Dr. Morgan Study Guide. Flashcards
1
Q
Side effects of minoxidil and hydralazine and nitroprusside. What drugs usually have to accompany minoxidil and hydralazine and why?
A
Hydralazine:
- reflex tachycardia (barrorecptor reflex) fixed with beta blocker
- volume expansion (use diuretic)
- Systemic Lupus Erythematosus like syndrome
Minoxodil:
- volume expansion
- reflex tachycardia
- **hypertrichosis (hair growth)
- Pericardial Effusion (Tamponade)
Need Beta Blocker for reflex tachycardia
Need Diuretic for volume expansion
2
Q
71.-Long term pharmacologic therapy s/p MI-
A
Beta Blockers Antiplatelet drugs ACEI Anticoagulants- ASPIRIN STATIN
ASA contraindicated- AFib, LV, Trombus wall motion abnormalities, severe Systolic Dysfunction
3
Q
70.-Lidocaine in acute MI-
A
ventricular dysrhythmias- the major cause of death following MI treated with lidocaine IV. 60% of Deaths- Don’t use.
4
Q
69.-Pregnancy and HTN. Which classes of drugs are contraindicated?
A
Chronic HTN during pregnancy leads to a placental abruption
give methyldopa alpha 2 agonist
5
Q
Patients who have been diagnosed with HTN but have other compelling indications such as:
Stable Angina or arrhythmia
Unstable Angina
S/P MI
A
Beta Blockers
6
Q
Patients who have been diagnosed with HTN but have other compelling indications such as:
BPH
Diabetes
CHF
ISH
A
BPH (alpha 1 antagonists, SINS)
Diabetes (ACE Inhibitor, ARB)
CHF (BETA OR ACE or ARB)
ISH (Thiazide and DHP- PINE)
7
Q
Stage A drugs
A
Cease high risk behaviors
Treat disease states that compound risks
8
Q
Stage B drugs
A
Cease high risk behaviors
Treat disease states that compound risks
Add ACE I / ARB plus BETA Blocker
9
Q
Stage C Drugs
A
ACE I / ARB
Diuretics
Digoxin
Isosorbide or Hydrolazine (to replace ACE/ARB)
Drugs to avoid stage C- Dysrhythmic agents- cause death make worse NONDHP DHP ONLY Amlodipine and Felodipine NSAIDS-- cause NA H2o retent
10
Q
68.-Lifestyle modifications for HTN-
A
Therapeutic Lifestyle Changes
*** Weight loss #1 way to help BP Sodium Resriction DASH Diet Alcohol Restriction Excercise
Smoking Cessation is a cardiac risk factor
11
Q
- -Pre-load vs Afterload -
A
Cardiac preload (veins)-how much volume gets to the heart reduced preload: over diuresis, dehydrated,vasodilater.
cardiac afterload (arteries):the force that the heart has to overcome to pump blood…the greatest determinant is arteriole vasoconstriction and vasodilation
12
Q
Name the afterload reducers-
A
Name the afterload reducers- Minoxadil Hydralazine DHP (Arteriole Vasodilators) Nifedipine sins
ADR=
Pheripheral Edema
Reflex Tachycardia
Volume Expansion
13
Q
Beta Blockers- NON DHP Verapamil and Diltiazem
SINs
Sodium Nitroprusside
A
Decrease Preload
14
Q
American College of Cardiology
A
based on the progression of the disease
Stage A- best- pt is at risk for developing HF No Symptoms or structural disease
Stage B- Structural Damage but no symptoms (remodeling)
Stage C- worst- advanced Structural damage- symptoms even at rest
Never go backwards so once a C never go back to a B ect..
