volume of distribution (Vd)?
Vd = Amount of drug in the body / Plasma drug concentration
32
What is the formula for loading dose?
Loading Dose = (Target plasma concentration × Vd) / Bioavailability (F)
Bioavailability is = 1 for IV drugs
33
What is the formula for maintenance dose?
Maintenance Dose = (Target plasma concentration × Clearance × Dosing interval) / Bioavailability (F)
Bioavailability is = 1 for IV drugs
34
Which dose is impacted by renal or hepatic disease: loading dose or maintenance dose?
Maintenance dose is affected by renal or hepatic disease because these conditions alter drug clearance (CL).
↓ Clearance = ↓ Maintenance dose needed
Risk of drug accumulation and toxicity
Loading dose is usually not affected, since it depends on Vd, not clearance.
35
Difference between first and zero order kinetics
36
Which drugs follow zero-order kinetics?
Drugs with zero-order kinetics are eliminated at a constant amount per unit time, regardless of concentration (saturation of elimination mechanisms).
Classic examples:
* Phenytoin
* Ethanol
* Aspirin
37
What are the increments of half-life?
50-75-87.5-93.75-97
38
How many half-lives does it take to reach steady state or eliminate a drug?
It takes about 4 to 5 half-lives to reach steady state during continuous dosing
Eliminate ~97% of the drug after stopping
This applies to first-order kinetics.
39
What does steady state mean in pharmacokinetics?
Steady state is the point during repeated or continuous drug dosing when the rate of drug administration equals the rate of elimination, leading to a stable plasma concentration.
Reached after 4–5 half-lives
Depends only on half-life, not dose
Higher dose = higher concentration, but same time to steady state
40
Mnemonic for CYP450 inducers
CRAP GPSS
* Carbamazepine
* Rifampin
* Alcohol (chronic)
* Phenytoin
* Griseofulvin (antifungal)
* Phenobarbital (all barbiturates)
* Sulfonylureas (antidiabetics)
* St John wort
41
What is the effect of CYP450 inducers?
CYP450 inducers increase the activity of cytochrome P450 enzymes, leading to:
Faster metabolism of drugs processed by CYP450
Decreased plasma concentrations of those drugs
Reduced efficacy of affected medications
Potential for therapeutic failure
42
What is the effect of CYP450 inhibitors?
CYP450 inhibitors decrease the activity of cytochrome P450 enzymes, leading to:
Slower metabolism of drugs processed by CYP450
Increased plasma concentrations of those drugs
Prolonged drug effects
Higher risk of toxicity
43
Are CYP3A4, CYP2D6, and similar enzymes part of the CYP450 system?
Yes, enzymes like CYP3A4, CYP2D6, CYP1A2, etc., are subfamilies within the cytochrome P450 (CYP450) enzyme system.
The CYP450 system is a large family of enzymes responsible for phase I metabolism (oxidation, reduction, hydrolysis) of many drugs.
44
Which two CYP450 enzymes are the most important in drug metabolism?
The two most important CYP450 enzymes are:
CYP3A4 — metabolizes ~50% of all drugs
CYP2D6 — metabolizes ~25% of all drugs and is highly variable genetically
45
What is the mnemonic for CYP450 inhibitors?
MAGIC RACKS
Macrolides
Amiodarone (class III antiarrhythmic)
Grapefruit juice
INH
Cimetidine
Ritonavir
Acute alcohol
Ciprofloxacin
Ketoconazole
Sulfonamides
46
What is the difference between amiodarone and amlodipine?
Amiodarone:
→ Class III antiarrhythmic
→ Blocks K⁺ channels, prolonging repolarization (↑ QT interval)
→ Used for atrial fibrillation, ventricular tachycardia
→ Has many side effects (pulmonary fibrosis, thyroid dysfunction, liver toxicity)
Amlodipine:
→ Dihydropyridine calcium channel blocker
→ Acts on vascular smooth muscle to cause vasodilation
→ Used for hypertension, angina
→ Side effects: edema, flushing, dizziness
47
What is the mechanism of action (MOA) of azole antifungals?
