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Pharmacology > Exam 7 > Flashcards

Exam 7 Flashcards

1
Q

Rapid acting insulin preps

A
  1. Rapid acting
  2. only insulin suitable for IV
  3. slower than native insulin (due to hexamer formation)
  4. time course similar to normal meal induced peak insulin
  5. SE: hypoglycemia, weight gain, allergic rxn, insulin resistance, atrophy of subQ fatty tissue at injection site, increase risk of CA
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2
Q

Humulin R

A
  1. Rapid acting insulin prep
  2. human sequence insulin
  3. only insulin suitable for IV
  4. Onset .5h, Peak 2-3h
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3
Q

Novolin R

A
  1. Rapid acting insulin prep
  2. human sequence insulin
  3. only insulin suitable for IV
  4. Onset .5h, Peak 2-3h
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4
Q

Insulin aspart

A
  1. Rapid acting insulin prep
  2. B28 proline replaced by aspartic acid
  3. Onset .25h, Peak .5-1.5
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5
Q

Insulin gluisine

A
  1. Rapid acting insulin prep
  2. B3 asparagine replaced by lysine residue
  3. B29 lysine replaced by glutamic acid residue
  4. Onset .25h, Peak 0.5-1.5h
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6
Q

Insulin lispro

A
  1. Rapid acting insulin prep
  2. normal proline-lysine dipeptide. positions B29 and B28 are reversed
  3. Onset .25h, Peak .5-1.5h
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7
Q

Intermediate acting insulin preps

A
  1. human sequence insulin aggregated with protamine and zinc (requires time to breakdown)
  2. action is more unpredictable
  3. can get mixtures of regular and NPH insulin
  4. SE: hypoglycemia, weight gain, allergic rxn, insulin resistance, atrophy of subQ fatty tissue at injection site, increase risk of CA
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8
Q

Humulin N

A
  1. Intermediate acting insulin prep
  2. decreased amount of injections required to control bg
  3. onset 1-4h, peak 4-9h
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9
Q

Novolin N

A
  1. Intermediate acting insulin prep
  2. decreased amount of injections required to control bg
  3. onset 1-4h, peak 4-9h
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10
Q

Insulin glargine

A

LONG ACTING INSULIN PREP

  1. asparagine at A21 replaced by glycine
  2. 2 arginines added to C terminus of B chain
  3. Soluble at pH 4, but poor at 7 (forms precipitant in interstitial fluids)
  4. SE: hypoglycemia, weight gain, allergic rxn, insulin resistance, atrophy of subQ fatty tissue at injection site, increase risk of CA
  5. designed to provide background insulin replacement
  6. onset 1-4h, duration 24-36h
  7. SE: hypoglycemia, weight gain, allergic rxn, insulin resistance, atrophy of subQ fatty tissue at injection site, increase risk of CA
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11
Q

Insulin detemir

A

LONG ACTING INSULIN PREP

  1. threonine at B30 omitted and C14 fa chain is attached to aa B29
  2. long acting dt self association at injection site and binding albumin in blood
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12
Q

Metformin

A
  1. Biguanide
  2. not bound to proteins
  3. taken 2x daily, or extended release
  4. 1st line tx for Type II
  5. prevents hyperglycemia but doesn’t induce hypoglycemia or weight gain (Euglycemic agent)
  6. decrease hepatic gluconeogenesis thru AMP activated protein kinase in hepatocytes
  7. can be used in conjunction
  8. decrease LDL/VLDL, decrease vascular disease, may decrease certain types of CA
    9: SE: GI disturbance (dose related), Lactic acidosis (rare but fatal)
    10: CONTRAINDICATIONS: any decrease in drug elimination or decrease tissue O2 predispose to lactic acidosis. alcoholism, renal hepatic, hypoxic pulmonary dx
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13
Q

Glyburide

A
  1. Sulfonylurea
  2. 2nd gen (1st gens less potent, longer t1/2)
  3. highly bound to plasma protein
  4. HAS LONGEST HALF LIFE=10h
  5. metabolized by liver
  6. taken 1 or 2x daily
  7. “insulin secretagogue”- requires functioning B cells
  8. only useful in early Type 2
  9. increase insulin release from B cells.
  10. inhibits K-ATP channel complex on B cell. depolarization of B cells. influx of Ca. insulin release
  11. can be used in combo
  12. SE: hypoglycemia, weight gain (increased appetite), Sulfur allergy, LONG TERM increase in CV mortality
  13. CONTRAINDICATIONS: hepatic, renal dx, pregnancy, breastfeeding, those at risk for hypoglycemia
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14
Q

Glipizide

A
  1. sulfonylurea

2. SHORTEST HALF LIFE=2-4h

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15
Q

Repaglinide

A
  1. Meglitide
  2. Rapidly aborbed in GIT
  3. Half life of 1 hr
  4. HIGHLY BOUND TO PLASMA PROTEINS
  5. insulin secretagogue. increase insulin release from b cell. inhibit B cell K-ATP channels.
  6. PREPRANDIAL DOSING (rapid action)
  7. can be used with sulfur allergies
  8. can be used in combo
  9. SE: hypoglycemia
  10. CONTRAINDICATIONS: hepatic, renal dx
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16
Q

