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Pharmacology > Exam 6 > Flashcards

Exam 6 Flashcards

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1
Q

Partial Seizure

A

Begins focally, in a single site in the cortex.
Simple = consciousness preserved
Complex = Loss of consciousness

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2
Q

Generalized Seizure

A

Involves both cortices from the start

Absence, tonic-clonic, and myoclonic seizures are examples of generalized seizures

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3
Q

Secondary Generalized Seizure

A

Starts as a partial seizure and then spreads to become generalized

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4
Q

4 Anticonvulsants that Inhibit Na+ Channels in neuron

A 
Carbamazepine
Oxycarbazepine
Phenytoin
Valproic Acid
These act by prolonging the "Inactive State" of the Voltage Gated Na Channels
COP-V
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5
Q

What types of channels are involved in absence seizures?

A

T-Type Calcium Channels

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6
Q

2 Anticonvulsants that inhibit T-Type Calcium Channels

A

Ethosuximide

Valproic Acid

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7
Q

Name 1 GABA reuptake inhibiting anticonvulsant

A

Tiagabine

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8
Q

Name 1 inhibitor of GABA degradation in the synapse

A

Vigabatrin

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9
Q

Name three drugs and their classes that have an inhibitory effect on GABA(A) receptors

A

Phenobarbital (Barbiturate)
Primidone (Barbiturate)
Diazepam (Benzo)

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10
Q

Only 2 drugs effective for monotherapy in treatment of absence seizures

A

Ethosuximide

Valproic Acid

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11
Q

What were the original anticonvulsants (prior to 1912)? Side effects?

A

Bromides

Profound sedation and skin lesions

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12
Q

Phenobarbital

A

Monotherapy for tonic-clonic and partial seizures
Potentiates synaptic inhibition via GABA(A) receptors (agonist of GABA(A) I guess)
Significantly protein bound and metabolized by liver CYP enzymes (drug interactions based on these features)
Induction of CYP enzymes can lead to rapid degradation of other drugs like oral contraceptives ):
Teratogenic
Can cause cutaneous allergic reactions

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13
Q

Primidone

A

Like Phenobarbital, Monotherapy for tonic-clonic and partial seizures (It’s not as effective though)
Also Potentiates synaptic inhibition via GABA(A) receptors (GABA(A) agonist I guess)
Is metabolized to phenobarbital. The rate at which this happens if variable between patients.
Similar side effects to phenobarbital, but can also cause nausea, dizziness, nystagmus, and ataxia.

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14
Q

Phenytoin

A

Monotherapy for tonic-clonic and partial seizures (IV fosphenytoin for status epilepticus)
Prolongs Voltage gated Na channels’ rate of recovery from inactive state
Highly protein bound (albumin)
** Plasma concentration increases disproportionately as dosage increases (half-life increases)
Metabolized by CYP enzymes in the liver (drug interactions with Warfarin and oral contraceptives)
Side effect = Gingival hyperplasia in 20%

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15
Q

Stevens-Johnson Syndrome

A

Drug reaction that causes rash with more than 10% surface area, 5% mortality
Starts with flu-like symptoms, progresses…
Toxic Epidermal Necrolysis is worse (>30% SA, 20-40% mortality)

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16
Q

Carbamazepine

A

Monotherapy for tonic-clonic and partial seizures
Prolongs Voltage gated Na channels’ rate of recovery from inactive state
Metabolized to 10,11 epoxide, which is just as effective
Induces its own metabolism, making achieving constant plasma concentration difficult
Other anticonvulsants also induce its metabolism
Many side effects.
Induces CYP enzymes = drug interactions (oral contraceptives)

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17
Q

Oxycarbazepine

A

Monotherapy, adjunctive treatment for partial seizures, even in patients 4-16 years old
Prolongs Voltage gated Na channels’ rate of recovery from inactive state
It’s a prodrug, converted to active metabolite by the liver
Conjugated to glucuronide and excreted
Does not auto induce metabolism
Similar side effects to carbamazepine
Induces CYP, but not as much as carbamazepine

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18
Q

Ethosuxamide

A

Monotherapy for absence seizures
Inhibits T-Type Ca channels
Not protein bound, few drug interactions
Side effects: nausea, vomiting, anorexia. CNS depression, lethargy. SJS, aplastic anemia.