15
Q
Aldosterone Antagonists Spironalactone and Eplerinone-
A
increase life expectancy NYC 3-4 symptoms
16
Q
New York Heart Association classification of CHF vs. American College of Cardiology
A
New York Heart Association
Class 1- HF no symptoms
Class 2 - Symptoms that worsen with exertion
Class 3- Minimal Exertion to get fatigued
Class 4- Symptoms at rest
17
Q
63.-Staging HTN
A
stage 1 HTN = __1____ drugs
Stage 2 HTN = ___2___ drugs
Normal BP - <120/80
Pre-hypertension 120/80 to 139/89
Stage 1 HTN- 140/90 to 159/99
Stage 2 HTN- greater than or equal to 160/100
18
Q
- -Digibind
A
Digoxin-can improve exercise intolerance, but does not improve their mortality rate or make you live longer. Try everything else then Digoxin. Positive ionitropic efects on the heart. makes the heart more efficient. Improves functional status, Decreases heart rate.
Digoxin and Potassium relationship. f K is even a little bit low, it can cause Digoxin Toxicity. This drug is very sensitive to low K.
It causes Arrhythmias and is a very low therapeutic index drug.
What would you see with Digoxin Toxicity. Bradycardia Arrhythmias GI: anorexia, nausea, vomiting CNS: fatigue and visual disturbances.
What is Digoxin’s therapeutic Range- 0.5 - 0.8 ng/ml
19
Q
Formula for arterial BP?
A
Arteriole BP= CO x PVR
20
Q
Formula for cardiac Output?
A
CO= SV x HR
21
Q
60.-Positive vs. negative symptoms of Schizophrenia-
A
Positive Symptoms-exageration or distortion of normal function such as hallucinations, delusions, paranoia, aggitation, combativeness, disorganized speech ect. Much easier to treat with drugs.
Negative Symptoms-loss of normal function such as: social withdrawl, emotional withdrawl, lack of motivation, poor self care, poor judgement, poverty of speech, flat affect, ect.. Meds don’t help.
Cognitive Symptoms-disordered thinking, memory difficulties, and focusing abilities.
22
Q
59-Michaelist Menten Pharmacokinetics-
A
Phenytoin-MM- mecalus mentin, small dosage adjustments can make tremendous jumps once it reaches the saturation point.
Which means that the metabolizing capacity of the liver has a saturation point and after it reaches that point the medication goes straight into the blood stream.
So you have to be very careful when dosing this medication.
**Phenytoin serum target-
10-20 mcg/ml
23
Q
- -Side effects of Tri-Cyclic antidepressants
A
Tricyclic Antidepressants ADR’s
Amitripyline
Desipramine
Nortriptyline
Orthostasis: from alpha1 blockade
Anticholinergic Side Effects: from muscarinic Blockade
Sedation: from histamine Blockade
Cardiac Toxicity- overdose and you die of ahrhythmia
Seizures: lowers the seizure threshold
Mania: not for use alone in a Bi-Polar Patient. Must have a mood Stabilizer with it. Toxicity of Tricyclics- 8 times the therapeutic dose.
If you give more than 8 days at a time, the patient will be able to overdose if suicidal.
common way to commit suicide, especially in women
go to sleep and never wake up
24
Q
Atypical Antidepressants
trazadone, ADR
A
causes Priapism
very sedating (sleep aid)
25
Atypical antipsychotics cause diabetes:
diabetes can develop or be exacerbated by atypical antipsychotics.
Causes metabolic syndrome. The hallmark signs of metabolic syndrome are overweight, high blood pressure, low HDL, high sugar, and their triglycerides are high.
This increases the patient's risk for coronary artery disease because diabetics are 4 to 5 times more likely to develop coronary artery disease than normal patients.
Also Cause Weight Gain
26
Adverse effects of Lithium during therapeutic Levels
```
GI issues (transient)
Polyuria
Polydipsia
Mild Tremor
Renal Toxicity
***** Hypothyroid disease- Medication induced
```
Pregnancy category D- Not that great
27
Adverse effects of Lithium during toxicity
```
Confusion
EKG changes
Fasciculations
seizures
hypotension
coma
death
```
28
phenobarb ADR
1. it is very sedating
| 2. potentially lethal due to suicide risks.
