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Auburn ECC > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Name the 4 types of vasopressin receptors

A

V1, V2, V3, oxytocin

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2
Q

Describe the tissues affected and effects of vasopressin on the V1 Rc

A

Vascular smooth muscle- vasoconstriction at high doses; vasodilation in cerebral, renal, pulmonary, and mesenteric vessels at low doses

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3
Q

Describe the tissues affected and effects of vasopressin on the V2 Rc

A

renal collecting duct-increased h2o permeability
endothelial cells- release of vWF
platelets- stimulation of aggregation
vascular endothelium-vasodilation

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4
Q

Describe the tissues affected and effects of vasopressin on the V3 Rc

A

Pituitary- adrenocorticotropic hormone release

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5
Q

Describe the tissues affected and effects of vasopressin on the oxytocin Rc

A

Uterus, mammary glands, Gi tract, endothelium- contraction, vasodilation

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6
Q

What is the half life of AVP?

A

10-35 min

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7
Q

Where is arginine vasopressin synthesized and stored?

A

synthesis- hypothalamus

storage- posterior pituitary

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8
Q

What are the 3 most potent stimuli for AVP release?

A

increased plasma osmolality, decreased blood pressure, decreased circulating blood volume

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9
Q

What are some uncommon stimuli for AVP release?

A

pain, nausea, hypoxia, hypercarbia, pharyngeal stimulation, glycopenia, drugs/chemicals, malignant tumors, mechanical ventilation

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10
Q

What are some chemicals/drugs that cause AVP release?

A

high dose opioids, histamine, glutamine, prostaglandings, angiotensin II, acetylcholine, dopamine

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11
Q

T/F - drugs such as glucocorticoids, low dose opioids, atrial natriuretic factor, and GABA can cause increased AVP release?

A

False- they cause decreased release of AVP

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12
Q

Name 6 causes of secondary hypertension

A

Kidney disease

Diabetes mellitus

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13
Q

What are the indications for use of ACE inhibitors?

A

Reduce blood pressure in all forms of hypertension
Mitral insufficiency and congestive heart failure
Reduce proteinuria by maintaining the heparan sulfate layer of the basement membrane

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14
Q

What type of receptors are vasopressin Rc’s?

A

G protein coupled Rc’s

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15
Q

How (physiologically) does the V1 Rc cause vasoconstriction?

A

activation of phospholipase C and phosphoinositide pathways; activate voltage gated Ca++ channels, which increases intracellular Ca++ levels

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16
Q

What are the indications for use of angiotensin II receptor blockers?

A

Used in humans for hypertension and cardiovascular disease.

Efficacy is unknown for treatment of hypertension in dogs and cats

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17
Q

T/F- vasopressin causes inactivation of the potassium-ATP channels in vascular smooth muscle cells

A

True

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18
Q

Vasopressin causes inactivation of the K+-ATP channels in vascular smooth muscle; how does this affect the muscle?

A 
These channels (when they are open) normally cause K+ efflux-->hyperpolarization-->decreased Ca++ into cells-->vasodilation
When the channels are inactivated vasodilation does not occur
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19
Q

What are the indications for use of adrenergic receptor antagonists?

A

B-adrenergic blockers are used when primary antihypertensive treatment fails to produce the desired decrease in blood pressure. Also used to manage HCM and supraventricular and ventricular tachycardias

A-adrenergic antagonists used as a primary or adjunct therapy for hypertension in dogs. Also used in micturition disorders to relax the smooth muscle of the urethra. Also used in treatment of hypertension associated with pheochromocytomas

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20
Q

What is the mechanism of action of angiotensin-converting enzyme (ACE) inhibitors?

A

Competitively inhibit the conversion of angiotensin I to angiotensin II resulting in systemic vasodilation

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21
Q

What is the mechanism of action of aldosterone blockers and what are some examples of this type of drug?

A

Spironolactone
Blocks the effects of aldosterone on the renal distal convoluted tubule and collecting duct thereby decreasing sodium resorption and potassium excretion

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22
Q

What are the indications for use of aldosterone blockers?

A

Hypertension due to its weak antidiuretic effects but also for its effects on the renin-angiotensin-aldosterone system

Used in treating hyperaldosteronism, iatrogenic steroid edema, refractory edema

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23
Q

What are the adverse effects of aldosterone blockers?

A

Hyperkalemia may occur but is uncommon in the absence of kidney insufficiency or concurrent use of a beta blocker, ACE inhibitor, angiotensin II receptor blocker, or potassium supplements

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24
Q

What is the mechanism of action of calcium channel blockers and what are some examples of this type of drug?