Nateglinide

A
  1. Meglitide
  2. safer in patients with reduced renal fxn
  3. Less frequent hypoglycemia
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17
Q

Pioglitazone

A
  1. Thiazolidinedione
  2. HIGHLY BOUND TO PLASMA PROTEINS
  3. taken 1x daily
  4. max effect at 1-3 mo dt gene expression
  5. tx for T2DM
  6. increase insulin sensitivity in target tissues
  7. PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA AGONIST (involved in lipid/glu metab)-expressed in adipose
  8. increase sens to nsulin stimulated uptake of glu and fa. altered adipokine production (leptin)
  9. increased in skel muscle and liver as well
  10. decrease tg levels and slight increase in HDL and LDL
  11. can be used in combo
  12. SE: weight gain, edema, osteoporosis, increase in CHF.
    SPECIFIC: increased risk of bladder CA
    CONTRAINDICATIONS: pregnancy, hepatic, heart dx.
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18
Q

Rosiglitazone

A
  1. Thiazolidinedione
  2. HIGHLY BOUND TO PLASMA PROTEINS
  3. taken 1x daily
  4. max effect at 1-3 mo dt gene expression
  5. tx for T2DM
  6. increase insulin sensitivity in target tissues
  7. PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA AGONIST (involved in lipid/glu metab)-expressed in adipose
  8. increase sens to nsulin stimulated uptake of glu and fa. altered adipokine production (leptin)
  9. increased in skel muscle and liver as well
  10. decrease tg levels and slight increase in HDL and LDL
  11. can be used in combo
  12. SE: weight gain, edema, osteoporosis, increase in CHF
    SPECIFIC: BLACK BOX WARNING FOR INCREASE CV EVENTS
    CONTRAINDICATIONS: pregnancy, hepatic, heart dx.
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19
Q

Acarbose

A
  1. a-glucosidase inhibitor
  2. minimally absorbed
  3. taken prior to each meal
  4. tx of TYPE II
  5. inhibitor of enteric a-glucosidase (bd complex carbs and saccharides)
  6. only monos can be absorbed…delays postprandial absorption of glucose
  7. breakdown of postprandial glucose increase (should be given emergency source of glucose)
  8. can be used in combo
  9. CAN BE USED IN PREDIABETICS
    10: SE: GI (bacterial metab of carbs in colon), will decrease with time
    11: CONTRAINDICATIONS: IBD, renal, GI dx
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20
Q

What diabetic drug can also be used in prediabetics

A
  1. Acarbose. a-glucosidase inhibitor
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21
Q

Colesevelam

A
  1. Bile acid sequestrant
  2. not absorbed systemically
  3. 2x daily
  4. Type II as adjunct to lifestyle change
  5. MOA unknown (decreased glu abs dt farnesoid rec.)
  6. SE: GI, incrase plasma triglycerides, decrease med absorption-vitamins, levothyroxine, OCPs, phenytoin, verapamin, warfarin)
  7. CONTRAINDICATIONS: hypertriglyercides, hx of pancreatitis, GI issues
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22
Q

Pramlitide

A
  1. Amylin Analogue (peptide secreted with insulin from b cells. acts at amylin receptor in hindbrain)
  2. PREPRANDIAL SubQ injection. don’t mix with insulin
  3. NOT HIGHLY BOUND
  4. metabolized/excreted by kidney
  5. used as adjunct to insulin (T1 and 2)
  6. insulin sparing agent. suppresses glucagon release, delays gastric emptying, promotes satiety
  7. can decrease mealtime insulin by 50%)
    8: SE: hypoglycemia, GI, weight loss
    9: CONTRAINDICATIONS: gastroparesis
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23
Q

Exanitide

A
  1. GLP-1 agonist-incretin normally secreted after meals and augment insulin release.
  2. SYNTHETIC exendin-4 is a peptide found in gila monster venom
  3. rapidly absorbed from injection site. SubQ injection preprandial
  4. excreted by kidney
  5. activated DLP-1 receptors in tissues. in b cells: increase insulin synthesis and release in glucose dependent manner
  6. ALSO: delayed gastric emptying and decrease appetite (dt CNS and GIT). suppress release of glucagon
  7. can be used in combo
    8: SE: GI disturbance, weight loss, hypoglycemia (when with sulfonylurea), pancreatitis, can alter OCPs and abx absorption
    9: CONTRAINDICATIONS: hx of pancreatitis
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24
Q

Sitagliptin

A
  1. DPP-4 inhibitor (prevents enzyme that degrades incretin hormones)
  2. increase circulating GLP-1 and GIP
  3. 95% inhibition for 12h
  4. NOT BOUND
  5. oral 2x daily
  6. TYPE II
  7. results in increased postprandial insulin secretion and decrease in glucagon
  8. can be used in combo
  9. SE: increased rate of infection (DPP-4 expressed in lymphocytes), HA, hypoglycemia (with sulfonylurea), hypersensitivity, pancreatitis
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25
Q

