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Pharmacology > Exam 6 > Flashcards

Exam 6 Flashcards

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
Q

Status Epilepticus

A

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)

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26
Q

What is one cause that long term AED use can cause?

A

Osteoporosis
Unknown mechanism (altered vit D metabolism?)
Monitor bone density in the elderly.

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27
Q

AEDs and Pregnancy

A

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

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28
Q

Carbonic anhydrase inhibitor

A

Acetazolamide

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29
Q

Complication associated with acetazolamide

A

Serious skin reactions because it is an sulfonamide

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30
Q

Structure of acetazolamide

A

Sulfonamide

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31
Q

Where do carbonic anhydrase inhibitors act?

A

Proximal convoluted tubule

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32
Q

Acetazolamide

A

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

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33
Q

Mannitol

A

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

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34
Q

2 loop diuretics

A

Furosemide (a sulfonamide)

Ethacrynic acid

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35
Q

How do loop diuretics get into the lumen?

A

Secreted by the organic acid secretory system.

Can increase Uric acid, bad for gout.

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36
Q

Loop diuretic mechanism

A

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

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37
Q

Uses of loop diuretics

A

Pulmonary Edema due to CHF
Edema due to cirrhosis, nephrotic syndrome
HTN if Thiazides fail
Hypercalcemia

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38
Q

Adverse Effects of Loop Diuretics

A

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

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39
Q

Name 4 thiazides

A 
Hydrochlorothiazide
Chlorothiazide
Chlorthalidone
Indapamide
CHIC
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40
Q

What chemical group do thiazides have?

A

Sulfonamide

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41
Q

How to Thiazides get into the lumen of the tubule?

A

Filtered through the glomerulus but also secreted by the organic acid secretory mechanism in the proximal tubule.

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42
Q

Which Thiazide is the most/least potent?

A

Chlorothiazide is the least potent

Indapamide is the most potent

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43
Q

Which Thiazide has the shortest/longest half-life?

A

Chlorothiazide has the shortest half-life

Chlorthalidone has the longest half-life

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44
Q

Thiazide mechanism

A

Inhibition of the Na+Cl- symporter in the distal convoluted tubule

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45
Q

Uses of Thiazides

A

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

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46
Q

Adverse effects of Thiazides

A

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…

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47
Q

Which Thiazide isn’t as bad when it comes to causing hyperlipidemia?

A

Indapamide

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48
Q

How do K+ wasting diuretics waste K+?

A

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+

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49
Q

Name 2 K+ sparing diuretics

A

Triamterene

Amiloride

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50
Q

How to K+ sparing diuretics get into the lumen of the tubules?

A

Via the organic BASE secretory system in the proximal tubules.

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51
Q

Mechanism of Amiloride and Triamterene

A

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+.

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52
Q

Uses of Amiloride and Triamterene

A

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)

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53
Q

Adverse effects of Amiloride and Triamterene

A

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

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54
Q

Name 3 aldosterone receptor antagonists

A

Spironolactone
Eplerenone
Drospirenone

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55
Q

What cells/where do aldosterone receptor antagonists act?

A

Principle cells of the collecting ducts

Intracellularly (max effects takes 2-3 days)

56
Q

Therapeutic uses of spironolactone and eplerenone

A

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
Q

Adverse effects of aldosterone receptor antagonists

A

Hyperkalemia
Use with caution with drugs that inhibit the RAAS system like ACE inhibitors
Think similar effects as Triamterene and Amiloride

58
Q

Adverse effects of spironolactone

A

Anti androgen effects in men. Affects the menstrual cycle in women.
Eplerenone is more selective and doesn’t have these effects.

59
Q

What is Drospirenone used for?

A

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
Q

Desmopressin

A

Synthetic ADH
Acts on principle cells in collecting ducts to increase water reabsorption
Used to treat central DI
Can cause water intoxication

61
Q

If a patient on a Thiazide presents with muscle weakness, cramps, and constipation what is the likely cause?

A

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
Q

How do caffeine and alcohol cause diuresis?

A

Caffeine increases GFR by increasing blood flow

63
Q

Which drugs are the first line treatments for HTN?

A

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
Q

What can happen if you decrease a patient’s BP too quickly?

A

Their cerebral blood flow can decrease due to the auto regulatory set point being used to higher systemic BP. This is bad.