A

Amlodipine, nicardipine
They act by blocking the influx of calcium into vascular smooth muscle cells that is necessary to cause smooth muscle contraction thereby decreasing systemic vascular resistance.

They inhibit the slow transmembrane calcium influx into the cell via voltage-gated L-type calcium channels

The dihydopyridines (amlodipine etc) are the family of CCBs that primarily act on blood vessels producing arterial vasodilation.

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25
Q

T/F- platelets have V1 receptors, which can lead to thrombosis due to increased intracellular Ca++

A

True

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26
Q

What is the mechanism of action of the arteriolar vasodilator hydralazine?

A

Acts on the smooth muscle of arterioles with a mechanism that is incompletely understood

Known to act as an antioxidant, inhibiting vascular production of reactive oxygen species. It may induce arteriolar vasodilation by preventing oxidation of nitric oxide thereby lowering blood pressure

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27
Q

What are the adverse effects of hydralazine?

A

Three types of adverse effects in humans:

  1. Reflex sympathetic activation
  2. Lupus-like reaction
  3. Nonspecific problems such as anorexia, nausea, vomiting, diarrhea, muscle cramps and tremor

In vet med, we see mainly reflex tachycardia, weakness and GI upset

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28
Q

Where are V2 receptors located?

A

basolateral membrane of the distal tubule, principal cells of cortical and medullary renal collecting duct

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29
Q

What are the indications for use of hydralazine?

A

Hypertension in dogs and cats (not a first line therapy)

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30
Q

In what 2 ways does AVP regulate water homeostasis?

A
  1. regulate the fast shuttling of aquaporin 2 to the cell surface
  2. stimulates synthesis of mRNA-encoding aquaporin 2
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31
Q

T/F: Most animals with nephrogenic DI have V1R mutations?

A

False; they have V2R mutations

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32
Q

How does the V2R activation affect coagulation?

A

release of plt from bone marrow, release of vWF and factor VIII from endothelial cells

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33
Q

What drug is used to release vWF and factor VIII?

A

DDAVP (1-deamino-8-d-arginine vasopressin)

Note: it also causes vasodilation

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34
Q

What happens inside the cell when V3R are activated?

A

releases intracellular Ca2+ after activation of phospholipase C and phosphoinositol cascade

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35
Q

What is the mechanism of action of angiotensin II receptor blockers and what are some examples of this type of drug?

A

Arterial and venous vasodilation
Losartan, Irbesartan, Telmisartan

They displace angiotensin II from its specific angiotensin type I receptor (AT1R) antagonizing all of its known effects (vasoconstriction, sympathetic activation, aldosterone release, renal sodium resorption).

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36
Q

What are the indications for angiotensin II receptor blockers?

A

Used in humans for hypertension and cardiovascular disease.

Efficacy is unknown for treatment of hypertension in dogs and cats

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37
Q

What are the adverse effects of angiotensin II receptor blockers?

A

These drugs appear to be safe with few adverse effects.

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38
Q

What is the mechanism of action of adrenergic receptor antagonists and what are some examples of this type of drug?

A

B adrenergic receptor antagonists: propanolol, atenolol
MOA: blockade of renin release, reduction of heart rate and contractility, decrease in peripheral vascular resistance, reduction in central adrenergic drive

A adrenergic receptor antagonists: prazosin
MOA: blocks activation of the post-synaptic alpha 1 receptors which are normally activated by circulating or neurally released catecholamines. This results in balanced vasodilation.

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39
Q

How does activation of V3R affect the CNS?

A

modulator of memory, blood pressure, body temp, sleep cycles, release of pituitary hormones

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40
Q

T/F: oxytocin Rc has equal affinity for AVP & oxytocin?

A

TRUE

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41
Q

Should exogenous AVP be given orally? Why or why not?

A

No- destroyed within the GI tract

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42
Q

What is the half life of exogenous AVP?

A

24 min

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43
Q

How is exogenous AVP excreted?

A

35% tissue peptidases, 65% renal

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44
Q

What Rc does selepressin work on?

A

V1R agonist; in healthy dogs they have a reduced risk of coronary ischemia compared with those given AVP

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45
Q

What is desmopressin acetate?

A

synthetic vasopressin analog; available in IN and inject form; binds to V2R; potent antidiuretic and procoagulant activity
Can cause a dose dependent increase in plasma factor VIII and plasminogen factor
Half life is 0.4-4 hrs

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46
Q

What is tolvaptan?

A

V2R antagonist; has aquaretic response and reduced cardiac preload; doesnt affect sympathetic NS, renal hemodynamics or RAAS; may be beneficial in CHF

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47
Q

How does vasopressin compare to epi in a meta analysis during CPR?