Canagliflozin

A
  1. SGLT2 inhibitor (prevents enzyme that transports filtered glucose from proximal renal tubule to tubular epithelial cells)
  2. decreased glucose reabsorption
  3. taken 1x daily before breakfast
  4. can be used in combo
  5. SE: genital infections, UTI, diuretic issues, can increase serum digoxin, long term safety unknown
  6. CONTRAINDICATIONS: SEVERE RENAL IMPAIRMENT
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26
Q

Bromocriptine

A
  1. Dopamine agonist
  2. tx hyperprolactinemia, galactorrhea, parkinsonism
  3. taken before breakfast
  4. may reset circadian rhythms. improve insulin resistance
  5. FIRST PASS METABOLISM
  6. can be used in combo
  7. SE: nausea, HA, fatigue, dizziness, HYPOTENSION, hypoglycemia (with sulfonylurea)
  8. CONTRAINDICATIONS: hypersensitivity to ergot drugs, syncopal migraines, breastfeeding, psych disorders, ppl on HTN meds
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27
Q

Glucagon

A
  1. 29aa peptide synthed by a cells in ISLETS OF LANGERHANS
  2. treat severe hypoglycemia
  3. rapidly metabolized by liver/kidney
  4. parenteral
  5. stimulated bd of hepatic glycogen. Binds to G protein coupled receptor in liver. stimulates adenylate cycles. increase in cAMP. increase in glycogen phosphorylase. decrease in glycogen synthase.
  6. no effect in skeletal muscle
  7. CAN BE USED FOR OVERDOSE OF B ADRENORECEPTOR BLOCKER
    8: SE: nausea, vomiting, inotropic events in heart similar to b adrenergic agonist. (Tachy and HTN)
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28
Q

Digoxin

A
  1. Digitalis glycoside
  2. Binds proteins
  3. oral is preferred when not serious. IV in serious
  4. ORAL: loading dose (may be large dose followed by some smaller doses) followed by daily maintenance dose (amount lost in 24h). safer to slowly acquire effective concentration
  5. inhibits Na/K exchange. increases Na. Decreases Na/Ca exchange. Increases Ca. increases contraction.
  6. POSITIVE INOTROPE
  7. CARDIOVASCULAR CHANGE: Increase in CO, Increased excretion of Na and H20 (increased urine output ONLY with CHF..and edema), improved renal perfusion, reversal of SNS reflex tachy and TPR
    8: SLOWING OF HEART RATE: dt reversal of SNS, BUT also VAGAL EFFECT (receptors at carotid, cardiac..stimulated), and EXTRAVAGAL SLOWING (lengthening of refractory period and decreased conduction velocity in AV node–with higher doses)–all this allows for increase filling time…increased CO
  8. DONT USE JUST TO SLOW HR
  9. DRUG INTERACTIONS: phenylbutazone (increase serum glycoside), phenobarbital (decrease plasma levels dt increase microsomal enzyme), quinidine (increase plasma levels by displacing it), verapamil (inhibits renal clearance) antacid gels, sulfasalzien, bile acid binding resins (decrease bioavailability)
  10. SE: low margin of safety. GI, Cardiac (arrhythmia), CNS (HA, fatigue, “digitalis delirium”), Vision (white halos on dark objects)
  11. Plasma Ca and digitalis make toxicity worse
  12. plasma K and digitalis make toxicity better. same binding sites
  13. acid base imbalance and low Mg make toxicity worse.
  14. Tx: discontinue, decrease diuretics, KCL, digoxin AB
  15. lidocaine and propranolol can tx arrhythmias.
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29
Q

Digitalis glycoside

A
  1. natural sources: dried foxglove, strophanthus gratis, venom of buffa auga
  2. inhibits Na/K exchange. increases Na. Decreases Na/Ca exchange. Increases Ca. increases contraction.
  3. POSITIVE INOTROPE
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30
Q

what electrolyte can decrease digitalis toxicity

A

K+

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31
Q

What antiarrhythmic drugs will you use to tx digoxin arrhythmias

A

lidocaine, propanolol

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32
Q

Digoxin immune Fab

A
  1. bind to digoxin and excreted in urine

2. when there is sever HyperK (so adding K will not help)

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33
Q

Dobutamine

A
  1. non-glycoside inotropic agent. catecholamine
  2. cardioselective B1 adrenergic agonist
  3. only given IV in intensive care. severe CHF
  4. causes Increase CO by increase B1 receptor action
  5. SE: tachycardia, increase in cardiac O2 demand and arrhythmia
  6. Tolerance
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34
Q

Dopamine

A
  1. Non-glycoside inotropic agent
  2. endogenous catecholamine
  3. ONLY IV for severe CHF
  4. at low doses: can increase renal BF, can enhance Na and H20 excretion
  5. SE: increase HR and 02 demand MORE THAN DOBUTAMINE, tolerance
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35
Q