29
57. -Low potency vs. high potency antipsychotics-
```
Low potency (Chlorpromazine)- This has more peripheral type side effects with it (outside of the CNS) such as sleepyness, or anticholinergic side effects.
High potency (Haloperidol)-.This is cleaner, but have more movement disorders associated with it. Such as psudoparkinsonism.
```
When deciding which Schizophrenic medication to use, you typically base it off of what type of side effects do you want the patient to have.For example: if a patient is agressive, you might want to give them a Low Potency (Chlorpromazine) because it will make them sleepy thus helping the agression.
You might use a high potency agent (Haloperidol) if a patient has urinary retention problems because the low potency agents have more anticholinergic side effects that would thus make the urinary retention worse.
30
56.-Anticholinergic Side Effects-
anti-cholinergic side effects are from muscarinic blockade.
You are more likely to see these effects with low potency agents like Chlorpromazine.
These effects are opposite of muscarinic man. No spit, urinary retention, blurred vision, constipation, tachycardia, and cannot sweat.
31
55. Neuroleptic Malignant Syndrome-
rare but serious, risks are worse with high potency drugs such as haloperidol.
```
The symptoms of neuroleptic malignant syndrome are:
leadpipe rigidity,
high fever,
sweating,
autonomic instability,
dysrhythmias,
altered consciousness,
seizures,
coma
death.
```
32
The treatment for neuroleptic malignant syndrome
syndrome:supportive measures. *****And immediate withdraw of antipsychotic agents. Minimizing the recurrence of neuroleptic malignant syndrome: do not reinitiate antipsychotic agents for at least two weeks or more. Consider the lowest dose possible, and possibly switching to an atypical antipsychotic agent.
33
54 -Seretonin Syndrome-
****What are the signs and symptoms of serotonin syndrome and what should you do to fix it? occurs within the first 3 days of initiating therapy and can kill you. Symptoms are:
```
Altered Mental Status
Incoordination
Myoclonus (seizure)
Hyperreflexia
Excessive Sweating
Tremor
Fever
```
****If these symptoms happen. must stop the SSRI immediately.
(caused by Fluoxetine (SSRI)
34
53-Anti-Seizure medications. Inhibitors vs inducers
Name the Antiseizure medications that are Enzyme Inducers:
Phenytoin, Phenobarbitol, and Carbamazepine
These cause warfarin levels to decrease. Need to bump it up
Name the Antiseizure Medication that is an Enzyme Inhibitor.
Valproic Acid.
Causes warfarin to build up to toxic levels need to decrease
35
52 -Phenobarbital side effects including respiratory side effects-
Phenobarbitol serum sodium target, 20-40 mcg/ml, There are two reasons we don’t use Phenobarbitol much anymore:
1. it is very sedating
2. potentially lethal due to suicide risks.
Pharmacokinetics of Phenobarbitol-Enzyme Inducer.
36
51.-Levadopa-Carbidopa mechanisms of action-
carbidopa has no therapeutic effects alone. This means that you can give somebody a boat load of carbidopa and it will not do anything.
It inhibits dopa-decarboxylase in the periphery which allows more of the inactive form of levodopa to cross through the blood brain barrier where it is then metabolized into dopa, thus increasing the dopamine levels in the brain.
37
50. -Lithium side effects and significant drug interactions-
Therapeutic Lithium levels 0.4 - 1
Plasma levels of lithium while being treated for mania- 0.8 - 1.4
```
ADR:
GI issues (transient)
Polyuria
Polydipsia
Mild Tremor
Renal Toxicity
***** Hypothyroid disease- Medication induced
```
```
What can cause lithium levels to rise in a patient:
Age due to loss of kidney fuction
NSAIDS
Cold Medications
Dehydration
Diuretics
And Low Sodium Diets
```
Pregnancy category D- Not that great
38
49.-MAOI inhibitors. Food and drug interations-
Monoamine Oxidase inhibitors (MAOI)
Phenelzine- ADR's-
CNS excitation
Orthostasis
***Hypertensive Crisis- there are certain drugs and food interactions that can cause increased levels or norepinepherine to be released into the body (causing ahrythmias and death)
Foods containing TYRAMINE are a trigger, and include Wines, aged meats and cheeses
These people have a strict diet
Drug interactions:
Ephedrine and Amphetamine- causes hypertensive crisis
Tricyclic Antidepressants
SSRI's- leads to serotonin syndrome
Meperidine (demerol) leads to hyperpyrexia
39
48.-Tolerance definition and application
What is tolerance?