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19
Q

Valproic Acid

A

Mono therapy of pretty much all types of seizures
Inhibits T-Type Ca channels, Prolongs Voltage gated Na channels’ rate of recovery from inactive state, and increases GABA synthesis
Highly protein bound, can inhibit certain CYP enzymes and increase hepatic blood enzymes (whatever that means)

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20
Q

Gabapentin

A

GABA molecule bound to a lipophilic hexane ring
Doesnt act on GABA receptors, but does decrease neuronal activity
Adjunctive treatment for partial seizures, neuropathic pain, and fibromyalgia
Mechanism isn’t really known, it binds to L-type Ca channels, but Ca flow doesnt change.
Not metabolized, excreted in its original form in urine (renal function important)
Side effects: fatigue/ataxia

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21
Q

Lennox-Gustaut Syndrome

A 
Childhood-onset epilepsy
Severe cog dysfunction
multiple seizure types
resistant to drugs
Can be deadly
Ketogenic diet?
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22
Q

Lamotrigine

A

Broad spectrum anti epileptic drug (partial and generalized seizures)
Prolongs Voltage gated Na channels’ rate of recovery from inactive state.
Also inhibits Ca channels to some extent
Other AEDs reduce its half life
SEs- dizziness, ataxia, blurred vision, nausea, rash, SJS

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23
Q

Topiramate

A

Broad spectrum anti epileptic drug (partial and generalized seizures and LGS)
Inhibits Na channels and AMPA-kainate receptors enhance GABA receptors
Not highly protein bound, excreted unmetabolized in urine
SEs- Anorexia, weight loss, fatigue, somnolence
Reduces plasma levels of oral contraceptives

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24
Q

Levetiracetam

A

Adjunctive treatment for generalized, partial seizures in adults, myoclonic seizures in children.
IV prep for status epilepticus
May prevent synaptic glutamate release???
high safety margin, rapid dose titration, 3-D printing?

