Exam 2 - ENT, pulm, cardio Flashcards

Question

When is nystatin used?

Answer 1

Used topically as powder for oral thrush. Good for I/C pts Prevent fungus growth Treat infection

Answer 2

Binds to sterols in fungal membrane to increase cell wall permeability; opens up for contents to spill out.

Answer 3

CMV - Leads to esophagitis, retinitis, colitis.

Answer 4

Famicyclovir Valacyclovir Valgancyclovir

Answer 5

Not active in current form, but when metabolized by liver are confirmed to "active compound"

Answer 6

A larger portion of drug goes through first pass; increase the bioavailability!

Answer 7

Inhibit viral DNA replication; guanine analogs are incorporated, but they're missing the sugar backbone so elongation can't occur. Triggers cell death.

Answer 8

Herpes simplex, Shingles, Herpes stomatitis

Answer 9

Valacyclovir, because its a prodrug. Has better efficacy.

Answer 10

Nephrotoxicity - worry about drug crystallizing in renal tubule causing interstitial nephritis. Bone marrow suppression. CNS affects - might increase risk of seizures or altered mental status in the elderly.

Answer 11

Drink a lot of water to prevent crystallization in the kidneys.

Answer 12

Herpes and Shingles Toxicity is worse so they're used less frequently than others; used mostly to step up therapy for resistant strains.

Answer 13

Famicyclovir

Answer 14

CMV for transplant patients and cancer patients. Can cause thrombocytopenis and CNS toxicity. Patients stop therapy due to side effects. Monitor CBC

Answer 15

Valgancyclovir

Answer 16

Resistant viral strains; there is no pro drug for it. >> CMV retinitis, acyclovir resistant HSV, shingles, ganciclovir resistant CMV Administered IV only and renally eliminated. Needs dose adjustment.

Answer 17

Inhibits DNA polymerase, directly.

Answer 18

Chelates cations - can lead to hypocalcemia, hypomagnesaemia, and hypokalemia

Answer 19

Aspirin (ASA)

Answer 20

Has anti-clotting effects and analgesic at higher levels. Old drug, good absoprtion, hepatically conjugated, and excreted in kidneys.

Answer 21

Irreversible inhibitor of COX 1, 2, 3 - no selectivity. Used to protect the heart against MI.

Answer 22

Inhibits PLT, causes bruising and bleeding. Do not use in bleeding disorder or pregnancy.

Answer 23

In children with fever (esp. viral), there is an increased risk of Reye's syndrome!

Answer 24

Fatty liver encephalopathy that affects children. Symptoms are similar to viral illness - fever, vomitting, lethargy etc., but can cause CNS damage -- can go unnoticed for a long period of time.

Answer 25

1 - rash on hands and feet, vomiting, high fever, lethargy 2 - encephalitis, hyperventilation, fatty liver 3 - coma, cerebral edema 4 - deeper coma 5 - siezures, organ failure, death

Answer 26

Peptobismol (Bismuth salicylate) - Has salicylate and can cause Reye's Syndrome.

Answer 27

Inhibits COX 1 and 2, nonselective Reversible inhibitor! - not as high risk as ASA.

Answer 28

Pain relief If you have a sprain or inflammation, better drug to use bc it works on the inducable COX.

Answer 29

RISK - COX1 helps prevent erosion with stomach acids, so use can lead to ulcers (since this is the target); can have acute kidney injury, can worsen hypertension

Answer 30

Decreases antihypertensives (ACEI) Leads to accumulation of Lithium Decrease secretion of methotrexate, which can lead to bone marrow suppression.

Answer 31

ASTHMATICS | Patients may have allergy to it that induces their asthma.

Answer 32

Inhibits COX3, which is located in CNS. Good for fevers! Not good for a sprain, because it doesn't target the periphery.

Answer 33

Liver toxicity; don't exceed 4000mg a day! Good for pain in pregnancy.

Answer 34

Mediates immune reactions. "Triple Response" - - redness - vasodilation - wheal - edema - flare - redness

Answer 35

Located on the heart and bronchial smooth muscle. | When activated, will see vasodilation.

Answer 36

H1 receptors increase post capillary permeability and vasodilation. This leads to increased mucus secretion, bronchus constriction, and smooth muscle tone.

Answer 37

Stimulate gastric acid secretion. Used in long-term complications of allergies, i.e. anaphylaxis.

Answer 38

Promote sleep and wakefulness.

Answer 39

Block smooth muscle and GI tract vasodilation, lowers edema (less itching).

Answer 40

OTC Sleep Aid | H1 receptor antagonist

Answer 41

euphoria, hallucinations at high doses

Answer 42

Don't cause sedation | Can't cross blood-brain barrier

Answer 43

allergic reactions, motion sickness, nausea, OTC sleep remedies.

Answer 44

Sedation, GI disturbance Antimuscarinic, so dry mouth and blurred vision

Answer 45

Second generation - Not antimuscarinic or antiemetic bc can't get into CNS

Answer 46

Intranasal spray; H1 receptor antagonist. Used for allergic and vasomotor rhinitis.

Answer 47

Nose bleeds, bitter taste No systemic side effects or activity. i.e. Doesn't help itching and rashes.

Answer 48

Nasal Corticosteroids | ONES AND IDES

Answer 49

Can be used over longer period of time, chronically, to decrease nasal allergic reactions. Do not use for acute allergies.

Answer 50

Decrease transcription from site of nucleus (gene transcription and protein production). Meds need to be taken consistently. Takes a week or so before effects are seen.

Answer 51

Don't want the pharmacist to fill inhaler version (for asthmatics only).

Answer 52

``` Epistaxis Septum perf (rare) ```

Answer 53

Synthetic adrenocortical steroid Used for drug hypersensitivity, severe rhinitis, asthma exacerbations.

Answer 54

They have glucocorticoid actions and mineralcorticoid actions GC is anti-inflammatory, while mineralcorticoid does fluid retention, salt retention, etc. to maintain good volume for cardiac status. MC effects cause worsening of CHF, HTN, fluid retention and weight gain. Can see glucose intolerance, because it can decrease insulin release. Bad for diabetics Can also see cataracts and increased IOP. Short course use only! Immunosupressive!

Answer 55

They're very potent anti-inflammatories. Good for asthma exacerbations, anaphylaxis, etc.

Answer 56

Decreased antidiabetic medications. Diabetics don't mess with dex. Electrolyte shift to hypokalemia = potassium deficiency.

Answer 57

Fungal infections, because it'll further depress immune system.

Answer 58

Adrenal gland insufficiency Exogenous corticosteroids causes the adrenal glands to secrete less. If on for over a week and stopped, the adrenal glands would be insufficient. Need to taper over a weeks time to prevent insufficiency.

Answer 59

ADR: Same as Dex. Don't use for fungal infections. Taper off of it or you'll have rebound symptoms.

Answer 60

Used intranasally MOA constricts alpha receptor in nose to decrease edema and leaky capillaries.

Answer 61

Local decongestant! Treats nasal congestion, but causes rebound hyperemia. Receptors are down regulated; none to be activated to reconstrict when off medication.

Answer 62

Rhinitis medicamentosa

Answer 63

Worsen HTN

Answer 64

Systemic decongestant; alpha agonist that constricts blood vessels in mucosa to decrease stuffiness. Sudafed can make erections go down, because it constricts blood vessels.

Answer 65

Can have some rebound congestion, but not like that in Afrin

Answer 66

Mucolytic - loosens mucus secretions in airway and decreases viscosity of them. Needs to be taken with water to decrease viscosity. Increase in drainage.

Answer 67

Shown in studies to have no fetal harm or harm in animals; totally safe. Ex: folic acid, water-soluble vitamins.

Answer 68

Animal studies may show some harm, but shows no harm to human fetus in any trimester. Ex: Amoxicillin

Answer 69

"Shrugging your shoulders" - not enough data to determine effect on humans. Majority of drugs! Ex: Albuterol

Answer 70

Evidence of risk to the fetus, but benefits of treating mom outweight the protection of fetus. Need to do risk-benefit analysis. Ex: Lithium

Answer 71

Definite harm and there's no case where its beneficial to give it to the mother. Ex: Teratogens

Answer 72

START OF PULMONOLOGY CARDS

Answer 73

Can target brain stem or the stretch receptors of the throat. Need to reduce number and severity of coughing episodes and prevent complications

Answer 74

Ace inhibitors

Answer 75

Hardest drug to dispense! Anesthetize stretch receptor in the lungs to prevent cough. Do NOT chew! Can numb mouth. Maybe not good for kids, might chew and can cause CNS depression.

Answer 76

Related to codeine; helps to supress cough center in the brain.

Answer 77

Proserotinergic effects - If you're taking other drugs that block reuptake of serotonin or decrease metabolism you may see tachycardia, altered mental status, hyperthermia. Too much serotonin in the synapse.

Answer 78

rhinovirus, coronavirus, influenza, adenovirus

Answer 79

AVOID ANTIHISTAMINES because it'll dehydrate the bronchial secretions and worsen symptoms.

Answer 80

Usually self-limited, give NSAIDs.

Answer 81

Bacterial - Those sick 3-5 days with a worsening of symptoms are bacterial: want to focus on atypicals. Use doxycycline or azithromycin

Answer 82

Doxycycline (teeth stain under 8yo) - treats mycoplasma resistant to macrolides!!

Answer 83

Don't want to use unless you had recent abx exposure; helps to cover for resistant strep pneumo (since they are more at risk for it). - levofloxacin - ciprofloxacin - moxifloxacin

Answer 84

Curb 65 PSI Guide if patient goes inpatient, outpatient, ICU

Answer 85

Over 65yo, had a beta lactam within last three months, alcoholism, immunosupressed, and medical comorbidities.

Answer 86

nursing homes, cardiopulmonary disease, medical comorbidities, recent abx therapy.

Answer 87

lung disease, corticosteroid use, broad spectrum abx therapy, malnutrition

Answer 88

1st line is a macrolide like Azithromycin or Clarithromycin Macrolides inhibit CYP3A4.

Answer 89

Treat with Beta Lactam AND Macrolide - - augmentin, cefuroxim - -azithromycin or clarithromycin If can't have beta-lactam, use resp FQ.

Answer 90

IV beta-lactam, ORAL macrolide Cefotaxime, ampicillin, and macrolide

Answer 91

IV treatment only and MRSA coverage (Vanco).

Answer 92

Cavity infiltrates and GPC clusters. Needs vancomycin (or linezolid, if CI to vanco).

Answer 93

Occurs from nursing homes, hospitals, or other healthcare settings. Infection not present at time of admission.

Answer 94

Hospitalized in acute care facility for more than two days in past 90 days. ``` Nursing home IV antibiotics recently Chemotherapy wound care dialysis patients ```

Answer 95

age, lung disease, depressed consciousness, large volume aspiration, hospitalization during winter months

Answer 96

mechanical ventilation, placement of NG tube, or ICP monitor. Preventing these lowers your risk for resistant bugs!

Answer 97

SPACE bugs ``` Psuedomonas E coli Klebsiella Acinetobacter Enterobacter ``` MRSA strep pneum

Answer 98

Fungal infection

Answer 99

Start therapy as soon as possible; don't wait for definitive culture! Initiate broad spectrum abx - Consider MDR, esp if at risk - Must cover MRSA and pseudomomas When cultures come back, you can streamline therapy to target the bug.

Answer 100

He has multiple risk factors for MDR pathogens. -- Need to go with 3 drug coverage. 2 for gram negative psuedomonas so on its hit, plus aminoglycoside, and MRSA coverage. Cefepime - antipseud CS Imipenem/Meri - antipseud carbapenem PLUS Gentamycin - aminoglycoside or antipseud FQ - levofloxacin. PLUS vanco (or linezolid).

Answer 101

3rd gen CS = Ceftriaxone OR levofloxacin OR ampicillin/sublactam OR ertapenem

Answer 102

Ceftazidime and Cefepime!

Answer 103

Imipenem - use with caution for patients with seizure history Meropenem

Answer 104

Piperacillin/tazobactam | Ticarcillin/clavulanate

Answer 105

ciprofloxacin levofloxacin Have good penetration to the lungs!

Answer 106

QT prolongation Tendon rupture in young patients - ciprofloxacin - levofloxacin

Answer 107

Once daily dosing, because they're conc-dependent killer. Also, need higher doses because they have poor lung penetration. Need TDM; nephrotoxicity and ototoxicity

Answer 108

Lungs, brain, and bones are hard to penetrate, so they require higher trough levels.

Answer 109

3-4th dose to make sure you're at a steady state

Answer 110

ototoxicity and nephrotoxicity

Answer 111

MRSA, VRE Can penetrate lungs Used when vanco isn't tolerated. NO DOSE ADJUSTMENT FOR RENAL FUNCTION.

Answer 112

Daptomycin

Answer 113

Could be a resistant pathogen and wrong therapy. May have been misdiagnosed. Complications, such as empyema or lung abscess.

Answer 114

7-8 days, but 10-14 for more resistant bugs

Answer 115

Laryngeal and lower airway edema, stridor, wheezing, rhinitis, GI symptoms

Answer 116

Worried about "leaky cappillaries" and intravascular depletion of fluid causing edema. Start with epinephrine and volume expansion!

Answer 117

Crystalloids are salt-based, ex: lactate ringers, NaCl. Good for intravascular volume replacement in anaphylaxis.

Answer 118

Albumen and starch.

Answer 119

Its a crystalloid isotonic solution - osmolarity is 308, which is isotonic to blood osmolarity (300). It will stay in intravascular space!

Answer 120

20ml/kg! (20kg patient gets 400ml bolus). Top off at 1-2 L and reassess. volume status.

Answer 121

Might need to give less than regular fluid bolus; also applies to peds patient.

Answer 122

4:2:1 rule 4ml/kg for first 10kg 2ml/kg for second 10kg 1ml/kg for every kg after 20.

Answer 123

100ml per hour.

Answer 124

Epinephrine

Answer 125

MOA: activates alpha and beta receptors Alpha - increases vasoconstriction to prevent the leak Beta - helps cause smooth muscle relaxation to release airway contraction and improve oxygenation. Know to relieve pruritus, urticaria, and angioedema.

Answer 126

Use preservative free product, because of allergy. If not possible, you treat allergy during tx.

Answer 127

IM or subQ | Can be given IV for SEVERE reactions, when patient isn't perfusing.

Answer 128

IV They're not perfusing so it won't be circulated if IM or subQ. without blood flow to these areas, it wont work well.

Answer 129

1mg in 1mL

Answer 130

1mg in 10mL

Answer 131

intercranial hemorrhage MI, pulmonary edema, etc.

Answer 132

1 in 10 via IV.

Answer 133

Histamine blockers! B/c there's a huge amount of histamine being released in reaction and these help alleviate itching, etc.

Answer 134

diphenhydramine and hydroxyzine | Most commonly used!

Answer 135

Rantidine Mainly GI drugs; optional add on drugs. H2 blockers prevent gastric acid in GI tract. They end up increasing pH of stomach so more things can grow and ulcers can occur.

Answer 136

bronchodilators, such as albuterol, which relax bronchial smooth muscle.

Answer 137

anxiousness, tremors, tachycardia

Answer 138

benadryl | dephenhydramine

Answer 139

zyrtec allegra claritin

Answer 140

``` Beclomethasone Budesonide Fluticasone Mometasone Triamcinolone ```

Answer 141

There are less systemic side effects; they work locally in the lungs.

Answer 142

Inhibiting the anti-inflammatory cascade by working at site of nucleus to decrease transcription of genes that makes inflammatory cytokines.

Answer 143

Inhaled corticosteroids take longer to work. Tell patient to take drug consistently, as prescribed, every single day. Takes 8 weeks for maximal effects.

Answer 144

Well tolerated compared to systemic CS. May develop oral candidasis, because the drug goes to the back of the throat and causes immunosuppression there. Must swish out mouth with water and spit afterward. Exceedingly high doses may suppress normal growth.

Answer 145

LABA like formoteral and salmeterol can be combined with ICS. LABA will provide some control throughout the day while the ICS start to kick in.

Answer 146

Symbicort (Formoterol/budesonide) Dulera (Formoterol/momentasone) Advair (Salmeterol/fluticasone)

Answer 147

Using ICS by itself. Combination products can be very expensive for patients. If its severe, do combination initially.

Answer 148

Leukotrienes are responsible for the bronchial constriction . If we get something to block at receptor site, it prevents them from bronchoconstriction in the first place and stops asthmatic symptoms.

Answer 149

Zafirlukast (Accolate) | Montelukast (Singulair)

Answer 150

Primary leukotriene modifier used clinically

Answer 151

CYP2C9 and CYP3A4 inhibition, which is hard to use clinically without causing drug interactions.

Answer 152

Block LTD4 receptors to prevent mucus secretion, edema, and inflammation. Considered a controller medication for asthma. Also works for aspirin induced asthma (non-atopic asthma).

Answer 153

Directly inhibits lipoxygenase to prevent leukotrienes from being formed in the first place.

Answer 154

Rarely used, inhibits CYP1A2 and CYP3A4. Can cause flu, drowsiness, hepatic elevation

Answer 155

Montelukast

Answer 156

Zileuton Works at source - Prevents leukotrienes from being made by inhibiting LOX.