A

is at least equivalent to epinephrine; in experimental models it improves cerebral O2 delivery and may improve chance of ROSC

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48
Q

T/F: hypovolemia or septic shock can cause a biphasic response in serum AVP levels (initially high, then depleted)?

A

True

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49
Q

What concentration of plasma AVP should be the goal for restoration of BP with minimal adverse effects?

A

AVP 20-30 pg/ml

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50
Q

What are the adverse effects of angiotensin II receptor blockers?

A

These drugs appear to be safe with few adverse effects.

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51
Q

What is the mechanism of action of adrenergic receptor antagonists and what are some examples of this type of drug?

A

B adrenergic receptor antagonists: propanolol, atenolol
MOA: blockade of renin release, reduction of heart rate and contractility, decrease in peripheral vascular resistance, reduction in central adrenergic drive

A adrenergic receptor antagonists: prazosin
MOA: blocks activation of the post-synaptic alpha 1 receptors which are normally activated by circulating or neurally released catecholamines. This results in balanced vasodilation.

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52
Q

What are the indications for adrenergic receptor antagonists?

A

B-adrenergic blockers are used when primary antihypertensive treatment fails to produce the desired decrease in blood pressure. Also used to manage HCM and supraventricular and ventricular tachycardias

A-adrenergic antagonists used as a primary or adjunct therapy for hypertension in dogs. Also used in micturition disorders to relax the smooth muscle of the urethra. Also used in treatment of hypertension associated with pheochromocytomas

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53
Q

What are the adverse effects of adrenergic receptor antagonists?

A

B-adrenergic blockers
Non-selective ones such as propanolol should not be used in cats due to bronchospasm.
May also cause hyperkalemia, bradycardia, insulin resistance, and depression

A-adrenergic antagonists
May cause hypotension nonresponsive to a-agonist therapy

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54
Q

What are some theories behind why septic shock causes lower levels of AVP?

A

degredation of released AVP, depletion of neurohypophyseal stores, enhanced sensitivity to AVP induced blood pressure changes, release may be inhibited by NO or high levels of norepi

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55
Q

T/F- many human papers have shown earlier weaning of catecholamines when giving vasopressin?

A

true

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56
Q

T/F- there have been human studies documenting decreased mortality rates in people with septic shock when giving vasopressin?

A

true

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57
Q

What are some adverse effects of AVP administration?

A

excessive coronary and splanchnic vasoconstriction, hypercoagulability, reduction in cardiac output, fatal cardiac events

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58
Q

What dose of AVP is used in dogs with refractory vasodilatory shock?

A

0.5 mU/kg/min IV, titrated up to achieve MAP >70 mm Hg and HR

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59
Q

How does AVP minimize blood loss from bleeding extremities?

A

redirects blood from skin, skeletal muscle and periphery

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60
Q

T/F- administration of AVP decreased fluid requirements and mortality in one human trauma study?

A

true

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61
Q

What drug is used to treat central diabetes insipidus?

A

DDAVP- monitor serial lytes and avoid water intoxication

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62
Q

What are some drawbacks to use of DDAVP for vWD?

A

expensive, short duration of activity, development of resistance

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63
Q

Name some adverse effects of AVP

A

contraction of bladder/gallbladder smooth muscle, increased peristalsis, decrease gastric secretions, phlebitis, skin necrosis, elevated LES, TCP, hyponatremia, anaphylaxis, abdominal pain, urticaria

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64
Q

What role might V1R antagonists play (in the future/not yet developed)? V2R?

A

V1R-mgmt of subarachnoid hemorrhage

V2R- CHF

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65
Q

T/F: Most animals with nephrogenic DI have V1R mutations?

A

False; they have V2R mutations

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66
Q

What drug is used to release vWF and factor VIII?

A

DDAVP (1-deamino-8-d-arginine vasopressin)

Note: it also causes vasodilation

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67
Q

What Rc does selepressin work on?

A

V1R agonist; in healthy dogs they have a reduced risk of coronary ischemia compared with those given AVP

How well did you know this?
1
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2
3
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68
Q

What is tolvaptan?

A

V2R antagonist; has aquaretic response and reduced cardiac preload; doesnt affect sympathetic NS, renal hemodynamics or RAAS; may be beneficial in CHF

How well did you know this?
1
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2
3
4
5
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69
Q

What is the mechanism of action of adrenergic receptor antagonists and what are some examples of this type of drug?