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25
Status Epilepticus
Series of seizures where full recovery doesnt happen before onset of next seizure (20% mortality) Treat with IV Lorazepam or Diazepam (lorazepam is better) Once seizures are controlled, give IV fosphenytoin (alternatives are levetiracetam, phenobarbital, valproic acid)
26
What is one cause that long term AED use can cause?
Osteoporosis Unknown mechanism (altered vit D metabolism?) Monitor bone density in the elderly.
27
AEDs and Pregnancy
They screw with oral contraceptives, making pregnancy 3x more likely. Also cause neural tube defects, fatal hydantoin syndrome (especially phenytoin) Mono therapy is preferable to combo Give vit K and folate to help prevent birth defects
28
Carbonic anhydrase inhibitor
Acetazolamide
29
Complication associated with acetazolamide
Serious skin reactions because it is an sulfonamide
30
Structure of acetazolamide
Sulfonamide
31
Where do carbonic anhydrase inhibitors act?
Proximal convoluted tubule
32
Acetazolamide
Diuretic Carbonic anhydrase inhibitor, acts in the proximal convoluted tubule CA normally converts bicarb to water and CO2, allowing the reabsorption of Sodium bicarb They aren't super effective because there are so many other places downstream where sodium can be absorbed. Loss of bicarb can lead to metabolic acidosis. Treats glaucoma by decreasing intraoccular pressure by inhibiting production of aqueous humor Treats respiratory alkalosis (acute mountain sickness) Treats cerebral edema (decreases CSF production) Can treat epilepsy Can be used to alkalinize the urine, enhancing excretion of weak acids (Uric acid and aspirin). This can cause kidney stones. Can cause hypokalemia due to indirect K+ excretion Sulfonamide allergic reactions
33
Mannitol
Osmotic diuretic It gets filtered through the the glomerulus into the tubule lumen Also decreases reabsorption of other solutes like sodium Can be used to induce urine flow in acute renal failure Can be used to decrease cerebral edema Can also lower intraoccular pressure Can pull water our of cells and into extra cellular space, which is dangerous in patients with CHF
34
2 loop diuretics
Furosemide (a sulfonamide) | Ethacrynic acid
35
How do loop diuretics get into the lumen?
Secreted by the organic acid secretory system. | Can increase Uric acid, bad for gout.
36
Loop diuretic mechanism
Inhibit the sodium potassium chloride transporter in the thick ascending limb of the loop of henle, inhibiting the reabsorption of all three ions. Leads to excretion of other ions like magnesium and calcium Drug of choice for CHF pulmonary edema Treats edema caused by liver and kidney problems Treats hypertension if thiazides fail Can treat hypercalcemia Leads to profound fluid/electrolyte loss Can cause metabolic alkalosis by increasing H secretion in the collecting ducts Can cause hypokalemia due to increased K secretion the collecting ducts Can increase glucose and lipids Can exacerbate gout by decreasing secretion of Uric acid and increased Uric acid reabsorption due to hypovolemia Can also cause ototoxicity Allergic reactions due to its sulfonamide structure
37
Uses of loop diuretics
Pulmonary Edema due to CHF Edema due to cirrhosis, nephrotic syndrome HTN if Thiazides fail Hypercalcemia
38
Adverse Effects of Loop Diuretics
Profound electrolyte/fluid loss can lead to hyponatremia, hypovolemia Metabolic alkalosis due to increased secretion oh H+ in the collecting duct Hypokalemia Increased serum glucose and lipids Can exacerbate gout because they are secreted into the lumen via the same organic acid secretory mechanism as uric acid and also because hypovolemia can cause increased uric acid reabsorption in the proximal tubule Ototoxicity Sulfonamide-like allergic reactions
39
Name 4 thiazides
``` Hydrochlorothiazide Chlorothiazide Chlorthalidone Indapamide CHIC ```
40
What chemical group do thiazides have?
Sulfonamide
41
How to Thiazides get into the lumen of the tubule?
Filtered through the glomerulus but also secreted by the organic acid secretory mechanism in the proximal tubule.
42
Which Thiazide is the most/least potent?
Chlorothiazide is the least potent | Indapamide is the most potent
43
Which Thiazide has the shortest/longest half-life?
Chlorothiazide has the shortest half-life | Chlorthalidone has the longest half-life
44
Thiazide mechanism
Inhibition of the Na+Cl- symporter in the distal convoluted tubule
45
Uses of Thiazides
Tx of mild-moderate pulmonary edema due to CHF Hypertension Kidney stones- Thiazides indirectly increase the reabsorption of Ca in the distal convoluted tubule Nephrogenic DI Can have a paradoxical anti-diuretic effect
46
Adverse effects of Thiazides