Azoles inhibit the fungal enzyme lanosterol 14-α-demethylase, a cytochrome P450-dependent enzyme, which:
→ Blocks the conversion of lanosterol to ergosterol
→ Disrupts ergosterol synthesis, impairing fungal cell membrane integrity
48
What is the INR target for therapy with Warfarin?
between 2 and 3
49
What does a high INR mean?
A high INR indicates increased blood clotting time (i.e., thinner blood).
Suggests over-anticoagulation, especially in patients on warfarin
Increases risk of bleeding
May require dose reduction or vitamin K if dangerously high
50
What does a low INR mean?
A low INR indicates decreased clotting time (i.e., thicker blood).
Suggests under-anticoagulation
Increases risk of thrombosis
May require increasing warfarin dose if patient is being anticoagulated
51
What is the normal INR ?
1
52
Would CYP450 inducers or inhibitors be responsible for high INR with warfarin therapy?
High INR = low coagulation = too much warfarin = decreased metabolism = CYP450 **inhibitors**
53
What are the 3 main subtypes of G-protein-coupled receptors (GPCRs)?
Gs (stimulatory)
Gi (inhibitory)
Gq
54
What are the pathways of Gs and Gi GPCRs?
Adenylyl cyclase = cAMP = PKA
55
What is the pathway of Gq receptor activation?
56
What are the popular mnemonics "HAVe 1 M&M" and "MAD 2s" for GPCRs?
Mnemonic: "HAVe 1 M&M" → Gq-coupled receptors
H₁ (Histamine 1)
A₁ (α₁-adrenergic)
V₁ (Vasopressin 1)
M₁, M₃ (Muscarinic)
Mnemonic: "MAD 2s" → Gi-coupled receptors
M₂ (Muscarinic)
A₂ (α₂-adrenergic)
D₂ (Dopamine)
All others (e.g., β₁, β₂, H₂, V₂, D₁) are typically Gs-coupled → ↑ cAMP
57
Dobutamine:
What receptor does it bind to most, and what type of G protein is it?
Binds most to: β₁ > β₂
β₁ is a Gs-coupled receptor → ↑ cAMP → ↑ heart rate and contractility
58
Dopamine (low dose):
What receptor does it bind to most, and what type of G protein is it?
Binds most to: D₁ > β₁ > α₁
D₁ is a Gs-coupled receptor → vasodilation in renal/splanchnic beds
(Increases HR but drops BP)
59
Dopamine (high dose):
What receptor does it bind to most, and what type of G protein is it?
Binds most to: α₁ > β₁ > D₁
α₁ is a Gq-coupled receptor → vasoconstriction
β₁ = Gs; D₁ = Gs
(increased pressure decreased HR)
60
Epinephrine (low dose):
What receptor does it bind to most, and what type of G protein is it?
Binds most to: β₁ > β₂ > α₁
β₁, β₂ = Gs → ↑ HR (β₁), vasodilation (β₂)
Drop in pressure, increased HR
61
Epinephrine (high dose):
What receptor does it bind to most, and what type of G protein is it?
Binds most to: α₁ > β₁ > β₂
α₁ is Gq → vasoconstriction
β₁/β₂ = Gs
62
Norepinephrine:
What receptor does it bind to most, and what type of G protein is it?
Binds most to: α₁ > β₁ > β₂
α₁ = Gq (vasoconstriction), β₁ = Gs (↑ HR), β₂ = Gs (minimal effect)
63
Phenylephrine:
What receptor does it bind to most, and what type of G protein is it?
Binds to: α₁
α₁ is a Gq receptor → vasoconstriction → ↑ BP, reflex ↓ HR
64
General rule for dose-dependent effect of dopamine and epinephrine?
Effect goes with the BP: high dose = high BP (through alpha-1)
Low dose = low BP and high HR (D1 vs B1)
65
What is the initial management of asthma?
Initial asthma management focuses on intermittent symptoms:
Use short-acting β₂-agonist (SABA) as needed
→ Example: albuterol
66
What is the management of persistent asthma?