A

B adrenergic receptor antagonists: propanolol, atenolol
MOA: blockade of renin release, reduction of heart rate and contractility, decrease in peripheral vascular resistance, reduction in central adrenergic drive

A adrenergic receptor antagonists: prazosin
MOA: blocks activation of the post-synaptic alpha 1 receptors which are normally activated by circulating or neurally released catecholamines. This results in balanced vasodilation.

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1
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70
Q

What is the mechanism of action of aldosterone blockers and what are some examples of this type of drug?

A

Spironolactone
Blocks the effects of aldosterone on the renal distal convoluted tubule and collecting duct thereby decreasing sodium resorption and potassium excretion

How well did you know this?
1
Not at all
2
3
4
5
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71
Q

What are the indications for use of aldosterone blockers?

A

Hypertension due to its weak antidiuretic effects but also for its effects on the renin-angiotensin-aldosterone system

Used in treating hyperaldosteronism, iatrogenic steroid edema, refractory edema

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72
Q

What are the adverse effects of aldosterone blockers?

A

Hyperkalemia may occur but is uncommon in the absence of kidney insufficiency or concurrent use of a beta blocker, ACE inhibitor, angiotensin II receptor blocker, or potassium supplements

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73
Q

What is the mechanism of action of calcium channel blockers and what are some examples of this type of drug?

A

Amlodipine, nicardipine
They act by blocking the influx of calcium into vascular smooth muscle cells that is necessary to cause smooth muscle contraction thereby decreasing systemic vascular resistance.

They inhibit the slow transmembrane calcium influx into the cell via voltage-gated L-type calcium channels

The dihydopyridines (amlodipine etc) are the family of CCBs that primarily act on blood vessels producing arterial vasodilation.

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74
Q

What are the indications for use of calcium channel blockers?

A

Hypertension and hypertensive crises

Amlodipine is the treatment of choice for hypertension in cats with chronic kidney disease

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75
Q

What are the adverse effects of calcium channel blockers?

A

Tachycardia, nausea, constipation, weakness

Afferent arteriolar vasodilation is greater than the efferent arteriolar vasodilation on the opposite side of the glomerulus which may result in decreased perfusion pressure with resultant decreased glomerular filtration

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76
Q

What is the mechanism of action of the arteriolar vasodilator hydralazine?

A

Acts on the smooth muscle of arterioles with a mechanism that is incompletely understood

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77
Q

What are the adverse effects of hydralazine?

A

Three types of adverse effects in humans:

  1. Reflex sympathetic activation
  2. Lupus-like reaction
  3. Nonspecific problems such as anorexia, nausea, vomiting, diarrhea, muscle cramps and tremor

In vet med, we see mainly reflex tachycardia, weakness and GI upset

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78
Q

Name two arteriolar vasodilators

A

Hydralazine

Sodium nitroprusside

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79
Q

What is the mechanism of action of the arteriolar vasodilator sodium nitroprusside?

A

Results in nitric oxide release, which stimulates the production of cyclic guanine monophosphate (cGMP) in the vascular smooth muscle. cGMP activates a kinase that leads to inhibition of calcium influx into the smooth muscle cell and decreased calcium-calmodulin stimulation of myosin light-chain kinase. This in turn decreases the phosphorylation of myosin light chains, which decreases smooth muscle contractions and causes vasodilation.

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80
Q

What are the indications for use of hydralazine?

A

Hypertension in dogs and cats (not a first line therapy)

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81
Q

What are the indications for use of sodium nitroprusside?

A

Hypertensive crisis
Rapid reduction of preload and afterload in acute heart failure
Controlled blood pressure reduction during surgery

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82
Q

What are the adverse effects of sodium nitroprusside?

A

Shock
Severe hyportension
Cyanide intoxication

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83
Q

What is the mechanism of action of fenoldopam?

A

Peripheral dopamine-1 agonist

Maintains or increased renal perfusion while lowering blood pressure

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84
Q

What are the indications for use of fenoldopam?

A

Severe hypertension

Hypertensive crisis

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85
Q

What are the adverse effects of fenoldopam?

A

Reflex tachycardia

Increased intraocular pressure

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86
Q

How do steroids cause hypertension?

A

Hepatic induction of angiotensinogen leads to over activation of RAAS

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87
Q

How does hyperthyroidism lead to hypertension?

A

Increased cardiac output due to effect of excess thyroid hormone on cardiac muscle

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88
Q

How does renal disease cause hypertension?

A

Renal regulation of blood pressure is from Pressure natriuresis and RAAS. Maladaptive increase in renin increases blood volume which leads to increased venous return. Or possibly inability of kidneys to process fluids and el leads to increased venous return. Increased vasoconstrictors (endothelin, thromboxane, adrenergic stimuli) and decreased vasodilators (nitric oxide, prostacyclin) may play a role

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89
Q

How does hepatic disease cause hypertension?