Inamrinone

A
  1. Non-glycoside inotropic agent
  2. Bipyridine derivative (PHOSPHODIESTERASE INHIBITOR)
  3. IV for severe CHF
  4. prevent cAMP inactivation dt phosphodiesterase inhibition. increase cAMP. increase Ca.
  5. improve diastolic relaxation. more SR Ca uptake
  6. NO TOLERANCE
  7. peripheral vasodilator effects
  8. SE: thrombocytopenia, increase myocardial O2 demand (fatal in ischemic HD–bc no tolerance forms)
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36
Q

Milrinone

A
  1. Non-glycoside inotropic agent
  2. Bipyridine derivative (PHOSPHODIESTERASE INHIBITOR)
  3. IV for severe CHF
  4. cAMP breakdown inactivation dt phosphodiesterase inhibition. increase cAMP. increase Ca.
  5. improve diastolic relaxation. more SR Ca uptake
  6. NO TOLERANCE
  7. peripheral vasodilator effects
  8. SE: thrombocytopenia, increase myocardial O2 demand (fatal in ischemic HD–bc no tolerance forms)
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37
Q

Captopril

A

More predictable dosing than other ACE

  1. ACE INHIBITOR
  2. Decrease A-II formed.
  3. inhibit vasoconstriction. decrease afterload
  4. inhibit aldosterone release. decrease retention of Na and H20. decrease preload
  5. indirectly increase CO and exercise capacity. does not affect HR much.
  6. can correct hypokalemia (digitalis tox)
  7. decrease high aldosterone related myocardial fibrosis
  8. may inhibit ACE-dependent production of A-II in myocardial tissue, where A-II contributes to hypertrophy
    9: SE: incombo: can cause too much decrease in BP, non productive cough (dt bradykinin), hyperkalemia, angioedema (dt bradykinin)
    10: CONTRAINDICATIONS: bilateral renovascular HTN (need to retain GFR), pregnancy, hepatotoxicity
    11: DRUG INTERACTIONS: hyperkalemia with other drugs, NSAIDS: impair antihypertensive effects of ACES by blocking bradykinin mediated vasodilation
    12: SPECIFIC: sulfdryl group responsible for rash, loss of taste, renal abnormalities, protein in urine
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38
Q

Enalapril

A

MUST BE ACTIVATED IN LIVER (which may be congested in CHF)

  1. ACE INHIBITOR
  2. Decrease A-II formed.
  3. inhibit vasoconstriction. decrease afterload
  4. inhibit aldosterone release. decrease retention of Na and H20. decrease preload
  5. indirectly increase CO and exercise capacity. does not affect HR much.
  6. can correct hypokalemia (digitalis tox)
  7. decrease high aldosterone related myocardial fibrosis
  8. may inhibit ACE-dependent production of A-II in myocardial tissue, where A-II contributes to hypertrophy
    9: SE: incombo: can cause too much decrease in BP, non productive cough (dt bradykinin), hyperkalemia, angioedema (dt bradykinin)
    10: CONTRAINDICATIONS: bilateral renovascular HTN (need to retain GFR), pregnancy, hepatotoxicity
    11: DRUG INTERACTIONS: hyperkalemia with other drugs, NSAIDS: impair antihypertensive effects of ACES by blocking bradykinin mediated vasodilation
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39
Q

Fosinopril

A
  1. ACE INHIBITOR
  2. Decrease A-II formed.
  3. inhibit vasoconstriction. decrease afterload
  4. inhibit aldosterone release. decrease retention of Na and H20. decrease preload
  5. indirectly increase CO and exercise capacity. does not affect HR much.
  6. can correct hypokalemia (digitalis tox)
  7. decrease high aldosterone related myocardial fibrosis
  8. may inhibit ACE-dependent production of A-II in myocardial tissue, where A-II contributes to hypertrophy
    9: SE: incombo: can cause too much decrease in BP, non productive cough (dt bradykinin), hyperkalemia, angioedema (dt bradykinin)
    10: CONTRAINDICATIONS: bilateral renovascular HTN (need to retain GFR), pregnancy, hepatotoxicity
    11: DRUG INTERACTIONS: hyperkalemia with other drugs, NSAIDS: impair antihypertensive effects of ACES by blocking bradykinin mediated vasodilation
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40
Q

Quinapril

A
  1. ACE INHIBITOR
  2. Decrease A-II formed.
  3. inhibit vasoconstriction. decrease afterload
  4. inhibit aldosterone release. decrease retention of Na and H20. decrease preload
  5. indirectly increase CO and exercise capacity. does not affect HR much.
  6. can correct hypokalemia (digitalis tox)
  7. decrease high aldosterone related myocardial fibrosis
  8. may inhibit ACE-dependent production of A-II in myocardial tissue, where A-II contributes to hypertrophy
    9: SE: incombo: can cause too much decrease in BP, non productive cough (dt bradykinin), hyperkalemia, angioedema (dt bradykinin)
    10: CONTRAINDICATIONS: bilateral renovascular HTN (need to retain GFR), pregnancy, hepatotoxicity
    11: DRUG INTERACTIONS: hyperkalemia with other drugs, NSAIDS: impair antihypertensive effects of ACES by blocking bradykinin mediated vasodilation
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41
Q