Persistent asthma (symptoms >2 days/week or nighttime symptoms) requires stepwise controller therapy:
Step 2: Low-dose inhaled corticosteroid (ICS)
Step 3+: Add long-acting β₂-agonist (LABA) or increase ICS dose
**Consider leukotriene receptor antagonists, theophylline, or biologics for higher steps**
Continue SABA as needed for rescue
67
What is the first-line treatment for COPD?
First-line treatment for stable COPD is a bronchodilator, depending on symptom severity:
Short-acting bronchodilator as needed (SABA or SAMA, e.g., albuterol or ipratropium)
68
Why can both β₂-agonists and muscarinic antagonists be used together in COPD treatment?
β₂-agonists and muscarinic antagonists have complementary mechanisms that provide synergistic bronchodilation:
β₂-agonists (e.g., albuterol, salmeterol):
→ Stimulate β₂ receptors (Gs) → ↑ cAMP → smooth muscle relaxation
Muscarinic antagonists (e.g., ipratropium, tiotropium):
→ Block M₃ receptors (Gq) → ↓ IP₃/Ca²⁺ → reduced bronchoconstriction
69
Which part of the autonomic nervous system (ANS) do muscarinic receptors belong to?
Muscarinic receptors are part of the parasympathetic nervous system (PNS).
They are cholinergic receptors activated by acetylcholine (ACh)
Found on target organs (e.g., heart, lungs, GI tract, bladder, eyes)
Key types:
M₂: heart → slows HR
M₃: smooth muscle & glands → bronchoconstriction, secretion, bladder contraction
70
What is albuterol?
Albuterol is a short-acting β₂-adrenergic agonist (SABA) used for rapid relief of bronchospasm in:
Asthma
COPD
Exercise-induced bronchoconstriction
Mechanism:
Stimulates β₂ receptors (Gs) → ↑ cAMP → bronchodilation
71
What is cimetidine?
Cimetidine is a histamine H₂ receptor antagonist used to reduce gastric acid secretion.
Mechanism of Action:
Blocks H₂ receptors on parietal cells in the stomach → ↓ acid production
Uses:
* GERD
* Peptic ulcer disease
* Zollinger-Ellison syndrome
Notable side effects:
CYP450 inhibitor → ↑ levels of other drugs (e.g., warfarin, theophylline)
72
What is theophylline?
Theophylline is a methylxanthine bronchodilator used in asthma and COPD (rarely first-line today). It has a **narrow therapeutic index**.
73
Is cigarette smoking an inducer of CYP450 enzymes?
Yes.
Cigarette smoke contains polycyclic aromatic hydrocarbons, which induce CYP1A2, a subtype of CYP450.
74
75
What is the mnemonic for the signs of acetylcholinesterase inhibitor poisoning?
Mnemonic: "DUMBBELSS" — for cholinergic toxicity (↑ ACh due to AChE inhibition):
D: Diarrhea
U: Urination
M: Miosis (pupil constriction)
B: Bradycardia
B: Bronchospasm
E: Emesis
L: Lacrimation
S: Salivation
S: Sweating
**Basically, all PNS functions are drastically increased**
76
What is a common cause of acetylcholinesterase inhibitor poisoning?
Organophosphate poisoning, often from insecticides or pesticides (e.g., parathion, malathion), is a common cause.
Seen in agricultural or industrial exposure
Organophosphates irreversibly inhibit acetylcholinesterase, leading to cholinergic overload
77
Why are women more prone to alcohol intoxication than men?
Lower gastric alcohol dehydrogenase (ADH) activity and decreased total body water volume.
78
What is the role of gastric alcohol dehydrogenase (ADH), and why does lower activity increase alcohol intoxication in women?
Gastric ADH is an enzyme in the stomach lining that begins the first-pass metabolism of ethanol before it reaches systemic circulation.
In men: Higher gastric ADH activity = more alcohol metabolized before absorption, lowering blood alcohol concentration (BAC)
In women: Lower gastric ADH activity = less first-pass metabolism, so more unmetabolized alcohol enters the bloodstream
79
How do acetaldehyde and NADH mediate the effects of alcohol intoxication?