Answer 157

Asthma attacks induced by NSAIDs and aspirin. Occurs when you block COX from making prostaglandins, it shifts over to the other side forming leukotrienes. Pathway is ramped up and can induce an asthma attack.

Answer 158

You can put them on leukotriene receptor antagonists to prevent symptoms from occurring in the first place. - Montelukast Pt who you wanted on aspirin, you can put on Montelukast as well to help aspirin induced asthma from occurring.

Answer 159

Put them on montelukast, which will "shunt" the path over to COX production, rather than LOX.

Answer 160

Liver Function Decline! | Anorexia, abdominal pain, nausea, jaundice, pruritis

Answer 161

Non specific headache or heartburn, but very well tolerated.

Answer 162

Adjuvant therapy if asthma symptoms aren't controlled by corticosteroids.

Answer 163

Remove trigger and stabilize the mast cells with MCS.

Answer 164

They're for prevention and only block one step of pathway. They aren't that effective, which is why they aren't used as often.

Answer 165

Mast cell stabilizers; an inhalation product. It has to be taken before the insult occurs to be effective against asthma. MOA not known, but prevent Ca from activating mast cells.

Answer 166

The drug takes 4 weeks before you see total efficacy. Tell patient it will take time so they won't discontinue drug.

Answer 167

Bad taste in mouth; well tolerated. Sore throat, stuffy nose, headache, cough... nothing important

Answer 168

Gets used regularly for patients who have significant allergies that are difficult to control and are on other medications. Used for kids with bad asthma at Nemours.

Answer 169

Monoclonal antibody - Used for AI conditions, rheumatology, Crohn's, and colitis. Ex: Omalizumab for asthma.

Answer 170

Targets a specific receptor, so these meds won't have as many side effects since they have one particular target. Less tissue damage, etc.

Answer 171

It is a protein, so any time you inject it into the blood stream, you're at risk for an immune reaction like anaphylaxis. Monitor patient during infusion. Also expensive to produce; used when other treatments are failed.

Answer 172

Subcutaneous injection. | Given every two to four weeks at the clinic.

Answer 173

Specifically targets against IgE.

Answer 174

Requires a Prior Authorixation, because insurance companies won't cover unless you have evidence of documented treatment failures. During administration, you have to monitor the patient for anaphylaxis until you know how they tolerate the treatment.

Answer 175

Secondary malignancy like leukemia may pop up, but is exceedingly rare.

Answer 176

Omalizumab Urticaria Anaphylaxis Injection site pain Bruising They're rare, but concerned about anaphylaxis.

Answer 177

Theophylline and Aminophyline Nonspecific phosphodiesterase inhibitor. Not used frequently, bc they're less effective and less well tolerated. Controller meds LABA and ICS are better.

Answer 178

IV form of Theophylline

Answer 179

Caffeine; same class as Theophyline

Answer 180

Nonspecific phosphodiesterase inhibitor -- Phosphodiesterase is an enzyme responsible for metabolizing cyclic GMP (secondary messenger), which is responsible for relaxation of smooth muscle. In asthma attack, bronchial smooth muscle constricts. So giving this drug will relax that muscle.

Answer 181

More smooth muscle relaxation.

Answer 182

Phosphodiesterase inhibitor.

Answer 183

Viagra. Used bc same enzyme is seen in lungs.

Answer 184

Narrow therapeutic index - therapeutic and toxic blood levels are close together. Need to draw troughs!

Answer 185

Arrhythmia, convulsions, nausea and GI issues. Its an older drug - will see in old women who physician never changed the drug.

Answer 186

IV Theophyline formulation to have extra bronchodilation.

Answer 187

COPD patients

Answer 188

Inhibit phosphodiesterase to have higher cGMP/cAMP to help bronchodilate. Adenosine receptor antagonist Anti-inflammatory reactions

Answer 189

Adenosine - Give to stop heart and reset the rhythm. If you block affects of adenosine, you have the tachy arrythmias. Theophyline can cause this, bc it blocks adenosine.

Answer 190

Seizures occur Theophyline can cause this, bc it blocks adenosine.

Answer 191

GI issues, smooth muscle relax in bronchioles, but also vascular smooth muscle = results in hypotension.

Answer 192

Renally eliminated drug; needs to be adjusted so levels don't get too high or drug can accumulate and get into CNS causing convulsions and sizures. Levels over 20mcg/mL are BAD!!!

Answer 193

5-20 is therapeutic Toxic effects start at 15 - nausea, vomitting, and cardiac effects. 30-40 TOXIC - siezures and arrythmias.

Answer 194

Drug accumulated in the CNS and caused a siezure. Levels over 20mcg/mL become toxic.

Answer 195

Dialyze drug off. CNS levels were so high, she ended up in non-convulsive epilepsy and died. Scary drug, not used frequently

Answer 196

Short acting rescue medications; block effects of muscarinic receptors which cause bronchodilation.

Answer 197

Used in provocative tests that induces an asthma attack.

Answer 198

short acting anticholinergic that lasts for eight hours

Answer 199

Long acting; only used for COPD and lasts 24 hours or more.

Answer 200

Albuterol inhaler Albuterol and ipratropium can be used synergistically to have more oomph into bronchodilation to see how reversible airflow obstruction is. Tells if you need another therapy.

Answer 201

Meter dose inhaler

Answer 202

Dry powder inhaler; comes in a discus where you turn it open and hit a trigger to puncture packet so patient can inhale drug itself. Relies on patient to inhale drug. May not be good for older or younger patients who dont have faculty to inhale.

Answer 203

Comes as a capsule. Capsule goes into inhaler and is punctured for inhalation.

Answer 204

Its not absorbed systemically. TEll patients not to store with normal medications.

Answer 205

CFC based propellent which damaged ozone layers, so they switched to HFA which is a new repellent.

Answer 206

By giving these drugs in lungs, you're less likely to see systemic effects. Midriasis, blurry vision, hallucinations, delirium, memory loss, psychosis, flushing, fever, hyperthermia, dry mouth/eyes, urinary retention, constipation, tachycardia, and hypertension.

Answer 207

Midriasis, blurry vision, hallucinations, delirium, memory loss, psychosis, flushing, fever, hyperthermia, dry mouth/eyes, urinary retention, constipation, tachycardia, and hypertension.

Answer 208

An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and the peripheral nervous system. Nicotinic receptors - skeletal muscle and nerve conduction through CNS. Muscarinic receptors - tissues.

Answer 209

Use short courses of systemic corticosteroids to decrease the inflammation occurring. Helps suppress and reverse the airway.

Answer 210

Systemic effect; take time to work, but work more quickly than ICS, bc they're more potent. This is why only used for exacerbations and short period of time.

Answer 211

Predinisone (oral tablet) Prednisolone (oral liquid) Methylprednisone (oral or parenteral IV, IM) Dexamethosone (Oral or parenteral IV, IM).

Answer 212

Adrenal suppression - exogenous steroids lower their secretions; start to shut down. If dose is less than a week, you don't need to taper it off. However, if dosed for longer, you must taper off so the adrenal glands start working again. Effects seen more with chronic dosing; not short-course therapy. IMMUNOSUPRESSION - leads to secondary infections. Growth supression Dermal thinning Hypertension Muscle weakness

Answer 213

Send them home with 5 days of corticosteroids. Stop at the end, no taper needed. Dose is less than a week, which is why no taper dosing is needed.

Answer 214

Need to taper off this dose to prevent the withdrawal that leads to adrenal insufficiency.

Answer 215

SABA PRN Exercise induced bronchospasm. They have a known trigger, so use beforehand to prevent from occurring.

Answer 216

More symptoms, want to add a controller therapy - ICS.

Answer 217

Can add LABA or increase ICS.

Answer 218

Med dose ICS and LABA

Answer 219

High dose ICS and LABA May add omaxilizumab. Keep journal of symptoms and nighttime awakenings.

Answer 220

Open tube that extends inhaler away from patients mouth

Answer 221

have a one way valve that do not allow patient to exhale into the device

Answer 222

Aerosolizes drug. Compressor with tubing, put drug into a cup, turn on compressor and the air will cause the aerosolization of albuterol to occur.

Answer 223

In six month old, putting a mask with nebulizer is easy, because they're passively breathing it in. Downside: more medicine is absorbed, which causes more systemic side effects.

Answer 224

2 puffs = 180mcg of albuterol Neb: inhale for 15 mins = 2.5 to 5 mg Inhale more, so you get jittery, increased HR, potassium shift inwards. Benefit: helps noncompliant patient get doses in.

Answer 225

Help patient get the dose in. Particle size is important. If its too big, you end up swallowing it. If its too small, you can exhale it. "Goldy Lock's" size to get to lungs where it will work.

Answer 226

Spacers and valve holding chambers; removes needs for coordinated activity. Drug is held in chamber and patient can breathe it in more controlled (if you go too fast, it whistles).

Answer 227

Equal efficacy, no additional toxicity with MDI.

Answer 228

Take cap off and shake inhaler to "prime" it (takes 3-4 puffs). Breathe it all out, when you start to inhale actuate inhaler so you have the best airflow down to lungs for drug to go. Hold for 10s and breathe out as normal.

Answer 229

Don't use multiple puffs in succession, bc puff needs time to work ~30 seconds First dose opens up smooth muscle of bronchioles, so second dose can penetrate even deeper.

Answer 230

rinse mouth and spit | avoids thrush

Answer 231

Chronic damage being done to lungs over time; effects aren't completely reversible like they are with asthma. Accelerated decline in FEV1 over time. Can be asymptomatic for long period of time as lungs start declining. More symptoms will appear as it progresses (graph). When not airing, need transplant.

Answer 232

smoking alpha 1 antitrypsin deficiency pollution

Answer 233

For rescue inhaler, start with b2 agonist to relieve acute symptoms.

Answer 234

Long acting cholinergic or beta agonist. Spireva.

Answer 235

Increased mortality rate; you need an ICS to start and then add a LABA.

Answer 236

Consider combination therapy. May add theophyline or ICS added. Asthma corticosteroids are initiated more early on than in COPD patients.

Answer 237

oxygen therapy

Answer 238

Nicotine is addictive; drugs used will try to replicate components, such as the dopamine pathway or nicotinic receptors itself. When people cut off nicotine cold turkey, they have withdrawals and lowered receptors. This is why we need drugs to stimulate during process.

Answer 239

Buproprion (Zyban) Nicotine transdermal (Patch) nicotine polacrilex (Gum) nicotine spray or inhaler Vareniciline (Chantix) Nitroglycerin tablets - sublingual.

Answer 240

Sustained release; long-acting drug. Stimulates "reward" pathway in the brain, dopamine, to decrease withdrawal effects of smoking.

Answer 241

Nicotine indirectly activates epinephrine and dopamine in CNS. Bupropion micmics these effects because it inhibits the uptake of norepinephrine and dopamine; increasing dopamine helps bc nicotine isn't stimulating the pathway anymore.

Answer 242

Used for weight loss.

Answer 243

Patients with seizure disorder - run risk of seizure threshold being decreased and causing seizures. Don't want them on other drugs that increase norephineprine; no monoamine oxidase inhibitors (MAOIs) or tricyclic antidepressant (TCA). Its an antidepressant, so it can interact with antidepressants - usually work by seratonin reuptake inhibitors.

Answer 244

7 to 12 weeks

Answer 245

Taper the nicotine dose, which is healthy since they're not inhaling tar or other carcinogens. Nicotine is activating receptor, so do not want smoking on top of this or increases risk of toxicity!

Answer 246

Make sure patient removes old patch before putting a new one on; don't want to experience toxicity. Leave on for 12 hours and then take off.

Answer 247

Cardio patients, bc it may cause tachyarrythmia or hypertension. Will affect antihypertensives

Answer 248

Newest drug Partial nicotine receptor agonist; it binds to receptor and activates, but not to the same degree (partial). If you smoke while on drug, it binds more tightly than nicotine and prevents it from activating. Can smoke on this drug and taper off to just this drug.

Answer 249

Vivid dreams, nausea, sleep disturbance Black box warning for neuropsychiatric events, like depression and SI. If your patient has a history of that, this isn't a good drug for them.

Answer 250

Annual influenza - if they get flu, they'd get a bad bacterial superinfection. Pneumococcal vaccine - more at risk for pneumococcal infections. Want to avoid.

Answer 251

START OF CARDIOLOGY CARDS

Answer 252

Bacterial infection on lining of heart or valve itself. Colonies of bacteria like to settle on valve.

Answer 253

Older patients > 60 yrs, male patients, IVDA, those with poor dental hygiene which leads to hematogenous spread, and valvular heart disease. If you can't treat with antibiotics, you need a valve replacement.

Answer 254

A thrombus is formed on an abnormal endothelial surface, where vegetation can start. Bacteria in blood colonizes here and starts proliferating.

Answer 255

Difficult to penetrate through and get a full kill of all the bacteria. This is a concentrated core of bacteria to penetrate. 6-12 weeks of treatment

Answer 256

Mainly gram positives! S aureus Enterococci HACEK Gram negatives in immunocompromised