Hypokalemia- increased K+ secretion in collecting ducts Metabolic alkalosis- increased H+ secretion in the collecting ducts Same negative effects with gout as loop diuretics Hyperglycemia- maybe due to decreased insulin release Hyperlipidemia Hypersensitivities to Sulfa (SJS) So pretty similar to adverse effects of loop diuretics...
47
Which Thiazide isn't as bad when it comes to causing hyperlipidemia?
Indapamide
48
How do K+ wasting diuretics waste K+?
They increase both Na+ and Cl- delivery to the collecting duct system. The collecting duct system is faster at reuptaking Na+ than Cl-, which leaves the lumen of the collecting ducts relatively more negative. This promotes more secretion of K+
49
Name 2 K+ sparing diuretics
Triamterene | Amiloride
50
How to K+ sparing diuretics get into the lumen of the tubules?
Via the organic BASE secretory system in the proximal tubules.
51
Mechanism of Amiloride and Triamterene
Inhibit apical Na+ channels in the collecting ducts This leaves more Na+ in the ducts and promotes diuresis It also makes the lumen more positively charged, inhibiting K+ secretion, sparing K+.
52
Uses of Amiloride and Triamterene
Often used in combo with K+ wasting diuretics to prevent hypokalemia Can decrease thickness of respiratory secretions in CF Also treats Liddel's Syndrome (pseudohyperaldosteronism)
53
Adverse effects of Amiloride and Triamterene
Hyperkalemia Contraindicated with aldosterone antagonists (spironolactone) Used cautiously with RAAS inhibitors Nausea/vomiting is common Triamterene is poorly soluble in urine and can cause kidney stones
54
Name 3 aldosterone receptor antagonists
Spironolactone Eplerenone Drospirenone
55
What cells/where do aldosterone receptor antagonists act?
Principle cells of the collecting ducts | Intracellularly (max effects takes 2-3 days)
56
Therapeutic uses of spironolactone and eplerenone
Often used with other diuretics to prevent hypokalemia Tx for primary and secondary hyperaldosteronism, especially for hyperaldosteronism caused by cirrhosis Also part of therapy for CHF
57
Adverse effects of aldosterone receptor antagonists
Hyperkalemia Use with caution with drugs that inhibit the RAAS system like ACE inhibitors Think similar effects as Triamterene and Amiloride
58
Adverse effects of spironolactone
Anti androgen effects in men. Affects the menstrual cycle in women. Eplerenone is more selective and doesn't have these effects.
59
What is Drospirenone used for?
It's part of Yasmin, the birth control. It's a Progestin derived from spironolactone May help counterbalance the fluid retaining effects of the ethanyl estradiol in Yasmin.
60
Desmopressin
Synthetic ADH Acts on principle cells in collecting ducts to increase water reabsorption Used to treat central DI Can cause water intoxication
61
If a patient on a Thiazide presents with muscle weakness, cramps, and constipation what is the likely cause?
Hypokalemia Remember that more Na+ is delivered to the collecting ducts, allowing more more to be exchanged with K+. Hypovolemia due to Thiazides can increase RAAS activity, leading to more aldosterone release which can lead to even more K+ wasting.
62
How do caffeine and alcohol cause diuresis?
Caffeine increases GFR by increasing blood flow
63
Which drugs are the first line treatments for HTN?
Thiazides They come after lifestyle modification fails to decrease BP to target (140/90 or 130/80 in its with DM or chronic kidney disease)
64
What can happen if you decrease a patient's BP too quickly?
Their cerebral blood flow can decrease due to the auto regulatory set point being used to higher systemic BP. This is bad.
65
What three types of diuretics are used to treat HTN?
Thiazides (distal convoluted tubule) Loop diuretics (thick ascending limb) K Sparing diuretics (collecting duct)
66
What is an important dosing principle of thiazide usage in treatment of HTN?
Patients will see most of the BP lowering effect at a low dose. Increasing the dose won't affect BP much more, but will increase the side effects (hypokalemia, increase in glucose and lipids)
67
What is something to watch out for in patients taking thiazides?
Signs of hypokalemia like weakness, fatigue, and cramping. | You can have them eat bananas to help prevent this (we all know this because of Honey I Shrunk the Kids)
68
Name three adrenergic neuron blockers used to treat HTN
Reserpine Methyldopa Clonidine
69
Reserpine Mechanism
Irreversible blockage of VMAT, which transports NE and DA into vesicles in the presynaptic nerve terminal. This causes NE and DA to be degraded by MAO and prevents their release into the synapse. This lowers BP by decreasing sympathetic tone.
70
Methyldopa mechanism