65
Q

What three types of diuretics are used to treat HTN?

A

Thiazides (distal convoluted tubule)
Loop diuretics (thick ascending limb)
K Sparing diuretics (collecting duct)

66
Q

What is an important dosing principle of thiazide usage in treatment of HTN?

A

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
Q

What is something to watch out for in patients taking thiazides?

A

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
Q

Name three adrenergic neuron blockers used to treat HTN

A

Reserpine
Methyldopa
Clonidine

69
Q

Reserpine Mechanism

A

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
Q

Methyldopa mechanism

A

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
Q

Clonidine Mechanism

A

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
Q

Name 3 alpha-1 adrenergic blockers.

A

Prazosin
Doxazosin
Terazosin

73
Q

Which Beta Blocker isn’t on our list of drugs used to treat HTN?

A

Esmolol

I don’t know why

74
Q

Which specific receptors do each of the 8 beta blockers act on?

A

Acebutolol, Atenolol, Esmolol and Metoprolol are all B1 selective.
Nadolol, Pindolol, Propranolol, and Timolol act on both Beta 1 and 2 receptors.

75
Q

Which two Beta blockers are partial agonists?

A

Acebutolol and Pindolol

76
Q

Which Beta blocker has high lipid solubility?

A

Propranolol.

Think propane, which is super non-polar…

77
Q

What are the main differences between B1 and B2 receptors?

A

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
Q

Labetalol

A

Mixed Alpha 1 and Beta 1-2 antagonist

79
Q

Nebivolol

A

Selective Beta 1 blocker that also potentiates NO (produces vasodilation)

80
Q

Name 2 direct arteriolar dilators

A

Hydralazine

Minoxidil

81
Q

Hydralazine

A

Direct Arteriolar dilator

Unknown mechanism, but it requires functional endothelium that can produce NO to work.

82
Q

Minoxidil

A

Direct arteriolar vasodilator
Mechanism may involve K channels
Used to treat hair loss (Rogaine)

83
Q

Calcium channel blockers mechanism in treating HTN

A

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
Q

Name 5 calcium channel blockers

A 
Verapamil
Diltiazem
Nifedipine
Felodipine
Amlodipine
85
Q

Verapamil

A

Ca channel blocker

86
Q

Diltiazem

A

Ca channel blocker

87
Q

Nifedipine

A

Ca Channel blocker

88
Q

Felodipine

A

Ca Channel Blocker

89
Q

Amlodipine

A

Ca channel blocker

90
Q

What are three classes of drugs that inhibit the RAAS system?

A

ACE inhibitors
Angiotensin II receptor blockers
Renin inhibitors

91
Q

Name 6 ACE inhibitors

A 
The all end in -pril
Captopril
Enalapril
Lisinopril
Fosinopril
Quinapril
Ramipril
92
Q

Name 3 Angiotensin II receptor blockers

A

They end in -sartan
Losartan
Valsartan
Candesartan

93
Q

Aliskiren

A

Renin Inhibitor

94
Q

What does renin do?

A

Converts angiotensinogen to Angiotensin 1.

95
Q

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?

A

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
Q

Name two Nitrates

A

Nitroglycerine

Isosorbide Dinitrate

97
Q

Nitrate Mechanism

A

Active Guanylyl cyclase, which converts GTP to cGMP

This leads to smooth muscle relaxation in blood vessels, decreasing angina.

98
Q

Nitroglycerine vs Isosorbide Dinitrate

A

Nitro is fast acting (3-5 minutes) but wears off quickly.

Isosorbide dinitrate works more slowly but for a longer period of time

99
Q

How to Calcium channel blockers treat angina?

A

They decrease the oxygen demand of the heart by decreasing after load (vasodilation) and decreasing contractility.

100
Q

Which 3 beta blockers are not used to treat angina?

A

Esmolol

Acebutolol and pindolol (these have partial agonist properties)

101
Q

Ivabradine

A

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
Q

Ranolazine

A

new Angina treatment

Inhibits the late inward sodium current in heart muscle.

103
Q

Which type of hyperlipidemia is not associated with increased CHD risk?

A

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
Q

Which types of hyperlipidemias have the greatest increased risk for CHD?