Answer 257

``` Haemophilus aphrophilus Actinobacillus actinomycetemcomitans Cardiobacaterium hominis Eikennella corrodens Kingella kingae ``` They live in the mouth. Common bugs of endocarditis.

Answer 258

Therapy needs to be geared towards culture since you're treating for several weeks. Start with empiric coverage and then you scale down.

Answer 259

MRSA, MSSA, Streptococci, and Enterococci Prefer bactericidal abx - leads to a better kill and gets rid of vegetation.

Answer 260

Vancomycin Good gram positive and MRSA. Tx may be needed for six weeks or longer.

Answer 261

They're PCN susceptible, so use PCN G 4-6x a day or a 24hr infusion to make sure you're above MIC. Alternatives: Ceftriaxone, Vancomycin (if can't recieve cephalosporin or PCN), and Gentamycin.

Answer 262

Gram positive synergy - one of the few cases an aminoglycoside is used to kill gram positives. Giving a cell wall killer like PCN or ceftriaxone loosens up the cell wall so Gentamycin can get in to inhibit protein synthesis at ribosome.

Answer 263

Inhibits protein synthesis at the ribosome. Bactericidal. Normally used for gram negatives.

Answer 264

It can shorten the therapy time in half and be very cost effective.

Answer 265

Don't want to accumulate too much drug because of renal toxicity and otoxicity.

Answer 266

Mostly PCN sensitive. Have to follow cultures. If susceptible to ceftriaxone and not PCN, treat with ceftriaxone.

Answer 267

Use synergy combination of gentamicin PLUS penicillin, ampicillin, or vancomycin. Generally resistant to PCN.

Answer 268

MSSA is treated by nafcillin, oxacillin, cefazoline +/- gentamicin. MRSA is treated with vanco.

Answer 269

nafcillin oxacillin dicloxacillin

Answer 270

Treated by ceftriaxone, ampicillin-sulbactam, or ciprofloxacin.

Answer 271

They inject particulate matter which can damage tricuspid valve, introduce skin flora, and use of saliva.

Answer 272

S aureus for more than half the cases. Followed by streptococci, enterococci, fungi and gram negatives.

Answer 273

Vanco for empiric coverage

Answer 274

Antibiotics may fail because they can't penetrate "foreign body". Often requires surgery, esp MRSA

Answer 275

Triple drug regimen - targets staphylococcus! Vancomycin Gentamicin Rifampin - add it as the last agent to avoid resistance

Answer 276

orange-red tears, urine, feces, sweat

Answer 277

It has a unique ability to kill staph that adheres to foreign material.

Answer 278

Add it as the last agent in the three drug regimen. If you use it first, resistance develops more quickly.

Answer 279

Inhibits bacterial RNA polymerase by blocking RNA transcription.

Answer 280

tuberculosis

Answer 281

It induces CYP enzymes like 3A4 so you see decreased level of other drugs. CYP3A4 is responsible for metabolism of half of all drugs.

Answer 282

By giving prophylaxis abx prior to bacteremia, you can prevent it from starting off in first place.

Answer 283

Prophylaxis beforehand, especially before dental procedures. Broncoscopy, tonsillectomy, etc. Mouth can spread into the blood stream.

Answer 284

30-60 mins prior to procedure Amoxicillin PO If PCN allergy, use cephalexin, clindamycin, azithromycin.

Answer 285

Prosthetic Heart Valves

Answer 286

Nonsuppurative complication of pharyngeal infection. Occurs 2-3 weeks following pharyngitis. Causes arthritis, carditis, nodules, erythema marginatum.

Answer 287

Group A streptococcus

Answer 288

Antibiotic therapy HF management Anti-inflammatory therapy

Answer 289

Amoxicillin and PCN Eliminate Group A Strep carriage

Answer 290

Aspirin to help deal with anti-inflammatory effect. Helps relieve symptoms. Treat CHF Valve surgery

Answer 291

Continue aspirin until symptoms are resolved. If it doesn't work, you can use glucocorticoids to manage inflammation, i.e. prednisone.

Answer 292

100g triglycerides a day | 250mg of cholestrol

Answer 293

Triglycerides and cholesterol are incorporated into chylomicrons. When chylomicrons are metabolized, the ratio of triglycerides and cholestrol change as we go along.

Answer 294

Emulsified by bile acids; the bile salts are sent to biliary tract, which contains cholesterol as well. Can reabsorb cholesterol in biliary tract. Cholesterol is absorbed into GI tract and then hits the liver first. Drugs work at second site to prevent reabsorption.

Answer 295

Hydrolyzes triglycerides in the core of the chylomicron. As time goes on, triglycerides go down as they're being converted to cholesterol.

Answer 296

A big portion of triglycerides, but as metabolism continues, you have higher cholesterol. LDL and HDL come from chylomicrons.

Answer 297

Synthesize cell membranes, hormone synthesis, and are disposed as bile salts.

Answer 298

When things are kicked out of biliary tract and reabsorbed through GI tract. Birth control, antiepileptics, and other drugs do this to increase their half life.

Answer 299

Carbohydrates and fatty acids

Answer 300

VLDL - higher portion of cholesterol, but made of triglycerides As metabolism goes on, TG is converted to cholesterol esters. - lipoprotein - lipase

Answer 301

Bad cholestrol, lead to artheriosclerosis and plaque formation.

Answer 302

LDL receptor, found in liver. How we metabolize and get rid of LDL. More LDL receptors in liver, the more that is cleared from blood stream, which is good.

Answer 303

Protein on surface of LDL that interacts with the receptor. Important for catabolism of LDL.

Answer 304

Main focus for medications. Have a half life of 1-2 days. ApoB interacts with LDL. Patients might not express LDL receptor or ApoB, which leads to high cholestrol since they can't metabolize it.

Answer 305

Liver gets saturated, LDL receptors down regulate or less expressed. Lower LDL receptors leads to atherosclerosis. Will start making plaques in arteries.

Answer 306

Take LDL into liver to make amino acids, bile salts, and recycles the receptor to put on surface of hepatocyte to take another LDL.

Answer 307

There's enough choleserol so you don't want to metabolize anymore. If you decrease the LDL in liver, you'll put out more LDL receptors to metabolize. Too high LDL in liver, you express less receptors.

Answer 308

Heterozygous familial hypercholesteremia - has half the normal number of LDL receptors. Cholesterol is twice the normal amount. Homozygous familial hypercholesteremia - No functional LDL receptors. Can be as high as 1000mg/dL.

Answer 309

60-70 LDL 20-30 HDL 10-15 VLDL

Answer 310

Main go to drug for dyslipidemia. Used for cardiovascular protection.

Answer 311

inhibits absorption of cholesterol

Answer 312

HMG-CoA reductase inhibitors

Answer 313

HMG-CoA reductase inhibitors HMG-CoA reductase produces cholesterol. By blocking it, we lower LDL in hte liver. Less cholesterol in the hepatocyte causes a response where more LDL receptors are expressed to metabolize the serum LDL. Decreased serum VLDL and IDL -- Done by increasing number of receptors so more can be taken out of blood stream.

Answer 314

Outside of its main use, it has pleiotropic effects which are positive and don't relate to main mechanism. You have stabilization of plaques, which have good effects on mortality and cardiovascular death. Frequently recommended for patients with Cardiovascular Disease - Need to be on a statin unless theres a contraindication.

Answer 315

Major enzymes: CYP3A4 - statins are metabolized by it. If you inhibit CYP3A4 via FQ or macrolide, you'll see high levels of statins and can lead to toxicity.

Answer 316

Macrolides inhibit CYP3A4, which lead to higher drug levels of statins in blood stream. Patients on FQ and macrolides should be on Resuvostatin or Pitavastatin to avoid toxicity with CYP inhibition.

Answer 317

Using combination therapy is good because synergism lead to better affects than drugs being used by themselves. Ex: Statin lowers LDL but is prescribed with resin.

Answer 318

The higher Triglyceride levels in blood, the better effect statins have on it.

Answer 319

START OF CARDIOLOGY 2 CARDS

Answer 320

Inhibit cholesterol formation in the liver , so you produce less cholesterol in the liver. Makes hepatocytes form more LDL receptors to take it out of the blood and process through liver. Serum lipids go down. Also have other pleiotropic effects - stabilization of plaques and prevent other cardio events.

Answer 321

Headache, fatigue, GI intolerance Increase in liver enzymes (AST and ALT can rise). Usually dose dependent. Increase dose increases risk for toxicity.

Answer 322

Reduce the dose or switch to a different agent. Rare to see liver problems by itself.

Answer 323

LFT. Beginning of therapy and a month or two after to see how they tolerate the drug.

Answer 324

Myalgias and myopathies; rare cases of rhabdomyolysis occur as well. Muscle pain is a common side effect. When dosing based on cardio risk, try to run up as high as you can until patient can't tolerate it anymore.

Answer 325

Muscles are broken down; kidneys take a hit, because myoglobin goes into the blood and causes interstitial damage to their kidneys.

Answer 326

Give them fluids to dilute the myoglobin to help the kidney.

Answer 327

Sign of rhabdo, urine is ice tea colored.

Answer 328

Decrease dose and do the best one they can tolerate. Avoid drug interactions.

Answer 329

Be very careful when prescribing statins and Gemfibrozil together, because it can lead to increase in statins and toxicity. Or when you do prescribe them togetehr, lower the dose of the statin.

Answer 330

Resuvostatin or Pitavastatin are not metabolized by CYP3A4.

Answer 331

Inhibit enzyme and metabolism, so less drug is metabolized, which increases risk for toxicity. Be cautious of it.

Answer 332

Hepatic disease Pregnancy - baby needs lipids to make cell membranes. Teratogenic.

Answer 333

Relative CI - you can get away with adjusting the dose. Gemifibrozil, niacin, and erythromycin ---- all will increase level of statins.

Answer 334

Rosuvastatin | Potavastatin

Answer 335

``` Verapimil Amiodarone Niacin Fibric acid derivatives (Gemifibrozil) Grapefruit Juice ```

Answer 336

Its an efflux transporter; things abosrbed from GI tract and this is responsible for kicking things back out. Inhibited by grapefruit juice as well. Inhibition of this can cause increase in drug levels.

Answer 337

Brain wants to keep toxins out, so PGP can help.

Answer 338

First line drug for hyperlipidemia, most efficacious. Not given to those who are pregnant or have hepatic disease.

Answer 339

Decrease the amount of absorption from cholesterol from your diet. By decreasing amount of cholesterol absorbed, liver doesn't think it has enough cholesterol. Starts producing more LDL receptors on the surface to absorb more cholesterol and LDL from the blood.

Answer 340

Statins are more potent and efficacious.

Answer 341

Ezetimibe can be used in combination with statins - synergistic. Statins work on directly producing cholesterol in the liver and Ezetimibe protects you from absorbing cholesterol from your diet.

Answer 342

Decreases cholesterol absorbed in diet. Less cholesterol is absorbed in the liver so the liver puts out more LDL receptors to lower levels.

Answer 343

Drugs that undergoes eneterohepatic reabsorption. -- Absorbed in GI, spit out through biliary tract, and reabsorbed = gives it a longer half life.

Answer 344

No CYP interactions

Answer 345

You can have an additional LDL reduction by 15-20% when adding a statin. Only have to take it once a day. Enterohepatic circulation prolongs half-life.

Answer 346

Enterohepatic circulation limits the systemic effects, may see GI upset, but minimal as far as side effects go. May also see elevation in hepatic transaminases when used with statins!

Answer 347

Shouldn't be used in breast feeding, pregnancy, children, hepatic disease, myopathy. When combined with a statin, you may see myopathy and hepatic disease.

Answer 348

Fibric acid derivatives - increases risk of cholelithiasis and myopathies. Bile Acid Sequestrants - work only in GI tract, so they can bind to this med and decrease the concentration. Antacids decrease concentration and cyclosporine increases concentrations.

Answer 349

Gemfibrozil (Lopid) Fenofibrate (Tricor) Bezafibrate (Bezalip)

Answer 350

Activate PPAR-alpha (nuclear transcription factor), which increases fatty acid oxidation. Leads to less secretion of triglycerides, which means less VLDL is produced and decrease LDL on cell surface (VLDL is precursor). Can see increase in HDL which is protective cholesterol.

Answer 351

Fenofibrate is metabolized by minor pathway in CYP3A4

Answer 352

Once daily medications lead to greater compliance. -- Fenofibrate or Bezafibrate.

Answer 353

When you have ingestion of dietary fats, you produce the most cholesterol. This oxidation of fatty acids lead to less triglycerides being released. Not as big of an effect as statin, but HDL increases and triglycerides decrease.

Answer 354

Nausea, abdominal pain, diarrhea. BIG RISK - Cholelithiasis, can affect movement of bile acids. By inhibiting that movement, you can have gallstones. Myopathy is also a risk. Can have synergistic effects with statins.

Answer 355

Pregnancy Hepatic or renal dysfunction Galbladder disease Adjust dose based on renal dysfunction.

Answer 356

Warfarin - see increased anticoagulant effects, could be related to protein binding interaction. Warfarin binds to albumin. If a fibrate drug is used, it will bind to albumin more tightly and plasma concentrations of warfarin will increase. More drug is available, so increase risks for bleeding.

Answer 357

With gimfibrozil, will see reactions that increase levels of statins, increasing risk for toxicity. See it in most fibrates, but highest effect in gimfibrozil. Decrease the statin by half.

Answer 358

Primary hypertriglyceridemia TG>1000mg/dL or low HDL. Can add it to increase those levels.

Answer 359

Resins. They work in the bile tract and are not systemically absorbed, which is why you can give them to children and pregnant patients :)

Answer 360

By binding cholesterol and bile salts, they're bound by resins and will be excreted in the feces. You absorb less cholesterol from diet and spit out diet tract to prevent that from being absorbed.. Increases LDL receptors to decrease cholesterol in the blood. Not as effective as statins, but are nice bc they're not absorbed systemically.

Answer 361

Cholesterol excreted in feces can lead to GI effects.

Answer 362

Children and pregnant patients! Children and pregnant women love resins

Answer 363

Cholestryamine Colestipol HCl Colesevelam Not absorbed, but bind cholesterol in GI tract to prevent them from being absorbed.

Answer 364

Most products come as tablets; these come as bulky powders or tablets. Patient may not tolerate as well, bc of the pulpy taste. Can mix with orange juice to mask flavor. There's a "plateau effect" where if you increase dose you get more ADR instead of efficacy from this.

Answer 365

That's when you have most fat in GI tract. Galbladder is actively secreting bile salts to help emulsify. Should give more bang for your buck.

Answer 366

They can bind to other medications. Can give a drug one hour before or two to four hours after to make sure the reaction doesn't cause binding.

Answer 367

bloating, flatulence, fullness, constipation, nausea.

Answer 368

Less absorption of water soluble vitamins -- ADEK and folic acid. Bile salts normally help emulsify these for absorption. Avoid this by separating medication times to one hour before or four hours after taking BAS.

Answer 369

digoxin, warfarin, thyroxine, beta blockers, and thiazide diuertics

Answer 370

avoid interaction by adminstering one hour before or four hours after bile acid sequestrant.

Answer 371

High levels of triglycerides (can make it worse) and familial dysbetalipoproteinemia.

Answer 372

Safest drug, because no systemic side effects. Good for pregnant patient and children. Poorly tolerated from GI standpoint. Can use with antilypemics as well since they have a differnt mechanism of action.

Answer 373

B complex vitamin; another derivative is nicotinic acid. Used an an antilipemic. Amide form is a niacinamide. Can cause flushing.

Answer 374

Less likely to cause side effects and hot flashes.

Answer 375

Immediate release Niacin supplment and Niacor Long acting Niacin Supplement Extended release Niaspan Inositolhexiancinate

Answer 376

Not well regulated by FDA.

Answer 377

Decreases free fatty acids released from the adipose tissue; will also see changes in synthesis of triglyercides which happen in liver. Less VLDL released = less LDL being produced, which lowers cholesterol in the blood. RECAP: Less triglycerides are getting in liver, less VLDL produced, more LDL receptors to clear LDL. Will see an increase in HDL.

Answer 378

Will see an increase in HDL. Extended release has more moderate side effects.

Answer 379

Its more tolerable to patients, i.e. less flushing

Answer 380

Tmax = 30 to 60 mins

Answer 381

How long it takes to get to highest concentration.

Answer 382

Longer duration of action so they're given less frequently.

Answer 383

Cutaneous flushing Nausea Abdominal discomfort Larger doses - increased LFTs, glucose, uric acid (bad for diabetics and gout), decreased glucose tolerance.

Answer 384

Too much prostanglandins production

Answer 385

Aspirin, because it prevents production of prostaglandins by inhibiting COX Also, ibuprofen.

Answer 386

Take aspirin or ibuprofen before to decrease production of prostaglandins beforehand. Or take extended release.

Answer 387

Increase in uric acid and decreased glucose tolerance. => Insulin produced isn't effective, so glucose goes up. Mitigated by extended release product.

Answer 388

Liver disease Symptomatic gout Type 2 diabetes Peptic ulcer disease (can get aggravated by it).

Answer 389

Statins - see mild increase in statin concentration, same thing with bile acid sequestrants (BAS increased). ETOH - can lead to increased flushing if you take with niacin bc acetaldehyde. Other herbal supplements can inhibit metabolism of it: kava-kava, germander, pennyroyal, comfrey, chaparral.

Answer 390

Other herbal supplements can inhibit metabolism of it: kava-kava, germander, pennyroyal, comfrey, chaparral.

Answer 391

Good for atherogenic dyslipidemia. Useful to lower LDL and increase HDL.

Answer 392

Lovastatin/Niaspan (Advicor) Reduces LDL, increaes HDL. Good effects on triglycerides.

Answer 393

hepatotoxicity, myopathy, and flushing

Answer 394

Statins | Resins can a little, but limited by side effects.

Answer 395

Niacin and fibrates

Answer 396

fibrates and nicotinic acids

Answer 397

Resins; don't give to those who already have high triglycerides.

Answer 398

LDL less than 100. HDL to be high, bc protective of cardio disease. TC less than 200 TG less than 150

Answer 399

treat blood choelsterol to reduce atherosclerotic cardio risk in adults, which is leadin cause of death and disability in US.

Answer 400

Statins can be moderate intensity or high intensity. Based on cardiovascular risk.

Answer 401

Individuals with ASCVD- stent placement, angina patients Individuals with LDL > 190 which means you are at risk for developing plaques and CAD Individuals with diabetes, 40 - 75 years old, that have LDL 70-189. Patients LDL 70-189 and estimated risk of ASCVD.

Answer 402

Moderate to high intensity statin

Answer 403

High intensity statins. They're at a big risk for developing more ASCVD.

Answer 404

Moderate intensity, bc they're older and at higher risk for toxicity.

Answer 405

High intensity statins

Answer 406

Gender, age, race, cholesterol, systolic BP, diabetes, smokers If over 7.5%, you get put on statins.

Answer 407

Atorvastatin and rasuvastatin; dosed to how well patient can tolerate it.

Answer 408

Decrease the dose.

Answer 409

Too much = volume overload and pulmonary edema. Too little = volume depletion and cardiovascular collapse.

Answer 410

Kidneys receive 22% of cardiac output and regulate BP in the body. If there's not enough pressure, they try to get more pressure going into them. Drop in BP will decrease ANP, increase ADH to counteract the drop, and increase BP. Can lead to renal cell hypertrophy.

Answer 411

Vasodilated - more blood can flow.

Answer 412

Prostaglandins

Answer 413

Decreases production of prostaglandins, so the afferent arteriole will have a smaller diameter. Less blood can get to the glomerulus.

Answer 414

Angiotensin 2!! Squeezes efferent arterioles, increases pressure on glomerulus, and causes more filtration to occur.

Answer 415

Reflexively decide to increase angiotensin 2 and prostaglandins. This dilates afferent arteriole and squeezes efferent arteriole to get as much blood to the kidneys as possible.

Answer 416

Where blood enters kidney and is filtered to proximal convoluted tubule.... to loop of henle, distal convoluted tubule, and collecting duct out to the urinary tract.

Answer 417

150-180 L filtered a day | 1 - 2 L excreted

Answer 418

First sight hit after glomerulus where 60-70% of filtrate is reabsorbed. There's reabsorption of glucose, organic solutes, and amino acids.

Answer 419

There will be more water in the nephron (following electrolyte concentration) and more fluid will be excreted.

Answer 420

Reabsorbs sodium. Site where loop diuretics work! Sodium is reabsorbed in ascending loop and is impermeable to water. Descending loop, water will leave to follow the sodium that was leeched out.

Answer 421

Na is reabsorbed here; site of thiazide diuretics.

Answer 422

Water movement is modified by aldosterone and antidiuretic hormone in collecting duct. Site of potassium sparing diuretics.

Answer 423

Helps absorb more water. ANTI diuretic. Gets turned off when drinking alcohol.

Answer 424

Work by inhibiting Na-2Cl-K carrier on the membrane in lumenal membrane of the thick Ascending Loop of Henle Inhibiting this transporter causes Na, Cl, and K to remain in lumen of renal tubule. Water flows and is excreted with them.

Answer 425

Furosemide Bumetanide Torsemide Ethacrynic acid -IDE

Answer 426

Furosemide

Answer 427

Bumetanide and Torsemide Dosage is less, bc they're more potent.

Answer 428

Concentration you have to achieve to inhibit 50% of transporters.

Answer 429

Ethacrynic acid. Furosemide and Bumetanide have sulfa moiety's in molecules.