A

Undetermined

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90
Q

What are the 4 mechanisms by which diabetes may cause hypertension?

A

Type I - effects on renal function (nephropathy with nephritic syndrome and glomerulosclerosis)Type II- 1. Hyperinsuliemia from insulin resistance leads to sodium and water retention and increased sympathetic activity, leads to increased PVR via changes in BV and vasoconstriction 2. Hypertrophy of VSM 2nd to mitogenic effects of insulin3. Elevated insulin leads to increased intracellular Ca which results in hyper responsive VSM contraction and increased PVR

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91
Q

How do pheos cause hypertension?

A

Release of epi and norepinephrine causes vasoconstriction and increased CO.

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92
Q

How does anemia cause hypertension?

A

Anemia leads to chronically dilated Capillary beds, when anemia resolves, overcompensation of capillary constriction happens causing increased PVR

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93
Q

How do ACEI’s control hypertension?

A

Prevent the cleavage of AG I to AG II (AG is a very powerful vasoconstrictor, inhibition results in vasodilation). This decreases AG I and II and increases bradykinin. Also these drugs induce arterial and venous vasodilation.

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94
Q

Other than vasodilation, what are some others affects of ACE inhibitors?

A

Reduced plasma volume from lack of sodium retention from decreased AG II, prevention of aldosterone release which leads to deceased Na and H2O retention and decrease BV. Decreased preload and after load, reduced intra glomerular pressure and inhibition of growth factors that lead to glomerular hypertrophy and sclerosis.

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95
Q

How do ACE inhibitors reduce proteinuria?

A

Maintaining the heparan sulfate layer of the glomerular basement membrane

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96
Q

What are 3 benefits of benazepril?

A

Lowering of glomerular capillary hypertension, decreased release of extracellular matrix and collagen from mesangial and tubular cells, and reduction in degree of glomerular and interstitial fibrosis

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97
Q

What is a rare side effect of ACE inhibitors?

A

Dry cough induced by increased bradykinin

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98
Q

How do AG II receptor blockers such as losartan work?

A

Displace AG II from it’s receptor ATIreceptor and possibly enhancing dopamine D1 signaling. Displacement form it’s receptor antagonizes all of it’s known effects and results in a dose dependent fall in PR with little change in HR or CO

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99
Q

How do beta blockers treat hypertension?

A

Blocks renin release, decreases HR and contractility, decrease in PVR and reduced central adrenergic drive

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100
Q

How do alpha adrenergic antagonists treat hypertension?

A

Selectively antagonizing alpha adrenergic receptors on systemic vessels. Prazosin acts as a competitive antagonist of postsynaptic alpha1 receptors and blocks activation of these receptors by circulating or neurally released catecholamines (which would typically cause vasoconstriction). PR falls with minimal changes in CO

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101
Q

What is eplerenone and what is it used for?

A

Antagonizes the aldosterone receptor- advantage over spironolactone is eplerenone does not bind to progesterone or androgen receptors like spiro. May cause hyperkalemia. Has been shown to reduce proteinuria and decrease renal fibrosis and inflammation.

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102
Q

List 5 secondary causes of hypertension

A

Kidney disease, Cushings, diabetes mellitus, hyperthyroidism, hepatic disease, less common: pheochromocytas, drugs (steroids, erythropoietin), chronic anemia, hyperaldosteronism, polycythemia

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103
Q

What is the MOA of maropitant?

A

Neuokinin-1 receptor antagonist that blocks the action of substance P in the central nervous system as well as at peripheral NK-1 receptors in the GI tract

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104
Q

What other effects can NK-1 receptor antagonists have other than as anti-emetics?

A 
Anti-inflammatory
Neuroprotectant
Hepatoprotectant
Reduction of diarrhea
Reduce visceral pain
Reduce the minimum alveolar concentration of sevoflurane
Possible anti-tumor activity
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105
Q

What is the MOA of 5-HT3 receptor antagonists?

A

Competitive blockers of the serotonin receptors both peripherally (where they are responsible for intestinal vagal afferent input) and centrally (in the chemoreceptor trigger zone and medullary vomiting center)

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106
Q

What is an unusual characteristic of ondansetron in people?

A

It inhibits emesis and low and high dosages; however, it increases it an intermediate doses.

The same has been seen with metoclopramide in people.

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107
Q

True or False: Ondansetron has been reported to increase the efficacy of tramadol

A

FALSE

It DECREASES the efficacy of tramadol

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108
Q

What is the MOA of metoclopramide?