Dual mechanism: 1. Inhibits DOPA Decarboxylase, which prevents production of DA from L-DOPA. This decreases production of both DA and NE, since NE is made from DA. 2. Gets converted to Methylnorepinephrine, which is an alpha-2 agonist. Remember that alpha-2 agonists have an inhibitory effect on the sympathetic nervous system.
71
Clonidine Mechanism
Treats high blood pressure by stimulating α2-receptors in the brain, which decreases peripheral vascular resistance, lowering blood pressure. It has specificity towards the presynaptic α2-receptors in the vasomotor center in the brainstem.
72
Name 3 alpha-1 adrenergic blockers.
Prazosin Doxazosin Terazosin
73
Which Beta Blocker isn't on our list of drugs used to treat HTN?
Esmolol | I don't know why
74
Which specific receptors do each of the 8 beta blockers act on?
Acebutolol, Atenolol, Esmolol and Metoprolol are all B1 selective. Nadolol, Pindolol, Propranolol, and Timolol act on both Beta 1 and 2 receptors.
75
Which two Beta blockers are partial agonists?
Acebutolol and Pindolol
76
Which Beta blocker has high lipid solubility?
Propranolol. | Think propane, which is super non-polar...
77
What are the main differences between B1 and B2 receptors?
B1 are more cardiac. They also increase renin secretion. B2 also acts on the heart, but not as much. Also affects glands, respiratory tract, GI tract, and peripheral resistance via dilation of peripheral vessels.
78
Labetalol
Mixed Alpha 1 and Beta 1-2 antagonist
79
Nebivolol
Selective Beta 1 blocker that also potentiates NO (produces vasodilation)
80
Name 2 direct arteriolar dilators
Hydralazine | Minoxidil
81
Hydralazine
Direct Arteriolar dilator | Unknown mechanism, but it requires functional endothelium that can produce NO to work.
82
Minoxidil
Direct arteriolar vasodilator Mechanism may involve K channels Used to treat hair loss (Rogaine)
83
Calcium channel blockers mechanism in treating HTN
They are mainly used to treat HTN because blocking Ca channels decreases contraction of smooth muscle in resistance vessels, decreasing TPR and therefore BP. They also act on myocardium to reduce force of contraction (not really sure if that's a good thing on not. It definitely has to do with some contraindications like Left sided heart failure).
84
Name 5 calcium channel blockers
``` Verapamil Diltiazem Nifedipine Felodipine Amlodipine ```
85
Verapamil
Ca channel blocker
86
Diltiazem
Ca channel blocker
87
Nifedipine
Ca Channel blocker
88
Felodipine
Ca Channel Blocker
89
Amlodipine
Ca channel blocker
90
What are three classes of drugs that inhibit the RAAS system?
ACE inhibitors Angiotensin II receptor blockers Renin inhibitors
91
Name 6 ACE inhibitors
``` The all end in -pril Captopril Enalapril Lisinopril Fosinopril Quinapril Ramipril ```
92
Name 3 Angiotensin II receptor blockers
They end in -sartan Losartan Valsartan Candesartan
93
Aliskiren
Renin Inhibitor
94
What does renin do?
Converts angiotensinogen to Angiotensin 1.
95
You have a patient on a thiazide for HTN. It's controlling their BP well, but they have signs of hypokalemia. What do you do?
Add on a K sparing diuretic like Triamterene or Amiloride. These won't affect BP that much, but will help the patient retain more K.
96
Name two Nitrates
Nitroglycerine | Isosorbide Dinitrate
97
Nitrate Mechanism
Active Guanylyl cyclase, which converts GTP to cGMP | This leads to smooth muscle relaxation in blood vessels, decreasing angina.
98
Nitroglycerine vs Isosorbide Dinitrate
Nitro is fast acting (3-5 minutes) but wears off quickly. | Isosorbide dinitrate works more slowly but for a longer period of time
99
How to Calcium channel blockers treat angina?
They decrease the oxygen demand of the heart by decreasing after load (vasodilation) and decreasing contractility.
100
Which 3 beta blockers are not used to treat angina?
Esmolol | Acebutolol and pindolol (these have partial agonist properties)
101
Ivabradine
Slows HR by inhibiting the so-called “funny” channel current in the SA node Used in high HR subjects intolerant of beta blockers or as add-on to beta blockers
102
Ranolazine
new Angina treatment | Inhibits the late inward sodium current in heart muscle.
103
Which type of hyperlipidemia is not associated with increased CHD risk?
Type I- Isolated Familiar Hyperchylomicronemias These people have way more than normal chylomicrons, but their LDL and VLDL are normal. Drug therapy is NOT indicated.
104
Which types of hyperlipidemias have the greatest increased risk for CHD?
Type IIa and IIb | Isolated Familial Hypercholesterolemia and Mixed Familial hyperlipoproteinemia
105
Ezetimibe
Cholesterol Absorption Inhibitor | Blocks Cholesterol absorption in the small intestine, forcing the liver to take more cholesterol out of circulation.
106
Name 3 Bile Acid Binding resins
Cholestyramine Colestipol Colesevelam They all have Chole or Cole
107
Bile Acid Binding Resins Mechanism