Answer 430

By inhibiting transporter, you have more sodium, potassium, and chloride on lumenal side. More water flows in that direction to be excreted. This can lower sodium, chloride, and potassium concentrations! Its important for patients on high-dose loop diuretics to look at potassium because they're excreting a lot of it.

Answer 431

Inhibiting the transporter, a lot of sodium, potassium, and chloride are excreted. Levels can become dangerously low.

Answer 432

Inhibit sodium chloride reabsorption by 20-25%, so can see big increases in urine output 4L a day. Also will see potassium, calcium, and magnesium excreted.

Answer 433

By losing more electrolytes, like potassium and magnesium, they're more prone to having arrythmias. Be aware of electrolyte shifts by giving these drugs.

Answer 434

The resulting hypokalemia can impair insulin release leading to high blood glucose levels (hyperglycemia). Because you're decreasing the pressure in the kidneys from diuretic, it activates SNS; releasing NE and dopamine. Catelcholamines: Activate a2 receptors = decrease insulin release. Activates B2 = increases glycogenolysis to produce more glucose. Leads to liver producing more glucose and see hyperglycemia from these drugs. Can worsen diabetes.

Answer 435

Hypokalemia (low K) impairs insulin release, which leads to high glucose levels and activation of A2, which further decreases insulin release and B2 which increases glycogenolysis. Leads to very high sugars and worsens diabetes.

Answer 436

Reflexive systemic vasodilation -- Prostaglandins will open up the afferent arteriole and have a direct relaxant effect on muscles. Opening up the smooth muscle and allowing more volume to hit the glomerulus.

Answer 437

It tries to counteract the drop in BP - Increase in the renin angiotensin system, aldosterone secretion, and ADH hormone. Kidneys say too much volume is lost, so trying to keep as much as they can. Reflex mechanisms like this can lead to medications being less effective.

Answer 438

If you give these chronically - Patient can have same dose of loop diuretic, which can be good in the beginning, but drop off over time and become a closer to normal output.

Answer 439

Put patient on loop diuretic and an ace inhibitor.

Answer 440

Increases in uric acid levels occur, because of fluid loss creates a more concentrated build up in plasma uric acid levels. By decreasing fluid volume, everything gets more concentrated to some degree. Increased risk for precipitating out.

Answer 441

Contraction metabolic alkalosis. Volume depletion leads to an increase in bicarbonate reabsorption, which is alkalosis response. You also excrete more hydrogen ions, contributing to this.

Answer 442

Mild increase in lipids; bad for patients who have uncontrolled lipids already.

Answer 443

Loop diuretics remain effective in patients with poor creatinine clearance and poor renal function ~ Even if 5ml/min. End stage renal disease, can still have increases in urine output with a loop diuretic. May not be true with other diuretics.

Answer 444

Used to manage fluid overload in pulmonary edema, nephrotic syndrome, ascites, hypercalcemia, renal failure, and heart failure. NOT used by itself to manage hypertension. If HTN pt is on loop diuretic, usually for something else.

Answer 445

Bodies tries to compensate and raises blood pressure when dosed chronically.

Answer 446

They have protein loss and can't regulate plasma fluid volume, which leads to fluid overload.

Answer 447

By blocking channel, you lose more calcium, causing you to go back to a normal level.

Answer 448

1. Volume depletion - reflex mechanism associated to keep volumes up. 2. Hypokalemia leads to cardiac arrythmias. 3. Hyperglycemia - diabetogenic effects. 4. Contraction alkalosis may occur. 5. Hyperuricemia can exacerbate gout. 6. Ototoxicity damages hair cells in cochlea. Occurs in high doses and other ototoxic meds, like vanco and aminoglycosides. 7. Hyponatremia leads to seizures. 8. Allergic reactions (Sulfa allergies to all except E. acid). 9. Azotemic due to increase in BUN (and uric acid). Azotemia is an increase in nitrogen containing elements in the blood.

Answer 449

These drugs can synergistically cause ototoxicity. Vanco, aminoglycosides, and loop diuretics.

Answer 450

NSAIDs - will oppose prostaglandin synthesis and blunt the diuretic response. Warfarin protein binding interactions - more warfarin in the blood will have increased anticoagulation. Lithium - body will want to retain sodium (lithium looks like sodium), and it will retain lithium as well. Can see increased levels in the blood = toxicity. Digitalis (antiarrythmic) - have increased risk for arrythmias when electrolytes are manipulated (K and Mg).

Answer 451

Chlorothiazide Hydrochlorothiazide (HCTZ) -THIAZIDE

Answer 452

Chlorthalidone Metolazone Indapamide Have some calcium channel blocking activity, but less elevation in lipids, less hypokalemia, and less hyperglycemia.

Answer 453

Haven't seen used clinically

Answer 454

Interesting, because, as a class, thiazide diuretics lose activity when Cr clearance is below 30ml/min. Loop diuretics stay active no matter what. Thiazides lose their activity when under 30ml/min or less, except for Metolazone, which still remains active.

Answer 455

You decrease sodium reabsorbed in ascending Loop of Henle, but there's an increased amount absorbed in distal convoluted tubule later on. DCT increases it, which is a blunting from loop diuretics.

Answer 456

By giving a thiazide with a loop diuretic you can overcome resistance and prevent DCT from reabsorbing as much.

Answer 457

Thiazide - Metozolone is usually used for that. Metolozone can make a rock pee!

Answer 458

The distal convoluted tubule to inhibit sodium and chloride reabsoprtion.

Answer 459

Instead of working on Na-2Cl-K channel like loop diuretics, it specifically works on a NaCl channel to inhibit reabsorption. Want it excreted. Not as potent as a loop diuretic.

Answer 460

Increased NaCl excretion (not as potent as a loop diuretic.), but has increase in fluid output. Will also see a lot of K and Mg being released. Has decreased calcium excretion, which causes it to be reabsorbed in the blood by PCT and DCT. More Calcium is reabsorbed in blood! IMPORTANT. Hyperglycemia Increases in uric acid levels, acutely. Decreased GFR - seen acutely with fluid loss, but chronically they adapt to maintain GFR.

Answer 461

Patients with kidney stones have kidneys precipitating calcium out in nephrons. By increasing reabsorption of Ca, it could have more in the blood and less in the urine - prevents stones from being formed in the first place!

Answer 462

Primarily used for HTN and for hypercalcemia (renal calcium stones). May also be used with other loop diuretics, etc. to get fluid off the body for renal failure, ascites, and CHF.

Answer 463

Elderly, obese, african americans, and those in Na retentive state. Work best in patients who are SALT SENSITIVE hypertensives - have a decreased ability to manage sodium in the body. Sodium can get stuck in interstitium of vessels causing "water logged" blood vessels. They can't dilate as well, so they have HTN.

Answer 464

Acutely, there's an increase in urine output, which causes a decrease in volume and cardiac output. The body uses Ang 2 to increase total peripheral resistance to squeeze down, but BP still drops. Over time, volume and CO will go back to normal, but BP will stay low because vessels are no longer water logged. :) Decreased wall thickness, increased diameter for flow , and decreasing response for vasopressors cause BP to go back to normal.

Answer 465

Acute - Start of thiazide diuretic decreases plasma volume and cardiac output immediately, from increased urine output. Body response by increasing total peripheral resistance, because you have less volume and want to maintain the same pressure so "squeeze down". Chronically -Want to increase cardiac output and plasma volume. Plasma goes back to normal and CO will increase. Systolic and diastolic may go down because there's decreased water logging effect. Chronically why these work better than loop diuretics. In loop diuretics, PV decreases, but they produce more ADH and it goes back to normal.

Answer 466

``` Hyperglycemia - Increases in glucose due to a decrease in insulin release. Hypokalemia Metabolic alkalosis Hyperuricemia hypercalcemia hyperlipidemia photosensitivity ```

Answer 467

More prone because body can't regulate hemodynamics as well. Sitting to standing, their blood pressure isn't as elastic to clamp down and maintain blood flow to the head.

Answer 468

When you give them an antihypertensive, it exacerbates further. Can see changes in mental status, dizziness, headaches. Dose at night time so they can sleep through that.

Answer 469

Do NOT have sulfa in them, so no allergies like you have with loop diuretics. Loop diuretics - all have sulfa, except for Ethacrynic acid.

Answer 470

Sexual dysfunction Constipation Thiazides are only effective above 30-40ml/min Cr clearance, but metolazone is a thiazide diuretic effective at lower clearance rates!

Answer 471

NSAIDs block PGs and blunt the effects of thiazide diuretics. Increase digitalis toxicity due to potassium excretion; the body wants to hold onto digoxin.

Answer 472

With loop diuretics, you can increase the dose and keep having more urine output. Ex: Start a patient on IV furosemide and you can drive dose up high. Thiazides, you hit a ceiling. HCTZ may only be 15-25mg; above that you don't see more increase on BP. You just see more ADR.

Answer 473

Low dose thiazides are preferred for hypertension, bc there will be fewer ADR.

Answer 474

Volume depletion leads to increase in Renin and Angiotensin 2, also increase ADH secretion and sodium/water reabsorption. Chronically, leads to decrease in BP especially in salt sensitive patients.

Answer 475

Work in the collecting duct. Can work to decrease aldosterone or decrease water channels, to have less water reabsorbed into the lumen.

Answer 476

Work by blocking luminal Na channels, inhibit Na Ca antiporters, and inhibit Na H ion antiporters. By blocking water channels in collecting duct, water can't be reabsorbed, so it is secreted. Has more sodium in lumen, so more urine outflow happens.

Answer 477

Potassium sparing diuretics are less potent than thiazide diuretics, so are given to patients on other therapies, but are used because they secrete less potassium. Raises potassium levels in the blood.

Answer 478

Amiloride (Midamor) Triamterene (Dyrenium) Frequently seen in combination with hydrochlorothiazide.

Answer 479

Same as others, just less potent - HTN, renal failure, CHF, ascites, edema. Frequently used with other antihypertensives

Answer 480

Hyperkalemia - Can be affected by ACE inhibitors and angiotensin blockers; also caution with potassium supplements, too high potassium can lead to arrythmias. Diabetics may have glucose intolerance.

Answer 481

Can have megaloblastic anemia.

Answer 482

Azotemia - medical condition characterized by abnormally high levels of nitrogen-containing compounds

Answer 483

Aldosterone antagonists

Answer 484

Hormone you secrete to regulate fluid volume in the body. Binds to receptor in nucleus and works to increase production of certain ion channels in sodium membrane to reabsorb more sodium and water. If anything, helps to increase BP by fluid volume. To block effects you'll get more water and salt excretion of kidneys.

Answer 485

DCT, but primarily in collecting duct

Answer 486

Works at the steroid receptors within the nucleus of the renal cells. Have increased number of sodium channels, which leads to sodium and water being reabsorbed.

Answer 487

Spironolactone (Aldactone) | Eplerenone (Inspra)

Answer 488

More frequently used; older, generic available, cheaper

Answer 489

Bind to the steroid receptor to prevent it from being activated. Prevents aldosterone from coming in and activating it. Good for patients with high circulating aldosterone levels, will have the most effect from these drugs. Inhibit channels on lumenal side to have less sodium reabsorption. Also has less potassium being excreted than other diuretics.

Answer 490

Potassium sparing diuretics and aldosterone antagonists

Answer 491

Modest effect on lipid, glucose, and uric acid levels.

Answer 492

``` Primary aldosteronism - hyper secretion of aldosterone. HTN CHF - class three or four ``` Edematous conditions like cirrhosis and nephrotic syndrome.

Answer 493

Hyperkalemia, esp. for patients with poor kidneys that can't manage potassium normally.

Answer 494

Spirinolactone has weak androgenic effects, which means it interacts with testosterone receptors, but not as tightly as testosterone. It will interact, but not to the same degree. Can block those receptors and prevent testosterone from working on them, which causes testicular atrophy and gynecomastia. Woman may get abnormal hair growth or irregular periods.

Answer 495

Switch to Eplerenone

Answer 496

Work in PCT, earlier end of neprhon, and increase amount of bicarbonate excreted within the kidneys. More excreted and water goes with that as well. Increased release of sodium and potassium, but is a poor diuretic. Won't have a good chronic antihypertensive effect from this.

Answer 497

Glaucoma for the eyes to decrease aqueous humor production.

Answer 498

Acetazolamide* main one used. Dichlorphenamide Methazolamide

Answer 499

Should acidify pH. Can prevent altitude sickness.

Answer 500

PCT - Inhibit carbonic anhydrase on outside of cell, so less is broken down to CO2 and water and is less likely to be reabsorbed. Bicarbonate will be excreted in the kidneys, which causes more water to go with it.

Answer 501

Glaucoma, by decreasing aq humor production. Epilepsy - because metabolic acidosis causes seizure threshold to be higher. Altitude sickness Treats metabolic alkalosis by inducing acidosis. Head injury to decrease the swelling; decreased production of CSF.

Answer 502

metabolic acidosis potassium depletion drowsiness

Answer 503

Increase amount of solute in kidneys, so more water will flow there. By inhibiting H2O reabsorption, esp in PCT allows for more fluid and water to be released. Can increase urine outflow.

Answer 504

Mannitol Glycerin Isosorbide Urea

Answer 505

Mannitol Given for head injury, can use to draw water out of CSF and decrease pressure.

Answer 506

Acute renal failure, acute tubular necrosis - questionable efficacy. Increased outflow but kidneys aren't working better.

Answer 507

START OF CARDIOLOGY 3 CARDS

Answer 508

Responsible for blood pressure regulation, secretion of aldosterone - retains sodium and fluid, affect renalblood flow and sodium excretion. Will be lookiing at drugs to inhibit pathway.

Answer 509

Renin is released from the kidneys in response to a drop in BP to regulate more flow to kidneys. Angio 1 converts to Angio 2 (drugs may work on angiotensin converting enzyme), which is responsible for metabolizing bradykinin. When Angio 2 is formed, it affects adrenal cortex to stimulate more aldosterone release to stimulate fluid retention and vasoconstriction to cause increase in BP.

Answer 510

renin baroreceptor macula densa SNS

Answer 511

Increased renin release, because baroreceptors aren't being stretched enough. Baroreceptors can recalibrate their baseline to be higher in HTN patients.

Answer 512

Macula densa responds to changes in sodium and chloride. Decrease in that from diuretics can stimulate renin release.

Answer 513

Renal nerve activity controls release of NE and epi to innervate juxtoglomerular cells to activate B1 receptors, whihc stimulate renin release.

Answer 514

Byproduct of renin release. Its a vasoconstrictor to stimulate aldosterone secretion. Causes renal vasoconstriction on efferent arteriole.

Answer 515

Vasodilator of afferent arteriole

Answer 516

Constricts the efferent arteriole, which is important to cause that pressure for flow to occur through nephrons.

Answer 517

Causes a negative feedback loop to inhibit further renin release. Increases NE release to stimulate thirst, sodium appetite, and ADH secretion to increase BP and fluid retention. Also helps with cell/tissue hypertrophy and cardiac remodeling after MI.

Answer 518

Patients with CHF and post MI are undergoing cell adn tissue hypertrophy and cardiac remodeling after MI. ACEI and ARBs help stop this remodeling. By blocking process, you slow disease progression of the heart.

Answer 519

Over activity of RAS leads to HTN, CHF, and diabetic nephropathy -- esp. when they have high pressures and sugars that push on glomerulus, which causes shredding. Myocardial remodeling.

Answer 520

Helps diabetics to protect the kidney from nephropathy.

Answer 521

effects on morbidity and mortality.

Answer 522

Decreased Ang 2 vasoconstriction bc less is made = decreased renal vasoconstriction, less synthesis of aldosterone = less sodium reabsorbed, less NE being send out, and less bradykinin metabolism. All decrease blood pressure on the system. Will inhibit the negative feedback loop. May release renin, but won't see much of an issue there.

Answer 523

If you give them a full dose of ACEI at once, it makes a large dilation, which can decrease pressure of kidneys causing an acute kidney injury. Even though its renal protective, want to start low and go slow so you don't have a dramatic effect on the kidneys.

Answer 524

Most are prodrugs. Must be metabolized by liver. Active form is eliminated through kidneys, except fosinopril.