During ethanol metabolism:
Ethanol → Acetaldehyde (via alcohol dehydrogenase, ADH)
Acetaldehyde → Acetate (via aldehyde dehydrogenase, ALDH)
Both steps use NAD⁺ → NADH, leading to ↑ NADH/NAD⁺ ratio in the liver.
80
Why does alcohol use cause hypoglycemia?
Alcohol is metabolized in the liver, leading to an ↑ NADH/NAD⁺ ratio, which disrupts normal glucose metabolism:
Gluconeogenic substrates are shunted away, leading to hypoglycemia, especially in fasting or malnourished individuals.
81
What are the main classes of non-insulin antidiabetic agents for type 2 diabetes?
Insulin secretagogues
- Sulfonylureas
- Meglitinides
Biguanides
- Metformin
Thiazolidinediones (TZDs)
- Pioglitazone
GLP-1 receptor agonists
- Exenatide, Liraglutide
DPP-4 inhibitors
- Sitagliptin, Saxagliptin
SGLT-2 inhibitors
- Canagliflozin, Dapagliflozin
82
What is the mechanism of action of insulin secretagogues?
↑ Insulin secretion by inhibiting pancreatic β-cell K+ ATP channels
→ Depolarization → calcium influx → insulin release
Example = sulfonylureas, meglitinides
83
What is the mechanism of action of metformin (biguanides)?
Stimulates AMPK
Inhibits mitochondrial gluconeogenesis
↓ Hepatic glucose production
↑ Peripheral glucose uptake
84
What is the mechanism of action of thiazolidinediones (e.g., pioglitazone)?
Activate nuclear transcription regulator PPAR-γ →
↑ insulin sensitivity
↓ insulin resistance
85
What is the mechanism of action of GLP-1 receptor agonists?
↑ Glucose-dependent insulin secretion
↓ Glucagon secretion
↓ Gastric emptying
86
What is the mechanism of action of DPP-4 inhibitors?
Inhibit DDP-4 enzyme, leading to:
↑ Endogenous GLP-1 and GIP
Enhances glucose-dependent insulin secretion
87
What is the mechanism of action of SGLT-2 inhibitors?
Block SGLT-2 in proximal renal tubules →
↑ Urinary glucose excretion
↓ Blood glucose levels
88
Which non-insulin antidiabetic class carries the highest risk of hypoglycemia?
Insulin secretagogues (especially sulfonylureas) carry the highest risk of hypoglycemia among oral agents.
They increase insulin secretion regardless of blood glucose level, which can cause blood sugar to drop too low
Examples: Glyburide, Glipizide, Glimepiride (sulfonylureas)
89
What is the first-line medication for hypertriglyceridemia?
Fibrates (e.g., gemfibrozil, fenofibrate) are the first-line treatment for severe hypertriglyceridemia (TG > 500 mg/dL).
90
What is the purpose and mechanism of drug-eluting stents?
Purpose:
Drug-eluting stents (DES) are used to prevent restenosis (re-narrowing) of coronary arteries after angioplasty.
Mechanism:
DES are coated with antiproliferative drugs (e.g., sirolimus, paclitaxel) that:
* Inhibit smooth muscle cell proliferation
* Reduce neointimal hyperplasia (scar tissue formation)
* Maintain vessel patency over time
91
What is the mechanism of action and indication of allopurinol?
Mechanism of Action (MoA):
Allopurinol is a xanthine oxidase inhibitor.
Blocks conversion of hypoxanthine → xanthine → uric acid
↓ Uric acid production
Indications:
Chronic gout (preventive therapy, not for acute attacks)
92
What is the mechanism of action of levothyroxine?
Levothyroxine is a synthetic form of thyroxine (T₄).
MoA:
Converted to active triiodothyronine (T₃) in peripheral tissues
**Binds thyroid hormone receptors → regulates gene expression**
Increases metabolic rate, oxygen consumption, and protein synthesis
93
What are the pharmacological treatment modalities for ADHD?