Tolerance, is a reduced responsiveness with prolonged exposure.
For example a person that has chronic pain such as cancer pain, their pain medication will stop working with prolonged exposure so it is absolutely appropriate for the doctor to crank up the dose to help them not be in pain.
40
47.-Carbamazepine side effects and monitoring
Carbamazepine
serum target level- is 4-12 mcg/ml
MOA- inhibits sodium channels
Unique Pharmacokinetics of Carbamazepine-it causes autoinduction.
Over time, the drug causes induction of itself.
so the metabolism causes the liver to eat iself(carbamazepine) faster.
Can make 1/2 life go from 50 hours to 15.
Adverse drug reactions of Carbamazepine-Ataxia, **hematologic Depression (need to monitor CBC), agranulocytosis, SIADH (check serum sodium, concentrates urine),
41
46. -Acute Dystonia-
Acute Distonia, typically happens quickly after administration of an antipsychotic agent.
You might hear a patient cry out and look over at them and they are twisted with their tongue hanging out.
It is a severe spasm of the tongue, face, neck, and upper torso. It is very painful.
Treatment is IM anticholenergic such as Benydryl, or Benztropine. These work very quickly.
42
45.-Potassium sparing diuretics. Identify them and know why they are used-
Aldosterone Antagonists, Spironolactone and Eplerenone
non-aldosterone antagonists- triamterene and amiloride
MOA- block sodium potassium pumps
USES- electrolyte benefits
43
-Aldosterone vs. ADH -
Aldosterone holds on to sodium and water and excretes K ,
ADH holds on to water.
44
43. -CHF potential drug if intolerant to ACEI or ARBS?
hydralazine or isosorbide
45
Name the ARBS (Angiotension 2 Receptor Blockers)
SARTANS
Losartan and Telmisartan
MOA- Does not interfere with the production of of angiotension 2 just blocks the receptor site.
Use SARTAN when you have ACE Cough, possibly angioedema
ADR-
Hyperklemia
Can still cause cough
Can Still cause Angioedema
CATEGORY X
CONTRAINDICATED- Renal Artery Stenosis
46
Name the aldoserone antagonists
potassium sparing diuretics
Spironolactone and Eplerenone (less Hormonal)
MOA- selectively blocks aldosterone receptors, eliminate volume expansion
***Uses-
HTN
HF NYC 3-4 (trophic agent)
ADR's Hypoklemia, Gynecomastia, Mentral Irregularity, Deep Womans Voice, Hairgrowth
47
What class are PRIL's?
Ace Inhibitors
MOA- Reduces levels of Angiotension 2, Dilates arteries and veins. Preload and afterload reducer.
Lisinopril, Captropril
```
ADR-
Hypotension
HYPERKALEMIA
cough
angioedema
```
DRUG OF Choice for diabetic nephropathy and heart failure.
CONTRAINDICATED- Renal Artery Stenosis
CATEGORY X
48
43. -CHF potential drug if intolerant to ACEI or ARBS?
Aldosterone Antagonists, Spironolactone and Eplerenone
????
Or Hydralazine or isosorbide not sure
49
42. -CHF front line therapies?-
Beta Blockers, Ace and Arbs
50
41. Which are drugs of choice?
| - ACEI side effects and monitoring parameters-
Ace Inhibitors
MOA- Reduces levels of Angiotension 2, Dilates arteries and veins. Preload and afterload reducer.
Lisinopril, Captropril
```
ADR-
Hypotension
HYPERKALEMIA
cough
angioedema
```
DRUG OF Choice for diabetic nephropathy and heart failure.