they bind to bile acids in the intestine and prevent their reabsorption. This makes the liver convert more cholesterol into bile acids to normalize their level, decreasing plasma cholesterol. They aren't used that often to decrease cholesterol since statins are better. they have other uses though...
108
What is another name for statins?
HMG-CoA Reductase Inhibitors
109
Name 5 Statins
``` Lovastatin Atorvastatin Rosuvastatin Pravastatin Simvastatin LARPS ```
110
Statin mechanism
HMG-CoA Reductase Inhibitors | They inhibit this enzyme, which produces mevalonic acid, an early precursor to cholesterol.
111
Niacin
Lowers LDL, VLDL, and triglycerides. Raises HDL The mechanisms behind this are complicated and uncertain as far as I can tell from google.
112
Omega-3-Acid Ethyl Esters
Used in patients with really high triglycerides. Reduce triglycerides and VLDL. Increases HDL Can dramatically increase LDL though...
113
Name 2 Fibric Acid Analogs
Gemfibrozil | Fenofibrate
114
Gemfibrozil and Fenofibrate
Fibric acid analogs Lower triglycerides, LDL, VLDL Raise HDL
115
Cholesterol Ester Transfer Protein Inhibitors
They all end in -CETraPib | They increase HDL levels
116
What are 5 important effects of insulin?
``` Decreased gluconeogenesis Decreased ketogenesis Decreased lipolysis Increased glucose uptake into fat and muscle Increased amino acid uptake in muscle ```
117
How do we produce insulin preparations today?
Recombinant DNA technology
118
Regular Insulin
Clear solution, human sequence Short-acting Only for IV use
119
NPH Insulin
Cloudy solution, human sequence | Intermediate acting
120
Pre-mixed insulin mixtures
Mix of NPH and regular insulin. | often 70% NPH, 30% regular
121
Insulin Lispro, aspart, glulisine
Short acting insulin preps Insulin that has been altered at specific amino acids to facilitate monomer formation. This makes them fast acting, good for postprandial administration (after meals) There are inhaled insulin preps that act similarly.
122
Insulin Glargine
Long-acting insulin prep (thing gLARGEine) Glycine replaces an aspartate (A21) 2 arginines are added to the c-terminus Poorly soluble at pH 7 Injected SQ, forms a micro-precipitate in the interstitial fluids, leads to long-steady action.
123
Insulin detemir
``` Long-acting insulin analog Threonine is omitted and a fatty acid chain is added to an amino acid. Self-injected SQ Binds albumin in the blood stream Acts faster than insulin Glargine ```
124
What is the fasting blood glucose goal with DM treatment?
70-130 mg/dL
125
What is the post-prandial blood glucose goal in DM treatment?
less than 180 mg/dL 2 hours after a meal
126
HbA1c target in DM treatment?
less than 7%
127
Describe a Split-Mixed Regimen of insulin dosage
Doses of 70:30 insulin given SQ | One before breakfast and one before dinner
128
Describe a three shot insulin regimen
Mixed injection before breakfast Regular injection before dinner NPH (intermediate-acting) injection at bedtime
129
Describe the Basal-Bolus regimen
Insulin glargine once per day (at bedtime) and a short-acting analog before each meal. This can be done with a continuous insulin pump instead of the insulin glargine injection at night
130
Adverse effects of insulin
``` Hypoglycemia Weight gain Allergic reactions Resistance Atrophy or hypertrophy of fatty tissue at injection site Atherosclerosis and cancer at high doses ```
131
Adverse effects of inhaled insulin
Throat irritation cough Decreased pulmonary function (do periodic pulmonary function tests) Long term safety TBD (that's good...)
132
Metformin
Biguanide First line of therapy for type 2 DM Reduces hepatic gluconeogenesis Prevents hyperglycemia, but does not induce hypoglycemia
133
Possible metformin mechanism
Inhibition of a mitochondrial specific isoform of glycerophosphate dehydrogenase, slowing the DHAP-glycerophosphate shuttle, through a few more convoluted steps decreasing hepatic gluconeogenesis.
134
Adverse effects of metformin
``` GI disturbances (most common, often transient) Lactic acidosis (rare, but dangerous, avoidable) ```
135
Metformin contraindications
Anyone predisposed to lactic acidosis (anyone with decreased tissue oxygenation or reduced drug elimination) Alcoholism Renal insufficiency Hepatic disease Hypoxic pulmonary disease Discontinue metformin for 48 hours up to administration of IV contrast
136
Metformin clinical use
1st line of therapy for type 2 DM Taken twice daily Often used in conjunction with other drugs (sulfonylureas, thiazolidonediones, or insulin)
137
Additional benefits of metformin
``` Weight loss Reduction in LDL, VLDL Lower BP Decreased risk of vascular disease May decrease risk of some cancers ```

Pharmacology (34 decks)

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