Answer 525

Fosinopril, eliminated throught the liver

Answer 526

Captopril and Lisinopril

Answer 527

``` END IN --PRIL Lisinopril Captoppril Enalapril > Enalaprilat Benazepril > Benazeprilat Fosinopril > Fosinoprilat Trandolapril > Trandolaprilat Quinapril > Quinaprilat Ramipril > Ramiprilat Perindopril > Perindoprilat Moexipril > Moexiprilat Perindopril ```

Answer 528

Enalaprilat; already active so you inject into the vein and it works.

Answer 529

Once daily dosing; good half life

Answer 530

Captopril; may be given twice a day

Answer 531

Shorter acting agents may lose some effectiveness towards end of the day and you may need to give it twice a day to get full 24 hour coverage. Ex: Lisinopril is usually given once a day, but might need it given twice a day for full coverage.

Answer 532

Steep dose response at lower doses, which flatten out the higher you get. Lower doses 5-10mg a day, you have a good decrease in BP, where 20-40 mg a day, you don't see as big of a decrease in hypertension.

Answer 533

Hypertension to decrease TPR, systolic, and diastolic pressures. Decrease LVH by relieving pressure and remodeling. Post MI - decrease remodeling and decrease in mortality when given post MI. Diabetic nephrophaty - decreases glomerular pressure and remodeling to prevent or delay progression of renal disease in diabetics. Also slows progression of renal disease in other nephropathies. Good for declining kidney function.

Answer 534

preferred in diabetics, bc of kidney protective effect - helps slow the diabetic nephropathy for longer periods of time.

Answer 535

Decreases remodeling that occurs with hypertrophy. Has decreased afterload by decreasing peripheral vascular resistance. Decreased preload and cardiac ouput, which will delay progression of CHF.

Answer 536

Based on symptoms - how much activity you can perform efore symptoms occur and function of heart activity. By decreasing remodeling, you prolong the amount of time it takes to go to stage two, three, and four. Decrease incidence of MI and hospitalizations.

Answer 537

Those with left ventricular hypertrophy

Answer 538

Heart failure is from reduced CO, which leads to further SNS activity and vasoconstriction. To respond to decreased CO, blood vessels want to clamp down to keep perfusion high. All lead to cardiac remodeling and increased Renin release. ALL cyclical and feed into one another. Renin increases remodeling to keep cardiac function as good as you can for as long as you can.

Answer 539

Dry cough Hyperkalemia Orthostatic hypotension Renal function impairment

Answer 540

Angioedema - swelling in nose, throat, mouth, larynx, lips, and tongue. Causes airway closure. Due to bradykinin accumulation. One third occur in first week, some first six months, or some years down road. Just cause on for two years, doesn't mean that it can't happen to them. Red flag is inspiratory wheeze! Fetal morbidity and mortality - CI for pregnant patients bc it can lead to birth defects and fetal death.

Answer 541

Dry cough - due to inhibit of ACE which increases bradykinin in body, which attacks cough receptors in lungs. Starts a week to six months after therapy, but not related to the dose or the agent. Women are more susceptible. No chronic ailments, but affects quality of life.

Answer 542

Hyperkalemia - bad for patients iwth poor kidney function. See reliable increase in potassium in patients, more pronounced when they have renal disease or are taking potassium sparing diuretics. Also done with aldosterone antagonists. Bad for potassium supplmenets, bc can have dangerous increase in it.

Answer 543

Orthostatic hypotension in elderly, especially with the first dose or upward titration. Give at night to sleep through bout and get used to over time. Also with CHF its more pronounced.

Answer 544

Renal function impairment - patients with renal disease whose blood flow is dependent on Ang 2. Giving tfull dose can drop GFR rapidly. Start low and titrate up with tolerance.

Answer 545

NSAIDs can decrease effects of ACEI, because if you have ACEI work to decrease constriction on efferent arteriole, kidneys try to vasodilate on afferent arteriole. ACEI decrease constriction on efferent arteriole and vasodilate afferent arteriole. NSAIDs block, which makes kidneys take a hit in the middle.

Answer 546

Angiotensin receptor blocker (ARBs).

Answer 547

Ace Inhibitors block effects of ACE, but there's other pathways for Ang 2 to be produced --- by trypsin, cathepsin, and chymase. Ang 2 works on ang receptors - AT1 and AT2. Continues to increase BP.

Answer 548

AT1 is expressed WIDELY in heart, endothelium, vascular smooth muscle and kidneys. AT2 is expressed during development in fetuses.

Answer 549

When Ang 2 is made, it affects AT1 and AT2. ARBs have high affinity binding and slow dissociation = have good sustained blockade of AT1 receptors. Will see vasodilation and renal vasodilation. Less aldosterone = less sodium reabsorption and less NE release to all lower the BP. Similar affects that you see with ACEI.

Answer 550

ARB reduce ang 2 at AT1 receptors and indirectly activate AT2 by increasing Ang 2 levels - By blocking receptors, body thinks its needs more Ang 2 and releases renin. Clinically, AT2 are stimulated, but may not be important. ARBs don't inhibit breakdown of bradykinin, which is a disadvantage for antihypertensives. Bradykinin cough might be a problem with ARB. ACEI renal elimination, while ARB is bile and renal elimination.

Answer 551

Do not need to know prodrugs vs not, just be able to distinguish from ACEI. ARB ends in -SARTAN PRODRUGS - Candesartan, Olmesartan, Losartan, Azilsartan NON - Eprosartan, Irbesartan, Telmisartan, Valsartan.

Answer 552

Mainly for HTN and in combination products with HCTZ (hydrochlorathiazide).

Answer 553

Salt sensitive HTN patients ACEI and ARBs are not as effective for salt sensitive patients. They can be mixed with thiazides for additional benefits.

Answer 554

Left ventricular dysfunction, post MI, CHF, and diabetic nephropathy prevention.

Answer 555

Hyperkalemia in renal disease or K+ sparing diuretics. Hypotension from first dose effect. Acute decrease in renal function from drop in GFR. Fetal morbidity or mortality -- Do not give in pregnancy! 2nd or 3rd trimesters

Answer 556

Use low doses and titrate up to avoid acute renal failure from drop in GFR. Do not cause cough (Main reason why you switch from ACEI to ARBs). Angioedema has a lower incidence in patients with ARBs. (May switch from ACEI to ARBs - won't have cross reactivity, bc there's no build up of bradykinin with ARBs).

Answer 557

Pregnant patient - Mom has AT1 and fetus has AT2, eventually there will be no AT1 to affect so it will continue to effect AT2. Selectivity is never absolute and will see cross reactvity with receptors.

Answer 558

L type - Found in sarcolemma within vascular smooth muscle of the heart, cardiac myocytes, and cardiac nodal tissue (SA and AV nodes). Important to cause muscle contraction. By blocking L type, see decrease in smooth muscle and myocyte contraction.

Answer 559

Dihydropiridines Nondihydropiridines (phenylakylamines and benzothiazepines).

Answer 560

SA node and AV node are primary pacemakers in heart. By blocking Ca channels, you decrease automaticitiy, which will cause heart rate and contractility to go down.

Answer 561

SA and AV nodes are slow response cells that have a "natural leak" to allow sodium to come in. Big influx of calcium occurs at action potential. By decreasing amount of calcium to get into the heart, you have a decreased peak of contractility and automaticity.

Answer 562

Non-pacemaker cells (or fast response cells) - By blocking calcium, there's less influx into cell. Calcium enters myocytes, which is important to interact with sarcoplasmic reticulum to initiate muscle contraction. Blocking the Ca influx will decrease contractility of the heart.

Answer 563

Fast response cells - When action potential comes along, it opens L type calcium channels, to activate the sarcoplasmic reticulum, which releases calcium and allows contraction to occur. During recovery, calcium goes back to SR and heart has channels to reset (get calcium out of cell). When you block calcium channel from SR, not as much gets out so the contraction isn't as strong.

Answer 564

Less calcium from SR = less Ca gets to myocyte, so less contraction occurs. Contraction not as hard.

Answer 565

Smooth muscle surrounds blood vessel - Calcium comes in and is released from SR to cause vasoconstriction. Inhibiting Ca influx causes vasodilation instead (antihypertensive effect)

Answer 566

At therapeutic doses, they're ineffective at decreasing venous tone. Not a lot of effect on vein. Because they can affect arteries - they decrease the afterload (afterload = arteries), which is the amount of pressure the heart is pumping against. Won't have an effect on preload with therapeutic doses.

Answer 567

Avoid, because CCB is a cardio depressant.

Answer 568

Myocardial cells depend on exogenous calcium from L type channels to come out and recirculating internal pool of calcium to be released from sarcoplasmic reticulum. Arterial blood vessels depend on exogenous calcium from L type channel, but they are three to ten times more sensitive to actions of CCBs than myocardial cells. Divide between DHP and Non-DHP - DHP work on blood vessels, but not directy depressant effects. Non-DHP work on heart and blood vessels.

Answer 569

Reduce slow inward current and decrease rate of recovery to slow AV conduction. Work on the heart.

Answer 570

Reduces slow inward current, but does not affect nodal tissue; works on blood vessels.

Answer 571

Angina, HTN, supraventricular arrythmias, diastolic heart failure, and rare cases of cerebral ischemia and migraine prophylaxis.

Answer 572

Non-DHP - Dilitiazem and Verapimil Okay affect on vasodilation, but primarily depress automaticity in AV and SA nodes.

Answer 573

DHP - work on vasodilation and have negligible affects in cardiac cells.

Answer 574

Non-DHP; available IV or PO. Controls supraventricular arrythmia, Afib, angina, HTN and supraventricular tachycardias.

Answer 575

Metabolized by CYP3A4 and will inhibit CYP3A4. Short half life, so when given IV it has to be a CONTINUOUS infusion or an extended release product PO.

Answer 576

Lots of bad affects which is why they aren't first line for HTN management. Vasodilation = Flushing, headache, hypotension, peripheral edema. Negative inotropic of Non-DHP effect can cause first degree, AV block, bradycardia, and exacerbations of CHF. GI - Can lead to constipation and affects smooth muscle by slowing down. More related to decrease perfusion, esp. in older patients. Drowsy, dizzy, depression. May have sexual dysfunction, gynecomastia, and GINGIVAL HYPERPLASIA.

Answer 577

Dilitiazem

Answer 578

Advanced heart block, hypotension, heart failure, liver disease, GERD GERD - esophageal sphincter isn't tight enough and meds relax smooth muscle and make it loser and worse.

Answer 579

CYP3A4 inhibitor, which affects statins, carbamazepine, propanolol, tacrolimus, and cyclosporine. Also a CYP3A4 substrate, so can be affected by other 3A4 inhibitors - atazanavir (HIV med) that inhibits CYP3A4 and increases levels of Dilitiazem.

Answer 580

Ritonavir, Indinavir, Saquinavir, and Atanzavir. -AVIR Other antihypertensives or cardio depressives could affect as well, synergistically.

Answer 581

Available IV or PO and sustained release for longer duration of action -- used for angina, HTN, Afib, and paroxysmal supraventricular tachycardia. Exact same as Dilitiazem!!! But may have more vasodilation and suppression in automaticity of SA node and AV node.

Answer 582

Inhibit CYP3A4 and substrate for it as well. Can see reactivity with CYP2C9, but not as often as CYP3A4 inhibitions do.

Answer 583

Constipation is more pronounced, other side effects similar to dilitazen. Peripheral vasodilation, negative inotropic effects, nausea, vommiting, dyspepsia, abdominal pain, elevation in liver function tests, CNS effects, gynecomastia, sexual dysfunction, GINGIVAL HYPERPLASIA, skin reactions.

Answer 584

Advanced heart block, hypotension, heart failure, liver disease and GERD Same as dilitiazen as well.

Answer 585

Substrate and inhibitor of CYP3A4. PGP - drug efflux pump in GI tract to kick out and prevent absoprtion. By inhbiting PGP there's increased levels of the drug being absorbed into system.

Answer 586

Indinavir, Ritonavir, Saquinavir, Atazanavir, Itraconazole, Cimetidine Similar to Dilitazen.

Answer 587

``` Amlodipine (long half life) Nifedipine (short half life) Nicardipine (few available IV form) Felodipine Isradipine Nisoldipine ``` DHP end in --IPINE

Answer 588

Dihydropyridines treat angina and HTN; not used for supraventricular arrythmias, because they DO NOT AFFECT NODAL TISSUE. Only the vasodilation of vasculature.

Answer 589

Nimodipine (DHP) - help prevent vasospasm in CNS after hemorrhage.

Answer 590

Drugs are so potent, you want to avoid short acting formulations. Blood pressure will drop fast and rebound back up. Use extended release prep or drugs with longer half lives.

Answer 591

Vasodilation is primary activity of DHP drugs!

Answer 592

Metabolized by CYP3A4, but DO NOT inhibit CYP3A4 like Verapimil and Dilitiazem. DHP will not cause increase in other drugs bc it doesn't inhibit CYP. Metabolism can be decreased by grapefruit juice.

Answer 593

Half life changes widely in DHP drugs. Nifedipine is a poor short acting agent, bc it has short half life and duration of action ~1.8 hrs. Amlodipine is good once daily, bc it has a longer half life ~35 to 50 hrs.

Answer 594

Vasodilation is more potent. Worsened peripheral edema (esp in CHF or PVD), gynecomastia being worse with Nifedipine, gingival hyperplasia. **Reflux tachycardia from heart wanting to pump harder from vasodilation.

Answer 595

Tachycardic and hypotensive - CCB like DHP. Bradycardic and hypotensive -- Dilitiazem.

Answer 596

Nifedipine - worst drug for that. Worse than Dilitiazem.

Answer 597

Severe aortic stenosis, unstable angina, or recent MI. Immediate release can lead to huge drop in blood pressure leading to ischemia of the heart.

Answer 598

Amiodarone, Digoxin, and Beta blockers can have a synergistic drop in BP. Won't see cardiodepressant effects, bc not working on heart as much.

Answer 599

Can be affected by CYP3A4 inhibitors, which can cause toxicity, but do NOT inhibit themselves. Indinavir, Ritonavir, Saquinavir, Atazanavir, Itraconazole, Cimetidine ~~ can cause increased levels of DHP. -AVIR drugs.

Answer 600

Competitive inhibitors, primarily see their effects on B1 receptors of the heart. They block normal substances that activate beta receptors (Epinephrine, Norepinephrine, Dopamine). Block will decrease cardiac output and an acute increase total peripheral resistance as they acclimate to decreased CO. Can also see impaired exercise tolerance. Blocking receptors, when you run, body can't pick up heart rate bc NE won't bind.

Answer 601

Can see competitive blockade of receptors that mediate renin release, which lower ang 2 and blood pressure.

Answer 602

In lungs, non selective BB could have competitive blockade of B2 receptors, which will increase bronchoconstriction. Bad for asthmatics!

Answer 603

CNS activity when lipid soluble - depresses SNS; may cause depression and migraines. Altered baro-reflex response.- can develop orthostatic hypotension.

Answer 604

Nonselective - Blockade of presynaptic B2 receptors decreases NE release.

Answer 605

Beta blockers can be selective to B1, B2, or can be nonselective affecting both. Metabolized by liver and kidney, but don't normally need a dose adjustment.

Answer 606

A partial agonist affect, which can lead to seizures, asthma exacerbations, heart failure, and bradycardia.

Answer 607

Membrane stabilizing activity stabilizes the myocardium of the heart to stop reentrant rhythms.

Answer 608

Non-selective

Answer 609

B1 selective

Answer 610

Grab bag of misc effects. Cause direct vasodilation by blocking A1, making NO, B2 agonist, calcium blockade, etc.

Answer 611

Affect B1 and B2 receptors; Nadolol, Penbutolol, Pindolol, Propranolol, Sotolol, Timolol Selective (A-M) Non-selective Beta Blockers (N-Z) KNOW EXCEPTIONS

Answer 612

High lipid solubility; want to avoid in elderly so you avoid altered mental status. Prevents stage fright and anxiety.

Answer 613

Affect B1; acebutolol, atenolol, bisoprolol, esmolol, metoprolol.

Answer 614

IV only Good short acting antihypertensive used in ER.

Answer 615

Acebutolol - Both Atenolol - Renal Bisoprolol - Hepatic Metoprolol - Hepatic

Answer 616

Carteolol Carvedilol Labetalol Betaxolol

Answer 617

Carteolol and Betaxolol

Answer 618

Carvedilol - has additional affects; a1 blockade. By blocking, cause vasodilation and decrease BP. Labetalol - IV for BP management; blocks a1 and activates B2 - relax bronchi and vasodilate vessels.

Answer 619

HTN (not first line) - First line = ACEI or thiazide diuretics. Works best in younger patients with increased catelcholamines, tachycardia, etc. Can cause fatigue and limit exercise tolerance. >>Not a first line agent for elderly.

Answer 620

(1/3 * sytole) + (2/3 * diastole)

Answer 621

Acutely, there's a decrease in CO, which leads to compensatory increase in TPR. Chronically, you decrease Ang 2 and NE release. Over time, altering baroreceptor reflex, you have a decrease in MAP, sustained decrease in CO, and long term decrease in TPR.

Answer 622

Timolol, Betaxolol, Carteolol | Decrease AQ humor

Answer 623

Propranolol and Timolol | Low dose to help vasospasms.

Answer 624

Propranolol; inhibits conversion of T4 to T3. Used to reduce tachycardia, tremor, anxiety.

Answer 625

Glaucoma, migraines, hyperthyroidism, angina pectoris (myocardial ischemia), acute MI, supraventricular arrythmias, panic attacks, tremors

Answer 626

Ischemia is due to too much oxygen demand from myocardium and not enough supply. Decrease CO and work heart is doing to allow for more blood flow to get to the ischemic areas.

Answer 627

Beta blockers with ISA activity; don't want to activate those receptors. Protects myocardium from NE/EPI. Protects ischemic myocardium by blocking receptors. Decreases mortality.

Answer 628

Block the AV node to slow transmission.

Answer 629

Blockade of B2 receptors on skeletal muscle. Non-selective Beta Blocker. Selective won't affect B2 receptors.

Answer 630

Start in hospital and titrate up slowly as they tolerate it. Carvedilol Metoprolol Bisoprolol Don't give a cardiodepressant or DHP. They have impaired left ventricular function, so by slowing the heart down, you can fill better and have a more controlled squeeze.

Answer 631

Bronchoconstriction is a concern with nonselective BB, can lead to asthma exacerbation and COPD pts. Less likely with B1 selective blocker for asthmatics. Cardiodepressive actions, which worsen negative inotropy, bradycardia.