CONTRAINDICATED- Renal Artery Stenosis
CATEGORY X
51
40.-Bipolar disorder treatment options. Drug of choice.
Valproic Acid
52
39. -Angina- how do our drugs relieve Angina?
Decreases pre-load- Pharmacotherapy is based on fixing demand issues. not supply. That is fixed with bypass or stents.
Drugs that decrease demand are:
Nitrates- work through preload by dilating the veins.
Beta Blockers- decrease HR, Contractility
Calcium Channel Blockers-
- Non-DHP= Deltiazem and Verapamil- decrease HR and contractility and dilate arteries which decrease afterload.
- DHP CCB- Nifedipine- All of the PINES, work purely on dilating arteries which is afterload reducers.
Antilipemics- Statin therapy- stabilizes the lesion and prevents it from progressing. Also can cause regression of the lesion.
ASA- Aspirin
53
38. -Where is heparin derived from?
secured from the lungs of cattle and intestines of pigs.
54
37. -INR and therapeutic range for most all indications-
1-2 is normal INR
55
36. -aPTT and therapeutic heparin range-
aPTT: want to thin blood enough to suppress coagulation, but not so much that you excessively risk hemorrhage.
- To do this, we measure the activated partial thromboplastin time (aPTT).
- Normal is 40 seconds.
- Therapeutic heparin is 1.5-2 times the normal (approx 60-80 seconds). Most hospitals have an algorithm for heparin dosing based on the body weight (bolus dose) and aPTT level.
- Initially, frequent monitoring is necessary (Q4-6 hours), but afterwords, can reduce to Q-day.
56
35.-Low Molecular Wt Heparins monitoring parameters-
CBC- if they are on it for a long time. to look at platelets and HH to check for bleeding. Do not check aPTT with lovanox
57
34. -Treatments of acute MI which have been proven to reduce mortality-
Antiplatelet and Beta blockers
58
32. -warfarin toxicity and treatment-
Give Vitamin K and hope they don’t die. Vitamin K- orally, IV, or Sub Q
FFP- If there is a serious bleed (fresh frozen plasma)
59
31. -STEMI diagnosis-
Has to have ST elevation
60
30. -nitrate free interval and tolerance-
When you start using nitrates, you have to have sulfhydyl in order for them to work.
You only have limited amount of sulfhydyl. In the first 24 hours you will run yourself out of sulfhydyl which is why you cannot use it as BP medication.
This is why you cannot list Nitrates as an Antihypertensive in someones chart.
To avoid tolerance, you have to have a nitrate free period of at least 8 hours per day.
Typically at night
do not abruptly discontinue the med. can cause vasospasm.
61
29. -niacin counseling-
**1. Start low and go slow
**2. Take it with food.
**3. Take an NSAID or Aspirn 30 min before Niacin
**4. Avoid taking with alcohol and hot or spicy foods or beverages.
**5.After a week or 2, you will become tolerant to that dose. Teach them to take IR at night.
**6. Avoid Interruption of therapy. If you run out of it, you have to start over with your tolerance level. (flushing, burning, itching)
7. 2 grams per day cap on SR niacin. Not a cap on IR Niacin
62
28. -Initial targets of choice for hyperlipidemia
LDL unless Triglycerides over 500
63
27. -Best drugs for LDL redx?
Statins
64
TG redx?
Fibrates
65
HDL improvement?
Niacin
66
26. -NCEP (ATP3) Risk Factors
1. Cigarette Smoking- 1 cig within the last month would count.
2. HTN- 140/90 - even if on BP meds and well controlled.
3. LOW HDL- if less than 40
4. Positive Family History for CHD
5. Age- male 55, female 65
This is the one negative risk factor. (meaning it is a good thing)
6. If HDL >= 60
67
25. -NCEP (ATP3) Risk Equivalents
Patients with:
1. Peripheral Vascular Disease
2. Carotid Artery Disease
3. Type 2 Diabetes
4. AAA
5. Framingham of <20% risk
These patients, along with pre-existing CHD are at greatest risk for an MI
68
24. -Myositis and rhabdo-
From Statins
1. Myalgia (1-5%)- myalgia simply means that something is going on with the muscles.
2. Myositis- (Moderate elevation in CPK) Inflammation of the muscles.
- Large muscles like thighs and butt, back.