Increasing Dopamine and NE in the synaptic cleft. Use stimulants like amphetamines and methylphenidate.
94
How does resistance to tetracyclines develop?
Efflux pumps
→ Bacteria acquire genes that actively pump tetracyclines out of the cell
Classic example is E Coli
95
How does resistance to fluoroquinolones develop?
Resistance to fluoroquinolones (e.g., ciprofloxacin, levofloxacin) commonly arises through:
Mutations in DNA gyrase or topoisomerase IV
→ ↓ Drug binding to target enzymes
96
How does resistance to macrolides develop?
Macrolide resistance (e.g., azithromycin, erythromycin) develops through:
Methylation of 23S rRNA
→ Alters the macrolide binding site on the 50S ribosomal subunit (via erm gene)
→ Prevents binding without affecting ribosomal function
97
What is ursodiol and what is its mechanism of action?
Ursodiol (ursodeoxycholic acid) is a bile acid therapy used to treat certain cholestatic liver diseases and cholesterol gallstones.
Mechanism of Action (MoA):
Reduces cholesterol absorption and secretion into bile
98
What is digoxin and what is its mechanism of action?
Digoxin is a cardiac glycoside used in:
Heart failure (especially with reduced ejection fraction)
Atrial fibrillation (rate control)
Mechanism of Action (MoA):
Inhibits Na⁺/K⁺-ATPase on cardiac myocytes
→ ↑ intracellular Na⁺
→ ↓ Na⁺/Ca²⁺ exchanger activity
→ ↑ intracellular Ca²⁺ → stronger myocardial contraction (positive inotropy)
99
What is the mechanism of acetaminophen (paracetamol) overdose?
In overdose, acetaminophen is metabolized by the liver's CYP450 system to a toxic intermediate:
↑ NAPQI (N-acetyl-p-benzoquinone imine)
→ Normally detoxified by glutathione
In overdose:
**Glutathione stores are depleted**
NAPQI accumulates → hepatocellular damage and necrosis, especially in zone 3 (centrilobular region) of the liver
100
What is the treatment for acetaminophen overdose?
N-acetylcysteine (NAC)
Replenishes glutathione
Directly binds NAPQI, the toxic metabolite
Most effective within 8 hours of ingestion
101
Why is aspirin not given to children?
Aspirin is not given to children due to the risk of Reye syndrome, a rare but potentially fatal condition.
* Mitochondrial dysfunction in liver and brain, leading to acute hepatic failure (microvesicular steatosis) and encephalopathy (cerebral edema)
102
What are the symptoms of aminoglycoside toxicity?
Major toxic effects:
Nephrotoxicity
→ Acute tubular necrosis (especially with other nephrotoxics like vancomycin)
→ Reversible
Ototoxicity
→ Cochlear: hearing loss, tinnitus
→ Vestibular: vertigo, dizziness, balance issues
→ Often irreversible
Neuromuscular blockade
→ Rare but can cause respiratory paralysis, especially in myasthenia gravis
Teratogenicity
→ Can cause deafness in the fetus
103
What are the most dangerous symptoms of fluoroquinolone toxicity?
Tendinopathy & tendon rupture
→ Especially Achilles tendon
→ Higher risk in older adults, those on glucocorticoids
QT prolongation
→ Risk of torsades de pointes
104
What is the mechanism of action (MoA) of nitroglycerin?
* Converted to nitric oxide (NO) in vascular smooth muscle
* NO activates guanylate cyclase → ↑ cGMP
* ↑ cGMP → dephosphorylation of myosin light chains → smooth muscle relaxation
Venodilation → ↓ preload → ↓ myocardial oxygen demand
105
What is the mechanism of action of the influenza vaccine?
Induces humoral immunity (IgG) against hemagglutinin (HA) and neuraminidase (NA) antigens
106
What is the mechanism of action of paclitaxel?
Paclitaxel is a microtubule-stabilizing chemotherapeutic agent.
* Enhances tubulin polymerization and stabilizes microtubules
* Prevents microtubule disassembly during mitosis
* → Cell cycle arrest in M phase → apoptosis