Losartan

A
  1. ARB. competitive antagonist at A-II receptor I
  2. decrease in vasoconstriction and aldosterone levels
  3. do not cause cough as ACE
  4. prevents A-II in heart which prevents hypertrophy (both ACE dependent/independent A-II–>ACE escape phenomenon)
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42
Q

Valsartan

A
  1. ARB. competitive antagonist at A-II receptor I
  2. decrease in vasoconstriction and aldosterone levels
  3. do not cause cough as ACE
  4. prevents A-II in heart which prevents hypertrophy (both ACE dependent/independent A-II–>ACE escape phenomenon)
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43
Q

Candesartan

A
  1. ARB. competitive antagonist at A-II receptor I
  2. decrease in vasoconstriction and aldosterone levels
  3. do not cause cough as ACE
  4. prevents A-II in heart which prevents hypertrophy (both ACE dependent/independent A-II–>ACE escape phenomenon)
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44
Q

Hydrocholorthiazide

A
  1. Diuretic. decrease ECF volume, decrease preload, decrease pulmonary congestion, decrease peripheral edema.
  2. USE THIS (thiazide) when GFR is greater than 30 mL/min
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45
Q

Furosemide

A
  1. USE LOOP DIURETIC (THIS) when GFR is less than 30 mL/min
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46
Q

Spironolactone

A
  1. K sparing diuretic. used to maintain K to decrease digitalis tox.
  2. also may prevent myocardial fibrosis dt elevated levels of aldosterone in CHF
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47
Q

Epleronone

A
  1. K sparing diuretic. used to maintain K to decrease digitalis tox.
  2. also may prevent myocardial fibrosis dt elevated levels of aldosterone in CHF
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48
Q

Hydralazine

A
  1. DIRECT VASODILATOR
  2. must monitor dt rapid actions. may decrease BP too fast.
  3. dilates thru mechanisms not specific for A-II, NE, or Vasopression, can work over all of them. Affects AFTERLOAD.
    ONLY AFFECTS AFTERLOAD
    PPL who benefit Most: severe CHF, right after acute with preexisting CHF
    SE: some can increase HR
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49
Q

Nitroprusside

A

can only be given IV
1. DIRECT VASODILATOR
2. must monitor dt rapid actions. may decrease BP too fast.
3. dilates thru mechanisms not specific for A-II, NE, or Vasopression, can work over all of them. Affects AFTERLOAD.
AFFECTS BOTH PRELOAD AND AFTERLOAD
PPL who benefit Most: severe CHF, right after acute with preexisting CHF
SE: some can increase HR

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50
Q

Nitroglycerin

A
  1. DIRECT VASODILATOR
  2. must monitor dt rapid actions. may decrease BP too fast.
  3. dilates thru mechanisms not specific for A-II, NE, or Vasopression, can work over all of them. Affects AFTERLOAD.
    ONLY AFFECTS PRELOAD THRU VENODILATION
    PPL who benefit Most: severe CHF, right after acute with preexisting CHF
    SE: some can increase HR
    TOLERANCE
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51
Q

Isosorbide Dinitrate

A
  1. DIRECT VASODILATOR
  2. must monitor dt rapid actions. may decrease BP too fast.
  3. dilates thru mechanisms not specific for A-II, NE, or Vasopression, can work over all of them. Affects AFTERLOAD.
    ONLY EFFECTS PRELOAD THRU VENODILATION
    PPL who benefit Most: severe CHF, right after acute with preexisting CHF
    SE: some can increase HR
    TOLERANCE
52
Q

Nesiritide

A

can only be given IV
1. DIRECT VASODILATOR PLUS DIURETIC
2. must monitor dt rapid actions. may decrease BP too fast.
3. dilates thru mechanisms not specific for A-II, NE, or Vasopression, can work over all of them. Affects AFTERLOAD.
SPECIFIC: decrease both arterial and venous SM by increasing cGMP. also natural natriuretic peptide.
PPL who benefit Most: severe CHF, right after acute with preexisting CHF
SE: some can increase HR

53
Q

What ACE inhibitor must be activated by liver

A

Elanapril

54
Q

Bisoprolol

A
  1. B-blocker (CARDIOSELECTIVE- B1)
  2. dangerous in pts with severe CHF–>low CO
  3. prevention of chronic adverse effects of catecholamines
  4. prevents down regulation of B receptors and functions
  5. prevents tachycardia and arrhythmias (which may prevent adequate vent. filling)
  6. CAN ALSO INHIBIT RAAS BY INHIBITING RENIN RELEASE FROM KIDNEY
  7. start with low doses
55
Q

Carvedilol

A

ANTIOXIDANT AND A BLOCKER TOO

  1. B-blocker
  2. dangerous in pts with severe CHF–>low CO
  3. prevention of chronic adverse effects of catecholamines
  4. prevents down regulation of B receptors and functions
  5. prevents tachycardia and arrhythmias (which may prevent adequate vent. filling)
  6. CAN ALSO INHIBIT RAAS BY INHIBITING RENIN RELEASE FROM KIDNEY
  7. start with low doses
56
Q