- Is terrible, like being beaten with a bat.
- It is BILATERAL, usually associated with a fever.
- Older people show signs of weakness and less pain
3. Rhabdomyolysis- this is where muscles start to break down. It can lead to kidney failure. (Very rare)
4. Transaminase Elevation- Approx 0.5-2%.- which is AST/ALT. When these are elevated it means that the liver is inflamed or irritated. Not indicative of function. Very Rare.
- For Liver function we test- Albumin is low, Billirubin is high, PT/INR is high. Those are indicative of liver function.
69
23. -Protamine sulfate-
Antidote for Heprin Toxicity
70
22. -Immediate release Niacin vs. sustained release. Differences.
Flushing (More common with IR)
GI Toxicity
Hepatoxicity (more common with SR)
Hyperglycemia - only 1/3 of diabetics will require any adjustment in dose
Hyperuricemia- (can cause gout)
71
21 -significant gemfibrozil drug interactions-
**It can cause irritation of the liver. So need to check baseline transaminase levels.
-If the patient complains of flu like symptoms or abdominal pain, you would want to repeat the transaminase levels and compare to the baseline.
**It can also produce myopathies similar to statins. You can use fibrates in combination with statins so that can double the risk of myalgias.
-need to council the patient on the symptoms.
72
20 -Framingham Risk Assessment-
High Risk Patient Population includes:Patients with CHD and CHD risk equivalents.(10 year risk of MI of >20%)Their LDL goal is < 130
Low Risk Patient Population includes:0-1 Risk Factor (10 Year risk of <160
73
-Counseling for trimethoprim-sulfamethoxazole therapy
drink 8-10 glasses of water a day while taking it.
74
-1st vs 4th generation cephalosporins. What are the differences?
AS one progresses from 1st generation to 4th generation
1. Increased activity against G- rods
2. Increased resistance to beta lactamase
3. Increased ability to penetrate the CNS (Meningitis).
75
-3rd generation cephalosporin that would be appropriate if Pseudomonas was a consideration-
CEFTAZIDIME IS THE ONLY ONE THAT HAS EXCELLENT PSEUD COVERAGE, AND EXCELLENT CNS PENETRATION.
76
-If a penicillin allergy, what antibiotics CAN you take and CANT you take
MRSA- Severe PCN Allergy- Give Vancomysin
Quinupristin / Dalflopristin (Synercid)- Safe in PCN allergic patients.
77
Macrolides- Erythromycin, Azythromysin, Clarithromycin
Enzyme inhibitor- caution with the open Theophylline, carbamazepine, and Warfarin. ( Erythromycin primary, but watch for all. )
Increases Warfarin
78
Rifampin
Inducer of CYP450
Decreases Warfarin
79
Remember all inhibitors except
Rifampin
80
Quinupristin / Dalflopristin
Sulfonamides and Trimethroprim(Synercid)
Inhibit CYP450
81
-Common upper respiratory pathogens-
H.Flu / Moraxella / Strep Pneumo
82
Bacteriostatic-
supperss growth, but don’t kill
83
Pathogen-
overgrowth or introduction of a new bacteria that causes an infectious response to the host
84
Superinfection-
secondary infection with resistant bacteria.
85
Nosocomial infection-
infection acquired in hospital/ nursing home. Typically very drug resistant.
86
Selective toxicity**
the ability of a drug to injure a target cell or organism without injuring other cells or organisms that are not targeted**
87
Selective toxicity** the ability of a drug to injure a target cell or organism without injuring other cells or organisms that are not targeted**
Disruption of the Bacterial Cell Wall:
Inhibition of enzymes unique to the bacteria:
Disruption of protein synthesis:
88
-Antibiotics with excellent anaerobic coverage-
Clindamycin-
| Metronidazole-
89
-Clavulanic Acid and Tazobactam. What are they for? What do they do? How does this help or hurt the antibiotic?