A

It is a 5HT-3 receptor antagonist as well as an antidopaminergic
Weak 5HT-4 agonist

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109
Q

Why is metoclopramide potentially less effective in cats?

A

They have very few dopamine receptors

110
Q

What is the MOA of promazine derivatives as anti-emetics?

A

They have antidopaminergic and antihistaminic effects that block the CRTZ and at higher dosages, the MVC as well

111
Q

What are some side effects of promazine derivatives when they are used as anti-emetics?

A

Increased central venous pressure
Brady or tachycardia
Anti-arrhythmic qualities in the dog
CNS signs in dogs with hepatic insufficiency

112
Q

What is aminopentamide?

A

It is an anticholinergic that has been used an an anti-emetic in dogs. There are cholinergic receptors in the brain involved in the vomiting center and in the upper GI tract via the vagus nerve.

It is less effective than metoclopramide, the 5-HT3 antagonists, and the NK-1 antagonists.

113
Q

True or False: In humans steroids have been used as anti-emetics?

A

TRUE

They are typically used in combination with other anti-emetics.

114
Q

What class of drug is the most effective prokinetics in veterinary medicine?

A

5-HT4 serotonergic agonists such as cisapride

115
Q

What is the MOA of cisapride?

A

5-HT4 serotonergic agonist
Enhances gastric emptying while increasing gastroesophageal sphincter pressure. It also enhances colonic and small intestinal motility (can be used in cats with idiopathic constipation).

It does not enhance esophageal motility as it is ineffective on striated muscle.

116
Q

What is the MOA of cholinomimetic drugs as prokinetics?

A

Ranitidine and nizatidine inhibit acetylcholinesterase which results in increased gastric emptying.

Bethanechol binds to muscarinic receptors which effects motility throughout the GI tract.

117
Q

True or False: The dose of metoclopramide needed to provide a prokinetic effect is lower than that needed for the anti-emetic effect

A

FALSE

Higher doses are needed to cause prokinesis and reduce gastroesophageal reflux.

118
Q

True or False: Misoprostol can be used to enhance colonic motility

A

TRUE

It has been used in patients with non-responsive constipation.

119
Q

What is the MOA of benzodiazepines?

A

facilitate the inhibitory actions of GABA, antagonism of serotonin, diminished release or turnover of Ach in CNS
Also have anxiolytic, sedative, hypnotic, skeletal muscle relaxant and anticonvulsant properties via limbic, thalamic, and hypothalmic areas of CNS

120
Q

T/F: benzodiazepines provide some analgesia

A

False

121
Q

What are the major differences between midazolam and diazepam?

A

Diazepam- not water soluble; formulated in a 40% propylene glycol and 10% alcohol vehicle
Midazolam- water soluble, well absorbed after IM injection, poorly bioavailable per rectum

122
Q

T/F: midazolam should only be given through a central vein?

A

false- midazolam is water soluble and can be given through a peripheral vein; diazepam should be given through central vein b/c propylene glycol may cause phlebitis

123
Q

T/F: midazolam and diazepam can also be given intranasally

A

true

124
Q

what adverse effects are associated with propylene glycol toxicity in animals receiving diazepam?

A

metabolic acidosis, hyperosmolality, neuro abnormalities, organ dysfunction

125
Q

what is a rare complication of oral diazepam administration in cats?

A

fulminant hepatic failure from acute hepatic necrosis (idiosyncratic rxn)

126
Q

How do benzodiazepines stimulate appetite?

A

at low doses they bind to benzodiazepine receptors and increase the attraction to tastes, especially in cats; may begin working within a few seconds of administration

127
Q

What is the controversy regarding use of benzodiazepines in animals with hepatic encephalopathy?

A

Human patients have been shown to increase arousal following flumazenil administration; there is a lack of arousal in other species including dogs and cats; improvement of HE signs has been shown in animals given the inverse agonist sarmazenil- this may be consistent with increased GABAergic activity in HE but not an increase in endogenous benzo ligands

128
Q

what are the recommended doses for sedation and anticonvulsant therapy for midazolam and diazepam?

A

Diazepam:
Sedation- 0.2-0.6 mg/kg, CRI 0.1-1 mg/kg/hr
Anticonv- 0.5-1 mg/kg, CRI 0.5-1 mg/kg/hr, per rectum 2 mg/kg
Midazolam:
Sedation- 0.1-0.4 mg/kg, CRI 0.1-0.5 mg/kg/hr
Anticonv- 0.2-0.5 mg/kg, CRI 0.2-0.5 mg/kg/hr

129
Q

T/F: flumazenil use is rarely indicated even in severe benzodiazepine overdoses if the patient is stable?