A

Type IIa and IIb

Isolated Familial Hypercholesterolemia and Mixed Familial hyperlipoproteinemia

105
Q

Ezetimibe

A

Cholesterol Absorption Inhibitor

Blocks Cholesterol absorption in the small intestine, forcing the liver to take more cholesterol out of circulation.

106
Q

Name 3 Bile Acid Binding resins

A

Cholestyramine
Colestipol
Colesevelam
They all have Chole or Cole

107
Q

Bile Acid Binding Resins Mechanism

A

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
Q

What is another name for statins?

A

HMG-CoA Reductase Inhibitors

109
Q

Name 5 Statins

A 
Lovastatin
Atorvastatin
Rosuvastatin
Pravastatin
Simvastatin
LARPS
110
Q

Statin mechanism

A

HMG-CoA Reductase Inhibitors

They inhibit this enzyme, which produces mevalonic acid, an early precursor to cholesterol.

111
Q

Niacin

A

Lowers LDL, VLDL, and triglycerides.
Raises HDL
The mechanisms behind this are complicated and uncertain as far as I can tell from google.

112
Q

Omega-3-Acid Ethyl Esters

A

Used in patients with really high triglycerides.
Reduce triglycerides and VLDL.
Increases HDL
Can dramatically increase LDL though…

113
Q

Name 2 Fibric Acid Analogs

A

Gemfibrozil

Fenofibrate

114
Q

Gemfibrozil and Fenofibrate

A

Fibric acid analogs
Lower triglycerides, LDL, VLDL
Raise HDL

115
Q

Cholesterol Ester Transfer Protein Inhibitors

A

They all end in -CETraPib

They increase HDL levels

116
Q

What are 5 important effects of insulin?

A 
Decreased gluconeogenesis
Decreased ketogenesis
Decreased lipolysis
Increased glucose uptake into fat and muscle
Increased amino acid uptake in muscle
117
Q

How do we produce insulin preparations today?

A

Recombinant DNA technology

118
Q

Regular Insulin

A

Clear solution, human sequence
Short-acting
Only for IV use

119
Q

NPH Insulin

A

Cloudy solution, human sequence

Intermediate acting

120
Q

Pre-mixed insulin mixtures

A

Mix of NPH and regular insulin.

often 70% NPH, 30% regular

121
Q

Insulin Lispro, aspart, glulisine

A

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
Q

Insulin Glargine

A

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
Q

Insulin detemir

A 
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
Q

What is the fasting blood glucose goal with DM treatment?

A

70-130 mg/dL

125
Q

What is the post-prandial blood glucose goal in DM treatment?

A

less than 180 mg/dL 2 hours after a meal

126
Q

HbA1c target in DM treatment?

A

less than 7%

127
Q

Describe a Split-Mixed Regimen of insulin dosage

A

Doses of 70:30 insulin given SQ

One before breakfast and one before dinner

128
Q

Describe a three shot insulin regimen

A

Mixed injection before breakfast
Regular injection before dinner
NPH (intermediate-acting) injection at bedtime

129
Q

Describe the Basal-Bolus regimen

A

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
Q

Adverse effects of insulin

A 
Hypoglycemia
Weight gain
Allergic reactions
Resistance
Atrophy or hypertrophy of fatty tissue at injection site
Atherosclerosis and cancer at high doses
131
Q

Adverse effects of inhaled insulin

A

Throat irritation
cough
Decreased pulmonary function (do periodic pulmonary function tests)
Long term safety TBD (that’s good…)

132
Q

Metformin

A

Biguanide
First line of therapy for type 2 DM
Reduces hepatic gluconeogenesis
Prevents hyperglycemia, but does not induce hypoglycemia

133
Q

Possible metformin mechanism

A

Inhibition of a mitochondrial specific isoform of glycerophosphate dehydrogenase, slowing the DHAP-glycerophosphate shuttle, through a few more convoluted steps decreasing hepatic gluconeogenesis.

134
Q

Adverse effects of metformin

A 
GI disturbances (most common, often transient)
Lactic acidosis (rare, but dangerous, avoidable)
135
Q

Metformin contraindications

A

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
Q

Metformin clinical use

A

1st line of therapy for type 2 DM
Taken twice daily
Often used in conjunction with other drugs (sulfonylureas, thiazolidonediones, or insulin)

137
Q

Additional benefits of metformin

A 
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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