E.BETA LACTAMASE INHIBITORS (not ABX)
1. CLAVULANIC ACID, TAZOBACTAM, AND SULBACTAM
2. MOA: Inhibits beta lactamase. Combined with PCNs to extend their spectrum to some beta lactamase bacteria (staph aureas, Staph Epi, B. Frag, Proteus, H.Flu).
90
Anti-staph penicillins-
NAFCILLIN -INDICATED for PCNase producing staph (staph aureus and staph epi
91
Enterococcus & Staph A.
Gram positive Cocci
92
Neisseria Gonococcus-
Gram Negative Cocci
93
E-Coli & Psudomonas
Gram Negative Rods
94
Signs of a worsening vs resolving infection?
A. Monitoring Clinical Response
1. Fever Curves
2. WBC: Bands
3. Regression of Erythema (For Tissue Infections)
4. Improvement in Chest Xray for Pneumona
5. General Improvement in health Status
95
prophylactic antibiotic usage. When is it appropriate?-
Prophylactic Antibiotic Use- ALMOST NEVER INDICATED EXCEPT
1. Surgery- ex Cefazolin pre surgery
2. Bacterial Endocarditis- individuals with congenital, valvular heart disease, or prothetic valves take antibiotics before dental procedures and surgery
3. Neutropenia- ex Bactrim DS in AIDS Patients to prevent Pneumonia
4. Influenza Outbreaks- Amantadine/ Ramantadine
96
-Two Drug Bug?
PSEUDOMONAS- usually nonpathogenic. Very resistant. TWO BUG DRUG.
97
Post?Antibiotic Effect
Aminoglycosides: Drugs: Gentamicin, Tobramycin, Amikacin.
Postantibiotic Effect= bactericidal activity persists several hours after serum levels have dropped below ***MBC.
98
Disk Diffusion Test-
DISK DIFFUSION- inoculating an agar plate, then place discs that contain different ABX on the agar plate. The degree of sensitivity is proportional to the size of the bacteria free zone around the disk.
99
-Cidal vs Static antibiotics-
Bactericidal- bacteria killers
| Bacteriostatic- supress growth, but don’t kill
100
Spontaneous Mutation vs Conjugation-
Spontaneous Mutation- random changes in a bacterial DNA. Leads to low level resistance. Additional mutation leads to greater resistance.
CONJUCATION- BACTERIA SEX- where bacteria “communicate” to one another and share/transfer DNA that leads to resistance (sometimes multi-drug resistance). Can even share with our normal flora. Takes place primarily with GRAM-NEGATIVE BACTERIA.
101
Broth Dilution Test-
Bacteria are grown in a series of tubes containing different
concentrations of different antibiotics. We can establish:
Minimum Inhibitory Concentration (MIC)- Lowest concentration of an antibiotic that produces complete inhibition of bacterial growth.
Minimum Bactericidal Concentration (MCB)- lowest concentration of drug that produces a 99.9% decline in the number of bacterial colonies.
102
Adjunctive Drug Therapy
ACEI after STEMI reduces short and long term mortality because of remodeling
PRILS
103
Adjunctive Drug Therapy
GPIIb/IIIa inhibitor used with ABCiximab for PCI
104
Adjunctive Drug Therapy
Clopidogrel (PLavix) ADP platelet receptor blocker
Aspirn
105
Adjunctive Drug Therapy
Heparin
Thrombolytics
PCI
to reduce the risk of re-thrombosis
106
Once you get to end stage heart failure, When you begin to have structural damage, need to have what medications right away
ACE or ARB
107
If you have NY Heart Failure class 3 or 4 you are given what drug?
Aldosterone Antagonists
Spironolactone and Eplerenone
108
What are the drugs of choice for heart failure?
Ace and arbs
| Beta Blockers