A

True, there is a possibility of severe adverse outcomes with flumazenil or sarmazenil use; overdose can usually be treated supportively with emetics and/or charcoal

130
Q

What types of things do platelets interact with in order to become activated?

A

vWF, subendothelial collagen, other activated platelets,

131
Q

Describe the two platelet receptors: P2Y1 and P2Y12

A

P2Y1: Agonism at this receptor is associated with platelet shape change and mild, reversible aggregation

P2Y12: Agonism at this receptor is associated with integrin activation and platelet granule secretion

132
Q

What are the thienopyridines and give an example?

A

A class of drugs designed to interfere with ADP-induced platelet aggregation through irreversible binding to the platelet P2Y12 receptor.

Clopidogrel

133
Q

How do the nucleoside analogues work as antiplatelet drugs?

A

They inhibit the effects of ADP on platelet aggregation through reversible inhibition of the P2Y12 receptor. They do not require hepatic metabolism for activation like the thienpyridines.

134
Q

How does aspirin results in platelet inhibition?

A

Aspirin administration causes irreversible blockade of COX-1 which decreases arachidonic acid formation necessary to create thromboxane-A2 (which is a potent vasoconstrictor and also plays a role in the recruitment and activation of platelets)

135
Q

How long do platelets last in circulation?

A

6 +/- 1 days

136
Q

Why are cats potentially less sensitive to aspirin therapy?

A

They have reactive platelets that are sensitive to other agonists thereby minimizing the importance of TXA2 activation

137
Q

Why are fibrinogen receptor antagonists potentially more effective than other antiplatelet drugs?

A

They target the final step in the platelet activation pathway (the expression of an active GPIIb/IIIa fibrinogen receptor). Because therapy is directed at the receptor itself variability in platelet response in minimized

138
Q

What may be responsible for variable response to clopidogrel or other thienopyridines?

A

They are prodrugs that require activation in the liver by the P-450 enzymes. Variation in this enzyme system between individuals and in certain disease states may result in altered pharmacokinetics

139
Q

Why are platelets more associated with arterial thromboembolism?

A

Sheer stress causes by fast-flowing arterial blood exposes platelet binding sites on vWF that increase the affinity for the platelet glycoprotein Ib receptor

140
Q

What morphological changes are seen with platelet activation?

A

The activated platelet changes from a smooth discoid shape to a more ameboid shape with filopodia

141
Q

What do the Alpha-granules of platelets contain? and the dense granules?

A

Alpha-granules: adhesion molecules (P selectin, vWF, thrombospondin, Integrin aIIbB3 (or GPIIb/IIIa)) and coagulation factors (V, VIII, fibrinogen)

Dense granules: smaller ions and nucleotides (Ca2+, ADP, adenosine triphosphate, serotonin, histamine)

142
Q

What change is seen with the platelet membrane after activation?

A

Rearrangement of the membrane phospholipids which provides a surface that supports the formation of the complexes that activate factor X (the tenase complex) and factor II (the prothrombinase complex)

143
Q

What is the name of classification scheme used for anti-arrhythmic drugs and what is it based on?

A

Vaughan Williams classification system

Groups drugs according to their major ion channel or receptor effects

144
Q

In general, how do Class I anti-arrhythmics work?

A

The act by inhibiting the fast sodium channel and decreasing the slope of phase 0 of the action potential

145
Q

What is an example of a class Ia anti-arrhythmic and what are its effects?

A

Procainamide

Depresses conduction velocity and prolongs the effective refractory period in many tissues including the atrial and ventricular myocardium, accessory AV pathways, and retrograde AV nodal pathways

146
Q

True or False: Procainamide is less effective than lidocaine for terminating ventricular tachyarrhythmias in humans

A

FALSE

It is more effective than lidocaine

147
Q

What are adverse effects of procainamide?

A

Anorexia, nausea, vomiting are seen most commonly.

In humans, rash and fever are seen immediately after use and myalgia, arthralgia, and agranulocytosis may be seen later.

In 1/3 of patients that take it longer than 6 months, systemic lupus erythematosus may be seen

148
Q

What is an example of a class Ib anti-arrhythmic and what are its effects?

A

Lidocaine

It inhibits the fast sodium channel, primarily in the open state with rapid onset-offset kinetics. There is also shortening of the action potential duration.

149
Q

In what conditions is lidocaine’s sodium blocking activity enhanced?

A

Acidosis, increased extracellular potassium concentrations, and partially depolarized cells

150
Q

Why are drugs that prolong AV nodal conduction given first for acute treatment of tachyarrhythmias?

A

Procainamide is not given first as it can enhance AV nodal conduction and worsen the ventricular response rate

151
Q

What are adverse effects of lidocaine?