Answer 632

Type 1 - When there is decreased glucose in blood stream, body increases EPI to have glycogenolysis. Allows gluconeogenesis to take place and increase glucose in blood. Beta blockers will block B receptors in liver, which block glycogenolysis, prolonging hypoglycemic episode. Responses are masked by BB. Might not notice for a while.

Answer 633

Type 2 - Have decrease insulin release leads to increased glucose in blood stream. When hypoglycemic, signs are masked.

Answer 634

BB blocks B2 receptors in blood vessels that are normally vasodilatory, cause constriction, which can lead to raynauds, muscle fatigue, and worsening of peripheral arterial disease. Also cause elevated triglycerides.

Answer 635

If you block B receptors, they start to upregulate. If there's more receptors and you takeaway drug, EPI affects more receptors leading to increased cardio effects. --- Acute angina, MI, increased BP.

Answer 636

Chance for depression, nightmares, vivid dreams, hallucinations, fatigue. >>Propranolol >>More lipid soluble, worse it will be.

Answer 637

Mix with CCB, both have cardiodepressive affects.

Answer 638

Clonidine, leads to decreases in BP and withdrawl.

Answer 639

Block A1 to cause vasodilation and hypotension. Decreases TPR and get reflex increase in HR.

Answer 640

Normally constrict vasculature. When you block cause vasodilation and hypotension.

Answer 641

A1 antagonist Not used frequently; added as third or forth agent to BB and diuretics or when CI to BB, CCB, etc.

Answer 642

Orthostatic HTN Postural dizziness Mild reflex tachycardia - related to decreased TPR. Increased renin, increase sodium and water retention. Blocking alpha receptors leads to impotence in males.

Answer 643

NSAIDs reduce the response. BB may worsen postural hypotension. Be careful with cardiac and renal failure. Can worsen bc of the vasodilation.

Answer 644

A1 selective agents used as antihypertensives and to help with benign prostatic hyperplasia. Less alpha constriction leads to relaxation and better urine outflow in BPH. Longer half life, once daily dosing. -ZOSIN

Answer 645

A1A selective antagonist, which is expressed on prostate. More specific and limits vasodilation. Better agent for BPH.

Answer 646

Can block A1 effects, which is an additive to antiHTN effects.

Answer 647

By stimulating post synaptic A2 receptors and imidazoline receptors; they cut amount of NE and EPI being released by CNS. Works on HTN from top down.

Answer 648

Nucleus of solitary tract and ventral lateral medulla. By activating receptors decreases sympathetic nerve activity.

Answer 649

Clonidine is central sympatholytic. By decreasing SNS effect; also decreases CO and vascular smooth muscle to lead to hypotension.

Answer 650

Decreased TPR Decreased HR Decreased CO

Answer 651

Decreased TPR and modest decrease in CO (no reflx cardio output like DHP). Efficacy independent of age, race, gender Works well in elderly No negative effects on lipids

Answer 652

Drowsiness, sexual dysfunction Narrow therapeutic index so dose change can lead to big changes in BP and CO. Kids are sensitive. Abrupt withdrawal syndrome - by blocking release of those catelcholamines, you uprgulate receptor which has big increase in HR.

Answer 653

A2A agonist, imidazoline agonist - Acute increase in BP. Can activate A1 and cuase vasoconstriction, but short-lived. Will see decreased BP and HR in long term.

Answer 654

Increases blood glucose bc decreased insulin release. Also causes sedation.

Answer 655

Decreased ADH secretion. Causes sodium retention, so should be given with diuretics.

Answer 656

Analgesic activity for surgery. Anesthetic with clonidine to decrease use of opioids post op. Causes sedation. Helps with opioid withdrawal, esp in neonate abscence syndrome.

Answer 657

Withdrawal reaction Orthostatic Hypotension Impotence Bradycardia

Answer 658

Less potent than clonidine, selective for A2 receptors. Less sedation. Could have withdrawal. Kids with ADD can be on a stimulant in the morning and use this to calm down at night.

Answer 659

Direct vasodilators work on arteries to cause dilation and decrease TPR. Last line agents for HTN, bc they have reflex sympathetic activation. Increase CO, fluid retention, renin, and tachycardia. Can lead to tachyphylaxis.

Answer 660

Process in which you are tolerant to a drug so you have to keep increasing the dose to see effects. Heroine abusers need more heroine to get high. In tachyphylaxis, you keep increasing your dose but you see no increased effect. Can increase anti-HTN and have no effect.

Answer 661

Hydralazine Minoxidil (Rogaine) Nitroprusside Diazoxide

Answer 662

Minoxidil and Diazoxide

Answer 663

Hydralazine with diuretic or beta blocker. Hydralazine is good for acute bouts of HTN via IV. Minoxidil as well.

Answer 664

Nitroprusside Diazoxide Fenoldopam Cause vasodilation to decrease HTN immediately.

Answer 665

Increases cGMP to increase nitrous oxide pathway. Causes good vasodilation. Blocks effects of calcium, works through nitrous oxide to increase cGMP, which causes vasodilation in smooth muscle.

Answer 666

Undergoes hepatic metabolism called acetylation. Can be fast or slow. Slow acetylators have increased drugs in the body, bc not metabolizing fast. Fast acetylators have levels go down more quickly.

Answer 667

Fast acetylators, because levels go down quickly.

Answer 668

Lupus like rash can develop in those who are slow acetylators. -- Happens with high doses, long term use, women, caucasians, and slow acetylators.

Answer 669

In slow acetylators, cause Lupus like rash.

Answer 670

Coronary artery disease, elderly, and ischemia.

Answer 671

Stools may turn black.

Answer 672

Activates ATP modulated potassium channels, which lets potassium out to hyperpolarize and prevent smooth muscle from contracting.

Answer 673

Can cause arrythmia, myocardial ischemia, and hair growth (hypertrichosis). Marketed topically for hair growth now due to systemic effects. If applied in large quantities, can see cardiovascular effects. Don't let kids get into it.

Answer 674

Good agent IV for hypertensive crises. Has 1 nitrous oxide particle to vasodilate and has 5 cyanide molecules. Body makes some cyanide, so its not abnormal. Body can metabolize, but if you have a patient with poor renal function or high dose it can cause toxicity.

Answer 675

Trembling, vomitting, convulsions, acidosis Can combat by giving with sodium thiosulfate, which donates sulfur molecules to liver to process cyanide better. Patients with renal toxicity can build up thiocyanate and develop toxicity. Not a good drug for those with poor renal function.

Answer 676

Dopamine agonist to stimulate cAMP. Good for renal natriuretic and diuretic properties to manage short-term blood pressure.

Answer 677

dysrhythmias

Answer 678

JNC 8 Guidelines - Goal BP is less than 140/90.

Answer 679

Thiazide diuretic or CCB DHP - amlodipine More salt sensitive patients - respond better to TD and CCB.

Answer 680

Start thiazide diuretics, CCBs, ACEI or ARB dependent on other disease states.

Answer 681

ARB or ACEI, because they're nephroprotective.

Answer 682

Increase dose of drug or add a drug from another class. Don't use ARB and ACEI at same time. Need two different types of classes of drugs.

Answer 683

Imbalance between myocardial oxygen supply and demand. Demand out strips supply and have signs of ischemia in cardiac tissue.

Answer 684

Atherosclerotic narrowing of one or more arteries. Can lead to unstable angina or acute MI.

Answer 685

Clinical manifestations of MI > chest pain.

Answer 686

Supply: Arterial hemoglobin conc of oxygen and coronary flow and distribution. Cardiac extraction of O2. Oxygen requirement: wall tension, heart rate, and contractility affect.

Answer 687

Heart rate, contractility, and wall tension affect oxygen demand of heart. Wall tension is function of preload and afterload.

Answer 688

Initial stretching of myocardiocytes prior to contraction. Can be related to ventricular and diastolic volume.

Answer 689

Pressure heart must pump against, related to systemic vascular resistance. As you have atherosclerosis, big plaques form and can cause major blockage of arteries.

Answer 690

Latent manifestation of ischemia that can occur with any degree of stenosis. Usually due to vasospasms. Can see when 50% of left main is occluded or 75% of other major coronary arteries being blocked. Can see in stenosis.

Answer 691

Defined as 90% blockage of artery with virtually no flow.

Answer 692

A vasospastic or variant angina that occurs in younger patients. Usually due to an issue with autonomic control where SNS clamps on coronary arteries. Can be so severe you see ST segment elevation (rare) and occurs at night or early morning hours.

Answer 693

Family history of premature CV event. | Age over 45 for males and 55 for females.

Answer 694

Sedentary life, diabetes, tobacco consumption, overweight, HTN, dyslipidemia.

Answer 695

Increase quantity of life by preventing acute coronary syndrome and increase quality of life by relieving symptoms.

Answer 696

Decreasing the myocardial demand by decreasing heart rate, contractility, and wall tension to decrease preload and afterload. Increase the myocardial oxygen supply to improve coronary blood flow and stabilize plaques to prevent acute coronary syndrome.

Answer 697

Reestablish flow through vessels by revascularization, via percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) to keep the vessel open and prevent re-stenosis. Pharmacotherapy - Antianginals like beta blockers, calcium channel blockers, nitrates. Vasculoprotective meds like antiplatelets, statins, ACEI.

Answer 698

CCB, nitrates, and beta blockers

Answer 699

CCB, nitrates, aspirin, clopidogrel Anti-PLT: aspirin and clopidogrel

Answer 700

Work to improve exercise capacity and reduce exercise induced ST segment changes. Decrease frequency of symptoms. Beta blockers, CCB: DH and, nonDHP, and nitrates.

Answer 701

Depends on degree of symptoms on exertion.

Answer 702

On demand, decrease HR, contractility, and wall tension. No effect on oxygen supply, because cause no coronary artery vasodilation.

Answer 703

First line in absence of contraindications. Useful for patients with limited exercise capacity from angina, preexisitng heart failure, and post MI to prevent mortality.

Answer 704

May use beta 1 selective or non-selective agent. B1 selective is better for asthmatics. B1 selective: metoprolol, atenolol Nonselective: propranolol, nadalol Third gen: carvedilol, labetalol

Answer 705

HR under 60bpm Systolic BP < 100mmHg AV block Acute decompensated heart failure

Answer 706

reactive airway disease, systolic heart failure, diabetes, and peripheral vascular disease.

Answer 707

Hypotension, bradycardia, hyperglycemia, dyslipidemia, fatique, sexual dysfunction, worsened claudication

Answer 708

Propranolol

Answer 709

non-DHP - Verapimil and Dilitiazen Demand: Decrease HR, contractility, and tension. Might have slight increase in HR but will decrease wall tension to affect preload and afterload. Supply: Might see mild dilation increase of stenosis and relief of vasospasm for those with vasospastic angina.

Answer 710

Non-DHP are good initial therapy for reduction of symptoms when pt can't be put on beta blocker or symptoms aren't fully controlled. NDHP go by themselves; DHP are prescribed with BB.

Answer 711

Used for those contraindicated to beta blockers, treats vasospastic angina, asthma, uncontrolled diabetes and LV dysfunction.

Answer 712

Don't want to further depress function.

Answer 713

BP less than 100 systolic, HR less than 60bpm, acute heart failure, ejection fraction and AV block. Precaution when using beta blockers and CYP 3A4 interactions.

Answer 714

Non-DHP verapimil and dilitazem Inhibit CYP3A4 and are metabolized by it.

Answer 715

Hypotension. DHP can cause headhace, flushing, and peripheral edema.

Answer 716

START OF CARDIOLOGY 4 CARDS

Answer 717

Nitrates donate nitric oxide to stimulate production of cyclic GMP. -- Guanosine triphosphate to cyclic guanosine monophosphate. -- Help increase activity of protein kinase G to decrease cytostolic calciucm. By decreasing calcium released in cell, smooth muscles will relax and vasodilate. Lowering BP! cGMP is normally broken down by PDE5 to decrease amount of cGMP there. Important drug interaction with erectile dysfunction meds, which work to inhibit PDE5. Might see synergistic effect which elads to increase cGMP and leads to synergistic vasodilation and decreases in BP.

Answer 718

Used for relieving acute symptoms of MI and aren't meant to be for long term control of symptoms. Sublingual tablets and sprays. Absorbed by mucosa in mouth, not the GI tract. Used at onset of angina and every 5 mins. If no relief after first dose, call EMS and continue to use every 5 mins.

Answer 719

Sitting or standing enhances effect. Store in original packaging in a cool and dry place, because nitroglycerin is easily broken down. Need an amber vile to stop light from destroying it. Replace tablets three to six months after opening to make sure they're in tact. Must spray under the tongue.

Answer 720

Used to help control symtpoms from occuring in long term control. Used as back up agents while CCB or BB can't be used or aren't well tolerated. If CCB or BB haven't been working, you can add a long acting nitrate. Shouldn't be a single therapy unless all others are contraindicated.

Answer 721

Isosorbide mononitrate (Imdur) - lasts 12 hours, dosed daily. Isosorbide dinitrate - duration three to six hours, dosed three times daily.

Answer 722

Comes in ointment and transdermal patch. Ointment is applied with a wax backed card that prevents it from being transmitted to healthcare provider. Transdermal patch - 12 hours on, 12 hours off. Same with ointment; want to avoid tachyphylaxis!

Answer 723

Headache, flushing, hypotension, reflex tachycardia. Heart responds by increasing cardiac output which causes tachycardia.

Answer 724

If you have a nitrate on 24hrs a day, body won't be able to maintain hypotensive or vasodilatory effect. Even if dose is increased. You will not see an increase in its efficacy or activity, which is why you need a nitrate free period. Nitrate free period is when patients have lowest symptom frequency. Nitrate free period is usually overnight.

Answer 725

Aortic valve stenosis, obstructive cardiomyopathy, and concurrent use of erectile dysfunction medications. BAD. Viagra, Cialis, Levitra -- When used with nitrates, concurrent use can lead to HTN, MI, or stroke.

Answer 726

1st line - beta blocker; non-DHP is a good alternative.

Answer 727

1st line is BB. Avoid calcium channel blockers.

Answer 728

First line treatment is Beta Blockers or Amlodipine. Avoid other CCBs.

Answer 729

First line treatment is DHP CCB. Alternatives include long acting nitrates. Avoid NDHPs and BB.

Answer 730

Frst line in Non-dhp or can use a long acting nitrate or cardioselective BB. Avoid nonselective BB because it causes hyperglycemia.

Answer 731

Treat with non-DHP and cardioselective BB. Avoid nonselective BB in asthmatics.

Answer 732

ACEI - good for patients with CAD, diabetes, or left ventricular systolic function. Prevents remodeling and progression of diease. Protective effects decrease mortality in long run.

Answer 733

Optimize dose and raise or add an additional long acting nitrate on a BB. Combination therapy. Third agent shoudn't be needed. Do a further work up via angiography.

Answer 734

Aspirin Clopidogrel Prevent blockages of arteries when theres' atherosclerotic plaques. PLT can often get stuck here and cause a clot.This can prevent it from occurring.

Answer 735

Decreases recurrence of acute coronary syndrome.

Answer 736

Anti PLT agent - put patients on a drug like this if they can't take aspirin.

Answer 737

Unless contraindicated, patient should be on aspirin. If they've had a prior MI, should be on beta blocker. If they have any DM or LV dysfunction, should be on an ACEI. "Renal protective effects". Look at lipid lowering therapy when appropriate. See who benefits from statins. Sublingual nitroglycerine is used for acute relief. Recurrent symptoms you can use prophylactic therapy with BB, CCB, or long acting nitrates.

Answer 738

Amlodipine Avoid beta blockers, because they lead to worsened symptoms.

Answer 739

Blood should remain fluid within vessels. Should be able to clot quickly when there's an injury. If thrombi occur, must be able to reestablish fluidity.

Answer 740

Vascular injury leads to vasospasm, done through mediators like TXA2 through arachodonic acid pathway. Limits blood flow to area and forms a platelet plug activated by collagent and mediators. Forms a fibrin clot from tissue factors. When done, fibrinolysis occurs, where clot is broken down by plasmin and vessels are normal.

Answer 741

Smooth part of endothelial surface has a mucopolysaccaride layer to prevent clotting cascade.

Answer 742

Thrombomodulin; binds thrombin and activates protein C, which inactivates clotting factors five and eight.

Answer 743

Natural anticoagulant that inactivates factor five and eight.

Answer 744

Circulates in blood to bind to thrombin and inactivate it.

Answer 745

Body produces this. Binds to Antithrombin III and kicks it into over drive to increase activity 1000 fold to deactivate factors 12, 11, 10, and 9.

Answer 746

inhibits PLT activation

Answer 747

stimulates PLT activation

Answer 748

Digests fibrin, inactivates factors 5, 8, and 12.

Answer 749

Collagen is exposed through injury; see Von Willebrand factor bind to collagen and release TXA2 and ADP. When interact with PLT, it causes conformational change exposing new receptors GPIIb/IIIa. Fibrinogen binds to receptors to form platelet plug. Thrombin, factor 2, interacts with receptors to sitmulate PLT activation. ADP activates receptors to further activate PLT

Answer 750

At rest, things that include inhibition of PLT activation are prostacyclin secreted by endothelium. to stop clotting. Collagen isn't exposed. Low levels of thrombin. PLT don't express the receptors on surface, so they can't bind to each other.