Metoprolol

A
  1. B-blocker (CARDIOSELECTIVE-B1)
  2. dangerous in pts with severe CHF–>low CO
  3. prevention of chronic adverse effects of catecholamines
  4. prevents down regulation of B receptors and functions
  5. prevents tachycardia and arrhythmias (which may prevent adequate vent. filling)
  6. CAN ALSO INHIBIT RAAS BY INHIBITING RENIN RELEASE FROM KIDNEY
  7. start with low doses
57
Q

Conivaptan

A
  1. Vasopressin antagonist
  2. V1a and V2 receptor antagonist
  3. IV treatment (blocks excess water retention)
  4. can help with hyponatremia
  5. don’t reduce mortality in CHF but treat SYNDROME OF INAPPROPRIATE ADH SECRTION (dt excessive ADH/vasopressin activity in kidney)
58
Q

Tolvaptan

A
  1. Vasopressin antagonist
  2. V2 alone receptor antagonist
  3. Oral treatment (blocks excess water retention)-adjunct to other tx
  4. can help with hyponatremia
  5. don’t reduce mortality in CHF but treat SYNDROME OF INAPPROPRIATE ADH SECRTION (dt excessive ADH/vasopressin activity in kidney)
59
Q

Class I antiarrhythmic

A
  1. Inhibit Na channels between APs (Phase 4 and 0)
  2. bind more readily to activated or inactivated cells than resting.
  3. better for tissues that are continuously depolarizing. good because it avoids cells depolarizing at a normal rate
  4. ALL INCREASE THRESHOLD FOR PHASE 0
60
Q

Class II antiarrhythmic

A
  1. Block Cardiac B receptor actions on Ca channels.
  2. can decrease inward Ca currents
  3. can diminish phase 4 depolarization, depressing automaticity in nodal tissues
  4. decrease phase 0 slope which slows conduction in nodal tissues
  5. Increase AP time and ERP in AV node (involving Ca activated K channels)
  6. can inhibit symp activity
  7. tx arrhythmias caused by increased symp activity or catecholamines, or a-flutter/fib, AV nodal reentrant tachy. prevents supra ventricular arrhythmias from reaching ventricles.
  8. can suppress DADs when caused by adrenergic stress in ventricles
61
Q

Class III antiarrhythmic

A
  1. inhibits K channels during AP. diminishes outward K current. prolongs repolarization at P3
  2. prolongs AP duration and ERP without altering AP phases or phase 4
62
Q

Class IV antiarrhythmic

A
  1. Block L-type calcium channels
  2. decrease inward current carried by calcium. P0, 2, 4
  3. prolong APD and ERP late in phase 3
    Phase 0 and 4 slopes suppressed
63
Q

Class IA antiarrhythmic

A
  1. Slow rate of rise of phase 0 of AP
  2. Inhibit P3 K currents
  3. increase AP duration and ERP
  4. INTERMEDIATE SPEED OF INTERACTION with P0 Na channels
64
Q

Class IB antiarrhythmic

A
  1. Less slowing effect no rate of rise of P0
  2. less slowing of conduction velocity than 1A
  3. inhibit late open Na currents, and decrease AP duration and ERP
  4. rapidly interact with P0 Na channels
65
Q

Class IC antiarrhythmic

A
  1. Markedly inhibit phase 0 Na currents
  2. depress rate of rise of P0. MOST slowing of conduction velocity.
  3. no effect on AP duration or ERP
  4. interact slowly with P0 Na channels
66
Q

Quinidine

A
  1. Class IA antiarrhythmic agent
  2. inhibits Na channels and K channels
  3. Prolong APD and ERP
  4. TX: supraventricular and ventricular (caused by excessive automaticity), to maintain normal rhythm after a fib cardioconversion
  5. Remember. intermediate speed of interaction with P0. slowed conduction velocity.
  6. SE: Tdp (bc prolonging AP duration..QT prolongation), GI, cinchonism (sweating,flushing and shit), a adrenergic blocking–decrease BP increase RSR, INCREASES BLOOD DIGOXIN LEVELS
67
Q

Procainamide

A
  1. Class IA antiarrhythmic agent
  2. K channels are inhibited by metabolite NAPA (little effect on 0, but is like class III)-eliminated via kidney
  3. prolonged APD and ERP
  4. SE: lupus (reversible, less common in rapid acetylators), CNS, GI, LESS a block THAN QUINIDINE, ventricular arrhythmias, tdp (less than quinidine)
68
Q

Lidocaine

A
  1. Class IB antiarrhythmic agent
  2. shortened APD and ERP dt inhibition of late Na channels opening during AP plateau (during ischemia).
  3. rapidly interacts with 0 Na channels
  4. actions manifested when rapid firing
  5. shortens 3 repolarization. decreased AP duration and ERP. not much decrease in 0 slope.
  6. TX: Emergent tx of ventricular arrhythmias during MI, suppresses ventricular arrhythmias caused by abnormal automaticity (bc decrease slope of p4. decrease excitability, threshold for 0), fixes rentry forms, stop tdp dt decreased AP duration.
  7. IV only dt first pass transformation
  8. SE: wide toxic therapeutic ratio, no impairment of ventricular contractile function, CNS, arrhythmias dt hyperkalemia.
69
Q

Flecainide

A
  1. Class IC antiarrhythmic agent
  2. interact more slowly with 0 Na channels. show effects at normal sinus rates
  3. Block P0 Na channels MOST compared to others in class 1
  4. marked slowing of conduction in most cardiac tissue
  5. no net effect on AP duration and ERP bc K channels inhibited in ventricles and Na channels blocked too.
  6. decrease in slope of P4
  7. sever arrhythmias resistant to other drugs
  8. SE: can aggravate CHF, HA, nausea, ventricular tachycardia (worse with hyperkalemia), INCREASED MORTALITY VS OTHERS)
70
Q

Propanolol

A
  1. Class II antiarrhythmic agent-B blocker
  2. reduces adrenergically driven arrhythmia after MI
  3. membrane stabilizing good for tx, but too much can cause SE.
  4. general SE: Bradycardia, decrease exercise ability, Rebound HTN, bronchoconstriction, insulin induced hypoglycemia more severe. DONT USE WITH CCB
71
Q

Acebutolol

A
  1. Class II antiarrhythmic agent-b blocker
  2. B1 specificity=less bronchospasm risk
  3. partial agonist activity decrease risk of too much suppression.
  4. general SE: Bradycardia, decrease exercise ability, Rebound HTN, bronchoconstriction, insulin induced hypoglycemia more severe. DONT USE WITH CCB
72
Q

Esmolol

A
  1. Class II antiarrhythmic agent-b blocker
  2. very short acting b blocker
  3. IV in acute setting. during surgery or ER
  4. general SE: Bradycardia, decrease exercise ability, Rebound HTN, bronchoconstriction, insulin induced hypoglycemia more severe. DONT USE WITH CCB
73
Q

Amiodarone

A
  1. Class III antiarrhythmic agent
  2. decrease cell to cell coupling in heart
  3. prolongation of APD and ERP dt blocking K channels
  4. TX: severe supraventricular and ventricular tachyarrhythmia. good for ppl with ICD
  5. IV action is rapid
  6. full clinical effects not until weeks after. lasts in tissues.
  7. contains iodine. like thyroxine
  8. SE: Interstitial pulmonary fibrosis, dizziness, hyper/hypothyroid, blue skin
  9. can cause tdp dt increase in APD in ventricular tissues
74
Q

Dofetilide

A
  1. Class III antiarrhythmic agent
  2. PURE. inhibits only K channels (mimics NAPA)
  3. prolongation of APD and ERP
  4. TX: supraventricular arrhythmias. good for A-fib
  5. oral and IV
  6. SE: tdp during IV
75
Q

Sotalol

A
  1. Class III antiarrhythmic agent
  2. blocks B receptors as well as Kchannels. prevents arrhythmia recurrences
  3. used in pts with ICD
  4. SE: tdp, b blocker stuff
76
Q

Verapamil

A
  1. Class IV antiarrhythmic agent CCB
  2. bind to L-type cardiac Ca channels
  3. decrease inward Ca. decrease slopes of P0 and P4. slow conduction and suppress automaticity.
  4. Increase APD and ERP in P3. less outward K current in P3 for repolarization.
  5. good for tissues that are Ca-dependent
  6. MORE EFFECTIVE AT SUPRAVENTRICULAR THAN VENTRICULAR (can stop DADs in both)
  7. TX: reentrant SVT, a-flutter/fib
  8. DONT USE IV WITH WPW PLUS AFIB
  9. care with hepatic dx
  10. SE: can decrease AV conduction too much and normal sinus rhythm. Avoid combo with B blockers.
77
Q

Diltiazem

A
  1. Class IV antiarrhythmic agent CCB
  2. bind to L-type cardiac Ca channels
  3. decrease inward Ca. decrease slopes of P0 and P4. slow conduction and suppress automaticity.
  4. Increase APD and ERP in P3. less outward K current in P3 for repolarization.
  5. good for tissues that are Ca-dependent
  6. MORE EFFECTIVE AT SUPRAVENTRICULAR THAN VENTRICULAR (can stop DADs in both)
  7. TX: reentrant SVT, a-flutter/fib
  8. DONT USE IV WITH WPW PLUS AFIB
  9. care with hepatic dx
  10. SE: can decrease AV conduction too much and normal sinus rhythm. Avoid combo with B blockers.
78
Q

Digoxin

A
  1. anitarryhtmic dt increased K current thru Ca-activated K channels. dt increased intracellular Ca caused by decrease N/K ATPase activity
  2. Shortens APD and ERP in atrial/ventricular cells
  3. lengthens ERP in AV node and purkinje fibers
  4. USE FOR A-fib/flutter
    SE: arryhtmia-tdp (can treat with lidocaine)
79
Q