Answer 751

Irreversible inhibitor of all COX enzymes. Acetylates COX1 and COX 2, which is irreversible for the life of the PLT. Also, prevent formation of thromboxine, which is a PLT activator. Inhibit COX1 prevents PLT from activation. 160mg/day has COX maximally inhibited.

Answer 752

Irreversible, 7-10 days.

Answer 753

``` Ibuprofen - 24hr Naproxen - 48 hrs Diclofenac - 48hrs Indomethacin - 48hrs Piroxicam - 72 hrs ``` Reversible; so have shorter duration of action for PLT inhibition than aspirin.

Answer 754

Inhibiting COX1, see increase in Dyspepsia, GERD, PUD, and bleeding in GI. Bruisng might be more common.

Answer 755

Has vasodilation properties; combines with aspirin to form Aggrenox to prevent transient ischemic attacks and stroke, bc vasodilation and anti PLT activity.

Answer 756

When ADP reacts with P2Y1 receptor, it induces a conformational change leading to PLT aggregation. When ADP reacts with P2Y12 receptors, it inhibits cAMP induced inhibition and leads to more PLT activation. For PLT activation, you need to activate BOTH receptors. Receptor blockers inhibit fibringoen and receptors. ALso interfer wtih the binding of von willebrand factor.

Answer 757

Ticlopidine Clopidogrel Ticagrelor Prasugrel

Answer 758

Inhibit PTY12 receptor.

Answer 759

Most have a delay in effects 2-3 days. Maximal effect at 8-11 days. Loading dose is used to get to steady state quicker. Can be synergisticlally used with ASA.

Answer 760

Prevent stroke, MI, PAD, and post-angioplasty. Given orally and good for long term use.

Answer 761

ADP receptor blocker; use is limited to those who can't tolerate aspirin. Its a prodrug thats hepatically activated.

Answer 762

Binds disulfide bridge of P2Y12 receptor to inhibit PLT activation.

Answer 763

Thrombotic thrombocytopenic purpura - AI reaction to drug; can cause death if not reated early. Hemorrhage Use is limited to those who can't tolerate aspirin.

Answer 764

Prodrug; binds sulfur on P2Y12 receptor, synergistic with aspirin. Hepatic activation; loading dose used.

Answer 765

Hemorrhage; less risk of TTP. Better than Ticlopidine

Answer 766

ADP receptor blocker; similar to clopidogrel. ADR include HTN, worsening hyperlipidemia, and bleeding risk.

Answer 767

Has a longer duration of action for ADP receptor blocker. Recommended over clopidogrel because it has more PLT inhibition. ADR increased uric acid, bleeding, and dyspnea.

Answer 768

Monoclonal antibody; protein that was formed against a specific target. Targetted against glycoprotein IIb/IIIa receptor. Further blocks binding of PLT.Immediate onset and works 18-24hr after infusion is stopped. Used intraoperatively or with acute coronary syndrome.

Answer 769

Bleeding, thrombocytopenia Repeated administration use you're worried about patient developing antibodies against the treatment.

Answer 770

Peptide inhibits fibrinogen from binding to IIb/IIIa receptors. Continuous infusion for 96 hours and given with ASA and heparin to prevent stensosis. ADR bleeding, thrombocytopenia.

Answer 771

Non-peptide inhibitor. Renallly eliminated. ADR include bleeding, bradycardia, and dizziness.

Answer 772

Abciximab Eptifibatide Tirofiban

Answer 773

Monitors intrinsic pathway.

Answer 774

Monitors extrinsic pathway. | Factor 7

Answer 775

Both paths meet to factor 10, where prothrombin is activated to thrombin to form fibrin and make a stable clot.

Answer 776

Antithrombin III | Protein C and S

Answer 777

Glycosaminoglycan; naturally occuring product found in mast cells in the body. Chains of varying lengths are formed. They attach to core protein.

Answer 778

Regular Heparin; helps antithrombin III cause breakdown of factors 2, 10, 9, 11, and 12. Forms scaffold for binding antithrombin III to bind to factor more easily. 1000 fold increase when heparin is around.

Answer 779

Heparin is extracted from porcine intestinal mucosa or bovine lung. Given IV or subQ. Immediae onset of action.

Answer 780

Doesn't cross placenta or BBB; also isn't found in breast milk. Heparin is preferred in pregnant woman.

Answer 781

Half life may be increased if patient has liver cirrhosis or renal failure.

Answer 782

aPTT (activated partial thromboplastin time). Patients aptt/normal aptt = Looking for therapeutic ratio of 1.5-2.5.

Answer 783

Venous thrombosis, PE, MI, coronary angioplasty.

Answer 784

Major bleeding, but can be reversed with protamine to prevent heparin from interacting with antithrombin III. Heparin induced thrombocytopenia (HIT) - Rare, 5-10 days after heparin infusion, antibodies are made to heparin and PLT factor 4. Works to activate PLT, which cause clots throughout the body and you won't have any circulating PLTs left.

Answer 785

Protamine will bind heparin to stop its effects.

Answer 786

Heparin induced thrombocytopenia (HIT) - Rare, 5-10 days after heparin infusion, antibodies are made to heparin and PLT factor 4. Works to activate PLT, which cause clots throughout the body and you won't have any circulating PLTs.

Answer 787

Same drug, but has a shorter molecule. 5K daltons. Use unfractionated heparin, but can enzymatically cleave the long monosaccaride chains to have a LWMH.

Answer 788

Enoxaparin (Lovenox) - used most frequently. Dalteparin Tinzaparin

Answer 789

Works on antithrombin III, but don't affect IIa. Have greater effort against Factor XA. Shorter chain is able to interact with antithrombin III and Factor XA. Factor 2A doesn't fit to bind. That's why it has low activity against it.

Answer 790

SubQ as a fixed dose or weight adjusted dose. To prevent DVT, standard dose of 40mg. To treat a clot, will be a higher, weight-adjusted dose. 60mg of Enoxaparin daily.

Answer 791

Monitor Anti-factor XA Assay. Only need to monitor for renal failure or extreme weights. Doesn't affect aPTT because you're not acting on IIa.

Answer 792

Less bleeding than heparin. | May cause HIT. Don't give to patient with history of it.

Answer 793

Pentasaccaride that works on XA. Not IIa.

Answer 794

Could monitor Antifactor 10A assay. Given Subcutaneously once a day. Renally eliminated - make dose adjustments for renal patients.

Answer 795

Lowest incidence of HIT, because its the shortest molecule to react with those antibodies. Good for patients with history of HIT.

Answer 796

Used for prevention of PE and treatment of active clots. Protamine has no effect to reverse Fondaparinux effects.

Answer 797

Lepirudin Bivalirudin Argatroban

Answer 798

Based off Hirudin, which is in salivary glands of leeches that inhibit thrombin (2A) itself.

Answer 799

Inhibit factor IIa itself. Can be monitored with aPTT.

Answer 800

Argatroban, hepatically excreted

Answer 801

Lepirudin and Bivalirudin, because they're both renally excreted.

Answer 802

Used in patients going into coronary angioplastly or patients with HIT to anticoagulate them until you can get them on a new therapy.

Answer 803

Mainstay for oral anticoagulation. Racemic mixture, S-enantiomer is more potent.

Answer 804

Vitamin K antagonist; that works to prevent recycling of Vitamin K, which inhibits active Vitamin K to liver to produce new clotting factors. Factors II, VII, IX, X, protein C, and S will be inhibited to prevent formation of clotting factors. Less clotting factors in the blood means it'll take longer to form clots in blood.

Answer 805

Decrease in vitamin K dependent cofactors by 10-40%. Does not work on existing clotting factors.

Answer 806

Can't act on existing clotting factors. Don't get therapeutic effect until 3 to 5 days after starting, because the body's current factors need to be depleted first to get the warfarin effect.

Answer 807

Protein C is the first one. When you initially begin warfarin, you have a procoagulant effect bc you're losing the protein C and its natural anti-clotting factors.

Answer 808

Because protein C is removed from the blood which loses an anticlotting protein.

Answer 809

Bridge with heparin until INR reaches appropriate level. Take hearpin off and leave them on the warfarin.

Answer 810

Given orally with 100% absorption. Long half life. Metabolized in liver. S warfarin - CYP2C9 (something inhibits it, you get increased effects).

Answer 811

3-5 days to get to steady state.

Answer 812

If another drug binds to albumen tighter, it causes warfarin levels to increase in the blood. Can lead to increased effects.

Answer 813

Crosses the placenta. Possibly okay to use in breast feeding though.

Answer 814

As you increase intake of vitamin K, you decrease warfarin efficacy! Don't eat green leafy vegetables. Need to dose a person's diet. Can't change it or medication will be less effective.

Answer 815

CYP2C9 inhibition Protein binding interaction that beats warfarin. Vitamin K increase, but then drop you see increase in warfarin. Disrupt flora of gut; can have increase activity bc it could remove vitamin k. Antibiotics could do this.

Answer 816

PT and INR

Answer 817

PT measures factors II, VII, and X.

Answer 818

Inernational normalized ratio to calculate sensitivity index for good INR value. Healthy = 1 Warfarin = Target 2 - 3 Valve replacement = 2.5 to 3.5

Answer 819

Have poor activity of CYP2C9, which cause high levels of warfarin. Happens in caucasians.

Answer 820

Bleeding - won't happen if INR is in range. Reversal of bleeding is Vitamin K. Can cause skin necrosis from protein C and S deficiency. Causes birth defects in pregnancy.

Answer 821

Fresh frozen plasma with Vitamin K to reverse warfarin.

Answer 822

Bothersome to use Warfarin, because it was diet dependent and you had to monitor INR often. WIth so many drug interactions, it becomes problematic. Alternatives were used so you could monitor less when on it. Dabigatran Rivaroxaban Apixaban

Answer 823

Oral direct thrombin inhibitor; works to prevent fibrinogen to fibrin and prevents activation of factors V, VIII, XI, and XIII. Used for DVT, PE, and Afib. No routine monitoring.

Answer 824

No antidote to stop bleeding. A monoclonal antibody can reverse it, but its expensive and not a lot of places carry it.

Answer 825

Oral product; inhibits factor XA. Used for DVT, PE, and Afib. No routine monitoring is needed. Renally excreted but DO NOT NEED A DOSE ADJUSTMENT.

Answer 826

Reversed with prothrombin complex concentration; this is just plasma and clotting factors.

Answer 827

Oral Factor XA inhibitor. Used for DVT, Afib, PE. No monitoring needed.

Answer 828

Can be reversed with prothrombin complex concentrate.

Answer 829

CYP3A4 If you have CYP3A4 inhibition board, you might have increased levels which lead to bleeding. If you have an inducer, you might see decreased effects and more clots.

Answer 830

STEMI - completely occlusion of coronary vessel. NSTEMI - Non STEMI and unstable angina (angina at rest).

Answer 831

In acute coronary syndorme, thrombus is formed in the coronary vessels. Coronary vessel with plaque, which occludes the vessels. When enclosed in fibrous cap, it doesn't trigger a clot. To begin thrombus formation, you need an endothelial injury to occur either spontaneously (where plaque ruptures) or a procedural injury (during a stent placement). Once you have exposed collagen, you have PLT activation, adhesion, and aggregation occuring. PLT bind by Willebrand pathway. PLT are activated and expose IIa/IIIb receptors. Clot cascade starts. Fibrin strands form and it creates an occlusive thrombus, with very little flow.

Answer 832

PLT inhibitors and direct thrombin inhibitors are used to prevent thrombus formation..

Answer 833

Key link between tissue injury, coagulation, and platelet response. Key mediator for pathways to activate formation of fibrin and more PLT activation. Crtical mediator.

Answer 834

Injured tissue has tissue factor to activate factor 7, which is important in extrinsick pathway, which afctivates factor X and factor 2. Thrombin is important to kick off extrinsic pathway as well. Amplification of factor 2 is done and more PLT activation as well. As you propagate, more PLT are activated and more thrombin is formed to lead to clot stabilization.

Answer 835

Reestablish blood flow, relieve chest pain, prevent MI, and prevent development of HF after acute coronary syndrome.

Answer 836

Aspirin at first sign of hest pain - chew and swallow to aid in release of drug to be absorbed faster. Nitrates - short acting, sublingual nitroglycerin, which can treat symptomatic part of chest pain. Beta blockers - good for those with unstable angina or angina at rest to risk progression to MI.

Answer 837

Allergy, recent GI bleed, or recent intercranial hemorrhage.

Answer 838

Start with a sublingual therapy until in hospital where you switch to IV infusion if patient is still symptomatic. Used to treat chest pain only.

Answer 839

Hypotension, headache, reflex tachycardia, which increases oxygen demand on heart and worsens the ischemia.... Be careful who you give it to.

Answer 840

Hypotension or PDE inhibitors can cause a bigger drop in BP.

Answer 841

Start in IV followed by PO.

Answer 842

Don't start them on a beta blocker right away. Later it can reduce after effects. Caution BB if they have bradycardia, hypotension, heart block or severe reactive airway disease.

Answer 843

Opioid analgesic to manage chest pain, when unresponsive to nitrates. Used in STEMI.

Answer 844

Can cause hypotension, due to release of histamine, and allergy.

Answer 845

MONA Morphine, Oxygen, Nitrates, Aspirin. Nitrates and morphine only treat pain; no mortality benefits.

Answer 846

Work to directly activate or inactivate conversion of plasminogen to plasmin. Plasminogen is inactive, but when converted to plasmin by tissue plasminogen activator (tPA) it lyses fibrin, cleaves fibrinogen, and inhibits factors II, V, and VII. This helps clear clot more quickly.

Answer 847

Fibrinolytic; that forms a stable 1:1 complex with plasminogen and exposes catalytic site, which helps to convert active plasminogen to plasmin. CLOT BUSTER - Endogenous tissue activator can also bind to plasminogen bound to fibrin to convert to plasmin and lyse the clot.

Answer 848

Fibrinolytics; activate circulating and fibrin-bound plasminogen. Lack specificity so could cause bleeds in other parts of body. Not used in the US as much anymore.

Answer 849

Only work on fibrin bound to plasminogen, which is more specific to clots and less risk for bleeding.

Answer 850

Bleeding; give a patient tPA but causes intercranial hemorrhage. Prefer to send patients to cath lab so you're less likely to cause systemic bleeds. Without access to cath lab, these will be administered. Allergic reactions can happen because they're protein based. Leads to fever, chills, and rash with streptokinase and urokinase. Ventricular arrythmias

Answer 851

9 CI of FIBRINOLYTICS 1. Surgery within ten days including organ biopsy, puncture of vessels, trauma or cardiac resuscitation. 2. Serious GI bleed within last three months. 3. Hypertension where diastolic is greater than 110! HIGH! 4. Active bleeding or hemorrhagic disorder. 5. Previous cerebrovascular accident or active intercranial process. 6. Aortic dissection 7. Acute pericardititis 8. STK prior exposure or alelrgic reaction 9. Pregnancy.

Answer 852

Aren't used in US. Streptokinase and urokinase are older and have a greater risk for allergic reactions. Can be used in Europe though.

Answer 853

Developed from human fetal kidney tissue, hence "urokinase". Not antigenic because its human tisssue.

Answer 854

More antigenic, because its a foreign protein.

Answer 855

Put a fibrinolytic like tPA in the line to break it down. Tissue Plasminogen Activator

Answer 856

Most commonly used fibrinolytic; made by recombinant DNA technology from Chinese hamster ovary cells. WTF. They activate fibrin bound plasminogen. Used for occluded catheter, ischemic strokes, and MI.

Answer 857

Fibrolytic. | Seen used for myocardial infarction.

Answer 858

"Time is tissue" - The sooner you get drugs working, the higher the benefit. Indications include those less than 75 years of age if you get within 12 hours of onset, you can get some benefit. If after that time, they won't really work. Relatively few patients use these. Most patients go to cath lab because systemic risk of bleeds from fibrinolytic is too high.

Answer 859

Glycoprotein IIb/IIIa inhibitors; can be used before percutaneous coronary intervention (PCI)

Answer 860

P2Y12 receptor antagonist; as a clot prophylaxis with stent placement.

Answer 861

Put on heparin in conjunction with Fibrolytics or antiPLT meds.

Answer 862

ADP receptor antagonists to prevent recurrence of stenosis and PLT aggregation.

Answer 863

Early treatment is similar - MONA. Fibrinolytics are NOT recommended in STEMI because the bleeding risk is too high. GlycoproteinIIb/IIIa receptor angtaonists, used more commonly, like Abciximab. Enoxaparin preferred over heparin.

Answer 864

Ischemic heart disease and MI is a large cause of CHF. ~ Most cases. Patients with HTN and cardiomyotpathies, from alcohol or drugs.

Answer 865

Chemo drug that causes cardio myopathies.

Answer 866

Due to decreased contractility of ventricles from loss of muscle mass, hypertrophy, or dilated cardio myopathy. Manifested by reduced ejection fraction.

Answer 867

Impaired relaxation. Seen with LVH - thicker and stiffer ventricles can't relax as well or fill as efficiently. Caused by ischemic tissue as well, because theres impaired removal of calcium in cytosol which causes more contraction. Decreased ventricular filling leads to decreased CO.

Answer 868

Increase preload - blood returning back to heart. Done by sodium and water retention. Vasoconstriction occurs. SNS activation leads to tachycardia and increased contractility. Leads to LVH which worsens CHF.

Answer 869

Peripheral edema, jugular venous dystension, hepatomegaly, bloating, constipation, ascites

Answer 870