Adenosine

A
  1. decreases conduction velocity and abnormal impulse formation in AV node
  2. inhibits Ca influx and activates Ach-sensitive K phase 4 current-hyperpolarization of resting membrane potential
  3. prolongs AV node refractory period
  4. tx acute paroxysmal SVT of AV node and WPW
80
Q

Magnesium

A
  1. Treatment for Torsades

2. unknown mechanism

81
Q

methicillin

A

not available in US

can cause interstitial nephritis dt type 4 hsn

82
Q

Natural Penicillins

A 
Pen G
Pen V Potassium
Pen G procaine
Pen G Benzathine
Pen G benzathine plus Pen G procaine
83
Q

Penicillinase Resistant Penicillins

A

used for staphylococcal infections and gram + infections

84
Q

Penicillinase Resistant Penicillins

A

methicillin
Nafcillin
Oxacillin
Diclozacillin

85
Q

Extended Spectrum Penicillins

A

-against some gram negative MOS
Ampicillin
Amoxicillin

86
Q

Antipseudomonal penicillins

A

Carbenicillin
Ticarcillin plus Clavulanate potassium
Piperacillin plus Tazobactam
Mezlocillin

87
Q

Other beta lactam drugs

A

monobactam
carbapenems
B lactamase inhibitors

88
Q

monobactams

A

Aztreonam

89
Q

carbapenems

A

imipenem pluscilastatin

90
Q

b lactamase inhibitors

A

clavulanic acid

tazobactam

91
Q

combo products using b lactamase inhibitors

A

amoxicillin plus clavulanic acid
ticarcillin pluse clavulanic acid
piperacillin plus tazobactam

92
Q

Imipenem

A

one of the broadest spectrum of pen family members

93
Q

Mostly likely MOS for AOM

A
  1. Strep pneumo
  2. hib
  3. moraxella catarrhalis
    (70-75% of cases)
94
Q

basic structure of penicillin

A
  1. thiazolidine ring
  2. b lactam ring
  3. side chain R group
95
Q

breaking of b lactam ring

A

lose antibacterial action (penicillinase)

96
Q

side chains are added to:

A

6-aminopenicillanic acid cor structure

97
Q

many penicillin family members are:

A

Na or K+ salts

98
Q

final step in production of peptidoglycan cell wall is complete cross linking of chains using

A

transpeptidase enzyme

99
Q

penicillin covalently binds to

A

transpeptidase enzyme (similar to D alanyl D alanine end of glycopeptide polymer)

100
Q

autolysin enzymes

A

released by bacteria when no cross linking. autolysis of bacteria

101
Q

other PBPs used for

A

cell shape and septum formation at cell division

102
Q

penicillins used in conjunction with:

A

aminoglycosides (Gentamycin)

103
Q

Structural differences in PBPs leading to resistance

A

Strep pneumo, Staph (MRSA). High molecular weight PBPs

104
Q

inability of penicillin to penetrate site of action

A
  1. penicillins must pass thru porins in G-bacteria
    2 PEN G has difficulty
  2. can also be pumped out by G- bacteria
105
Q

P. aeruginosa

A

lacks high permeability porins

106
Q

P. aeruginosa, E. coli, N. gonorrhoeae

A

active efflux

107
Q

b lactamase

A

staph. aureus

gram- produce in between membranes

108
Q

mycoplasma

A

not killed by penicillin bc no cell wall

109
Q

intracellular bacteria

A

cannot be reach by penicillin

110
Q

Amoxicillin

A

only drug that is not affected by food

111
Q

Oxacillin/Nafcillin/Dicox-anti staph

A

highly bound to plasma proteins-lead to clinical failure

112
Q

poor tissue penetration

A

eye, prostate, bbb

113
Q

Nafcillin

A

eliminated by biliary excretion. no adjustment for renal failure

114
Q

oxacillin and dicloxacillin

A

eliminated by biliary excretion and kidney. don’t adjust for renal failure

115
Q

probenacid

A

blocks secretory mechanism. less elimination of Pen G

116
Q

creatinine clearance less than 10 mL/min

A

1/4 to 1/3 normal dose

117
Q

major penicillin antigenic determinant

A

benzylpenicilloyl

oral administration less sensitizing

118
Q

most important adverse rxn

A

type 1 hsn

119
Q

topical penicillin use

A

highest rate of sensitization

120
Q

extended spectrum and rash

A

usually viral infection and give ampicillin or amoxicillin

121
Q

excess na and K with penicillin

A

cardiac and renal tox

122
Q

GABA

A

penicillin antagonizes

123
Q

negative control for skin testing

A

albumin saline

124
Q

positive control for skin testing

A

histamine

125
Q

Skin test

A
  1. percutaneous Skin test 2x2 with erythema is pos

2. intradermal skin testing if percutaneous is negative. 6x6 with erythema and 3 mm greater than neg control is pos

Pharmacology (6 decks)

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