dyspnea on exertion, orthopnea, tachpnea, cough, pulmonary edema, hemoptysis

Answer 871

CHF symptoms are exacerbated at rest. Can have decreased exercise tolerance or worse symptoms at rest. Frequently, due to lack of compliance with salt and water diet or not staying on medications apropriately. Caused by arrhythmia, uncontrolled HTN, or fluid overload.

Answer 872

Limit fluid and sodium restriction to decrease symptoms. Physical activity can improve functional status and work off extra fluid.

Answer 873

Diuretics are good to get rid of fluid, but don't provide any mortality benefits in the long term. Thiazide diuretics aren't potent enough, so Looooop Diuretics are the go to drug for HF therapy!

Answer 874

Monitor the patients weight so you can detect fluid overload, which is a one pound increase in weight over several days.

Answer 875

Symptomatic relief; not a mandatory therapy. Decreease sodium and water retention and get rid of extra fluid. If patient doesn't have fluid overload or weight gain, they don't need a diuretic.

Answer 876

ACEI - decrease preload and afterload, decrease SNS activation, and prevent remodeling of left ventricle. Slows progression of disease to decrease mortality.

Answer 877

ARB is backup

Answer 878

Hemodynamic improvement, improved exercise tolerance, slower progression of disease, less hospital admissions, and prolonged survival.

Answer 879

Can acutely impair renal function (start at a low dose and titrate up), elevated potassium levels, cough, angioedema.

Answer 880

Carvedilol Metorpolol succinate XL (long form) Bisoprolol

Answer 881

Start at a low dose and in hospital, so you can monitor their perfusion. Titrate the dose up throughout six to eight weeks. Carvedilol Metorpolol succinate XL (long form) Bisoprolol

Answer 882

Improved exercise tolerance. Normally, impairs it, but by slowing heart, ventricles have more time to fill for improved exercise. Increase in ejection fraction and slower disease progression. Decreases hospitalization, need for transplant, and mortality.

Answer 883

Class 2 to $ - BB are a first line therapy, esp if they're post-MI. Also need something like ACEI to inhibit angiotensin 2.

Answer 884

Steroid based molecule used for heart failure. Works by inhibiting Na-K-ATPase. Digoxin inhibits this pump to have more sodium in the cell, which increases activity of exit pump which brings sodium out and ends with more calcium in the cell! -- Leads to stronger contractions, which is why it benefits heart failure. However, more activity is from neurohormonal effects. Using digoxin at lower concentrations, can see decrease in SNS and increase in PNS activity, resensitize baroreflex, and decrease RAAS system.

Answer 885

Leads to decrease HR, better conduction from AV node, and better pumping actions

Answer 886

0.5-1ng/mL. Higher levels lead to worsened outcomes in heat failure patients.

Answer 887

Provides symptomatic relief, improved exercise tolerance, but no survival benefit.

Answer 888

Doesn't slow disease progression. Just used with ACEI and BB to control symptoms.

Answer 889

Atrial fibrillation ot prevent clotting.

Answer 890

Need therapeutic drug monitoring. Anorexia, nausea, visual disturbance. If patient has photophobia or halo around lights, big indicator of toxicity. Yellow vision = xanthopsia.

Answer 891

Can see delirium, fatique, and abnormal dreams.

Answer 892

Digoxin induced depolarization, -- PVC, bradycardia. Nodal slowing, esp in overdose.

Answer 893

Patients with advanced AV block, severe bradycardia, PVCs or ventricular arrythmia. Hyperkalemia and WPW.

Answer 894

Digoxin Immune Fab, which is an antibody that will target digoxin. It binds to digoxin to relieve body of the toxicity. Works quickly.

Answer 895

Helps reduce mortality in grade 3 or 4 HF. Mechanism has neurohormonal inhibition and slows remodeling of LV. Spirnolactone Do not give if patient Cr < 2.5 or K>5. May cause gynecomastia. Eplenerone used to avoid gynecomastia.

Answer 896

In decompensation, they help to increase squeeze on heart or increase intotropy. Mirinone Inamrinone

Answer 897

Introptropic agents; work on PDE3 - work on heart instead of elsewhere. They increase contractility and have some vasodilation to have heart beat harder and lead to decrease in afterload. Will decrease CO.

Answer 898

Approved for short term IV use in decompensated heart failure. Helps patient during decompensation and low ejection fraction to get throug the hump and recover.

Answer 899

Intropic agent; IV infusion for acute exacerbation. Selective beta 1 agonist to increase heart rate and cardiac output.

Answer 900

Inotropic agent via IV infusion. Helps increase output from heart and activates dopamine, A, and B receptors.

Answer 901

Striated in nature. Tissues have automaticity. Electrical conduction is all or none phenomenon, because you need to reach an electrical threshold for myocytes to contract. Intercalated disks allow muscle contraction to occur between cells.

Answer 902

Starts with SA node, down to AV node, to bundle of his, where is goes to purkinje fibers to allow signal to transmit through ventricles.

Answer 903

Leak channels that allow for slow influx of sodium to reach a threshold to kick off the action potential. Atrial muscle has no automaticity so they wait for the signal to come in. SA node triggers atrial muscle.

Answer 904

Fast cells; have no automaticity. Phase 0 - inward Na currents start; signaled by action potential. Phase 1 - outward K+, inward Cl-. Lowers membrane potential. Phase 2 - Plateau effect due to inward flux of Ca2+. Makes cell more positive. Phase 3 - outward flow of K+ to reset cell for next contraction. Phase 4 - Na/K ATPase works to maintain normal potential for cells.

Answer 905

Phase 0 has rapid spike in membrane potential, because Na influx. Phase 1 has K out and Cl- going in to lower potential. Phase 2 is plateauing, because of Calcium influx. Phase 3 has potassium pushed out of cell to get back to the normal electronegativity. Phase 4 goes back to membrane potential.

Answer 906

IK channel is important to prevent QT prolongation. When it is blocked, QT prolongation will occur and it delays resetting of myocytes.

Answer 907

No matter what signal comes along to trigger, muscle is in a state where it absolutely can't contract again. Earlier on in deporlization.

Answer 908

If strong enough signal comes along, it can start up a reentrant rhythm.

Answer 909

SA and AV nodes; have automaticity to allow for cardiac conduction. Generate the intial action potential. Phase 4 - Na/K ATPase to maintain electronegativity, but there's a leaky influx of sodium. Phase 0 - when you hit a threshold, calcium influx. Phase 2 - Calcium stilll coming in, but K is going out. Phase 3 - outward flux of potassium to reset cells.

Answer 910

Outward flux of potassium allowed it to be more electronegative.... SO If you decrease outflux, you're cell is more positive and you can reach the threshold for action potential sooner.

Answer 911

Cholinergic increase outward flux of potassium making cell more negative. Lower resting potential makes the cell take a longer time to get the influx of sodium to hit for the action potential to be triggered.

Answer 912

From abnormal impulse formation - automaticity from ectopic pacemaker or changing influx/depolarization. Can also have abnormal impulse conduction.

Answer 913

Ischemic areas of heart conduct through tissue slower. Because ischemic tissue is slowed, reentrant rhythms can start, due to different in refractory period of healthy tissue to ischemic tissue. Can cause heart blocks!

Answer 914

Fix underlying and precipitating causes first, like hypoxia, ischemia, and electrolytes.

Answer 915

Work to decrease excitability. Less sodium influx has less automaticity from SA and AV node as well as fast response cells.

Answer 916

AP prolongation occurs when you prolong potassium channels. Prolonging refractory perid stops reentrant rhythms.

Answer 917

Prolong AV refractorniness and conduction, you increase energy required for atrial fibrillation.

Answer 918

Decrease slow response cells excitability.

Answer 919

Sodium Channel Blockers SVT, VT, V fib prevention and PVC prevention

Answer 920

Sodium Channel Blockers VT, V fib prevention, symptomatic ventricular beats

Answer 921

Sodium Channel Blockers Life threatening VTACH, Fib, refractory SVT.

Answer 922

Beta Receptor Antagongists SVT and Fib

Answer 923

Prolong repolarization by blocking K channels. Refractory VT, A fib, futter, SVT

Answer 924

Calcium Channel Blockers SVT

Answer 925

Good for rapid conduction from SA and AV node to ventricle. SVT, A flutter. Work on nodal tissue.

Answer 926

Useful for ventricular tachycardia, A fib, V fib.

Answer 927

Resting state of membrane prevents sodium from influxing to myocyte until you reach threshold. Sodium channels activate and then llow inward flux, which causes increase in AP. Inactivated phase - come in and close off further flux of sodium. Hasn't reached resting state, but blocks inward flux of sodium. Each class works different on chanenls.

Answer 928

Blocks channels to have slow phase 0, slow conduction, and prolong action potential. Prefer open channel to inactivated. When channel is open, they go in and inhibit. Have a slow dissociation.

Answer 929

Class 1A antiarrythmic. D-isomer of Quinine. Works by slowing conduction and prolonging refractory period to prevent reentrant rhythms, especially in ischemic tissue. Slows Phase 0 and increases threshold for excitability. Takes stronger AP to trigger cell to have action potential. Decrease automaticity in SA and AV node.

Answer 930

Has anticholinergic affects. A blocker at higher doses; may see effects on BP due to that.

Answer 931

Used to maintain rhythm in patients with atrial flutter or atrial fibrillation. Helps control ventricular tachycardia. Can be used with anticoagulants for clots in atria during atrial fibrillation or flutter.

Answer 932

CYP2D6 enzyme, when inhibit you can see higher levels of codeine and morphine.

Answer 933

N/V/D very frequently! Quinidine makes you queezy. Can induce its own arrythmia or Torsades... Torsades risk , because action potential is prolonged!!!!!!!!!!!!!!!! May cause hypotension due to alpha block effect. Thrombocytopenia is rare, but may be fatal. :( Cinochism occurs! New word.

Answer 934

Tinnitus, dizziness, and blurred vision.

Answer 935

Amide derivative of procaine; has a short duration of action. Less anticholinergic activity and alpha blocking activity. NAPA byproduct formed - has some class three activity to block potassium channels.

Answer 936

More NAPA byproduct is produced, because they metabolize procrainamide fast. Can lead to arrythmias!!

Answer 937

Hypotension, slowing of conduction, lupus like syndrome in slow acetylators! Get that warm rash, because they metabolize or acetylate slow and drug levels are high. IV version is tolerated better than quinidine. Oral form is not.

Answer 938

Like quinidine, but has more anticholinergic actions and negative inotropic affects - decreased contractility. Used for ventricular tachycardia and supraventricular arrythmias like A fib or A flutter.

Answer 939

Hypotension, antimuscarinic effects... Decreased contractility could worsen CHF. Torsades at risk.

Answer 940

Disopyramide

Answer 941

Procainamide, Disopyramide, Quinidine

Answer 942

Shorten phase 3 and decrease ectopic foci automaticitiy. They target inactive channels, but have higher affinity for ischemic tissue than normal tissue.

Answer 943

Local anesthetic used to numb areas for sutures, etc.

Answer 944

Has extensive first pass metabolism, so should be given IV. Can be given intravensouly to treat WPW, VTACH, premature beats, and Vfib.

Answer 945

Binds to open/inactive channels. More effective on sodium channels in iscemic tissues. Good for patients iwth active MI and ventricular arrythmias.

Answer 946

CNS toxicity in patients with poor hepatic function! Can see drowsiness, confusion, muscle twitches, nystagmus. Seizures can occur - this might lower threshold so don't give to patients with pmhx of seizures.

Answer 947

Analog of lidocaine that has oral availability.It decreases automaticity and conduction in ventricles. Used to treat congential long QT syndrome and prevent torsadaes. IMPORTANT.

Answer 948

N/V/tremor Blood dyscrasias, changes in granulocytes and platelets.

Answer 949

Mexiletine | Lidocaine

Answer 950

Slow phase 0 and conduction to prolong the refractory period. Affect normal heart tissue. Focuses on open channels. Ver slow dissociation.

Answer 951

Blocks sodium channels and has class 3 activity where it blocks potassium too.. Prolongs PR, QRS and QT. Long half life; can be oral or IV. PRevents PVCs.

Answer 952

Life threatening sustained ventricular arrythmias. Supraventricular arrythmias. Can only be used in patients without structural damage to the haert.

Answer 953

Blurred vision, tremor Induce a VTACH, which can be resistant to other treatments since sodium channels are blocked. Can cause bronchospasm, seizures, adn death for MI patients.

Answer 954

B blocking activity to work on SA and AV node; similar to flecainidie.

Answer 955

Can cause arrythmia; see bradycardia, bronchospasm from non-selective BB activity in drug. Decreased contractility from BB can also worsen CHF.

Answer 956

Work to slow conduction and decrease automaticity to prolong AV conduction and decrease phase 4 depolarization.

Answer 957

Non selective beta blocker to slow AV conduction and decrease speed and contracility of the heart. Can supress PVCs and membrane stabilizing effect..

Answer 958

Supraventricular arrythmias Ventricular ectopic beats MI

Answer 959

Worsen heart failure, can see heart block, hypotension, hyperglycemia, bronchospasm, heart failure, and digitalis toxicity

Answer 960

B1 seelective blcoker | less bronchospasms here

Answer 961

Given IV, short acting agent good for SVT to decrease sinus rate.

Answer 962

Prolong repolarization due to potassium efflux. Prolong phase 3, refractory period, and duration of action potential. Used to treat A fib and A flutter.

Answer 963

Very long half life of 40 days. Has a slow onset and slow elimination. May need a loading dose to get to steady state.

Answer 964

Recurrent ventricular tachycardia or fibrillation resistant to other drugs to maintain normal rate in atrial fibrillation. Replace lidocaine in MI. Lidocaine used to be used, but amdiodarone is now go to for ventricular arrythmias during codes.

Answer 965

Blocks potassium channels, inactivated sodium channels, calcium channels, and alpha and beta receptors to decrease automaticity and decrease automaticity to prolong refractory period.

Answer 966

Occur when dosed chronically; can see hypotension from alpha and beta affects. Pneumonitis, pulmonary fibrosis - fatal. Neurotoxicity, neuropathy, muscle weakness BLUE GREY SKIN COLOR photosensitivity thyroid abnormalities

Answer 967

Increases digoxin, warfarin, flecainide, phenytoin, and procrainamide levels.

Answer 968

Prolongs opening of sodium channel, which coutneracts opening of potassium channels. Prolongs repolarization and action potential.

Answer 969

Used as a way to convert A fib or A flutter.

Answer 970

Due to blocking of potassium channels, can see prolonged QT and heart block!

Answer 971

Frequently prescribed; helps maintain normal rhythm in A fib and ventricular arrythmias. Used in VA hosp. a lot.

Answer 972

Torsades and marked QT prolongation - do EKGs before hand and any time you change your dose. Eliminated by kidneys, so monitor the kidneys and electrolytes to prevent risks of torsades and other arrythmias.

Answer 973

EKG before you start and any time you change dose. Also monitor the kidney function and electrolytes to make sure you're not putting patient at risk of torsades or another arrythmia.

Answer 974

Beta blocker that inhibits potassium channels; decreases phase 4 depoarlization.

Answer 975

A flutter, A fib, ventricular tachyarrythmia

Answer 976

Torsades due to potassium blocking affects | Bronchospasm

Answer 977

Block L type calcium channels for slow av node conduction and decreased automaticity

Answer 978

Only non-DHP are here; work on vasculature, not the heart. Blocks activated and inactivated channels. Targets most active tissue causing arrythmia. Decreases AV conduction nad supresses SA node.

Answer 979

Control A fib and PSVT

Answer 980

Hypotension, edema CYP3A4 inhibition Don't use in ventricular arrythmias, sick sinus syndrome, or depressed cardiac function.

Answer 981

Natural product body makes consistently that inhibits molecules in CNS to prevent seizures by activating adenosine receptors. It inhibits hearts by blocking calcium channels. You hyperpolarize cell with potassium and prevent it from being triggered again. Can stop heart for two to three seconds. Can give to heart to reset itself and get rid of arrythmia.

Answer 982

WPW and paroxysmal supraventricular tachycardia

Answer 983

Flushing, shortness of breath, burning in chest.

Answer 984

Has a short half life, so needs to be administered apropriately. Push drug fast via IV and flush with fluids afterwards to ensure it reaches heart ASAP

Answer 985

Works to slow AV conduction, inhibits calcium channels in AV node, and increases parasympatheic tone and decreases SNS. Can induce heart block

Answer 986

Slow ventricular rate Induce heart block DO NOT use with calcium channel blcokers or beta blockers, becuase you odn't wanna decrease the activity of the nodal tissue too much.

Answer 987

N/V/D anorexia, CNS confusion, delirium, headache, seizures.

Answer 988

Used to treat Torsades de Pointes via IV to get patient out of rhythm. Can cause bradycardia, flushing, headache, and respiratory paralysis.

Exam 2 - ENT, pulm, cardio Flashcards

(1021 cards)