A

Nausea, vomiting, lethargy, tremors, seizures

152
Q

Why are lower doses of lidocaine recommended in cats (if it is used at all)?

A

The incidence of adverse effects is much higher in cats, with earlier reports of bradyarrhythmias and sudden death

153
Q

Give an example of an oral class Ib anti-arrhythmic

A

Mexiletine

154
Q

Name two class Ic anti-arrhythmics

A

Flecainide
Propafenone

They block the fast sodium channel with greater effects as the depolarization rate increases. They are uncommonly used in veterinary medicine

155
Q

What are class II anti-arrhythmics and how do they work?

A

B-adrenergic antagonists or B-Blockers

They work by:

1) Inhibiting the If current that also promotes pro-arrhythmic depolarization in damaged cardiomyocytes
2) Inhibit the inward calcium current indirectly by decreasing tissue cyclic adenosine monophosphate levels.

156
Q

What are the effects of beta blockers?

A

Slowed AV nodal conduction in supraventricular tachyarrhythmias

Slow sinus nodal discharge rate in inappropriate sinus tachycardia

Suppression of ventricular tachyarrhythmias thought to be caused in some part by increased sympathetic tone

157
Q

Give an example of a short acting injectable beta blocker

A

Esmolol

158
Q

What is an example of a class III anti-arrhythmic and how do they work?

A

Sotalol and Amiodarone

They block the repolarizing potassium current which results in prolongation of the action potential duration and effective refractory period

159
Q

What accounts for the pro-arrhythmic effects of class III anti-arrhythmics and in what conditions are the pro-arrhythmic effects enhanced?

A

They block the rapid component of the potassium current rather than the slow component making their effects more accentuated at slower heart rates (puts them at risk for early after-depolarization)

Accentuated with hypokalemia, bradycardia, intact status in females, increasing age, macrolide antibiotic therapy

160
Q

What is unique about amiodarone in terms of its anti-arrhythmic effects?

A

It has the broadest spectrum and exhibits properties of all four anti-arrhythmic classes

161
Q

Name some side effects of amiodarone?

A

Vomiting, anorexia, hepatopathies, and thrombocytopenia

162
Q

What is an example of a class IV anti-arrhythmic and how do they work?

A

Diltiazem

They are calcium channel blockers and slow AV nodal conduction and prolong the effective refractory period of nodal tissue. This effect is most notable at faster stimulation rate and in depolarized fibers

163
Q

What are adverse effects of class IV anti-arrhythmics?

A

Hypotension

Bradyarrhythmias

164
Q

How does digoxin work?

A

Digoxin binds to the Na-K-ATPase and inhibits it, this leads to increased intracellular Na, which causes the Na-Ca exchanger to move Ca into the cell to reduce intracellular Na.

Increased intracellular Ca causes increased sensitivity of the cardiac myocytes and increased contractility which leads to a decreased heart rate

165
Q

Why is hypokalemia a risk factor for digoxin toxicity?

A

Digoxin binds to the Na-K-ATPase pump at the same site as potassium. When potassium is decreased, Digoxin has more readily available binding sites. This results in inhibition of the Na-K-ATPase pump which leads to increased intracellular sodium.

Increased intracellular sodium causes the Na-Ca exchanger to move calcium into the cell in order to decrease intracellular sodium. Increased intracellular calcium results in increased contractility of the heart.

This is the mechanism for why digoxin works; however, when there is less potassium we see a larger effect for the same amount of drug decreasing the therapeutic window (which is narrow to begin with

166
Q

Name 5 things that predispose a patient to digoxin toxicity?

A 
Renal dysfunction
Hypokalemia
Advancing age
Chronic lung disease
Hypothyroidism
167
Q

When is magnesium indicated as an anti-arrhythmic and what are some potential adverse effects?

A

Indicated in torsade de points, and drug refractory ventricular tachyarrhythmias

Adverse effects: central nervous system depression, weakness, bradycardia, hypotension, hypocalcemia, QT prolongation

168
Q

TRUE OR FALSE: Adenosine is an effective treatment for dogs with AV node dependent tachyarrhythmias

A

FALSE

It is ineffective at slowing AV nodal conduction in dogs

169
Q

T/F- a recent Cochrane review reported a significant reduction in blood loss and need for blood transfusions after the use of EACA in patients undergoing major surgery?

A

true

170
Q

when are antifibrinolytic drugs contraindicated?

A

in patients that have prothrombotic diseases- DIC, aortic thromboembolism, IMHA, Cushing’s, upper urinary tract hemorrhage (obstruction can occur)

171
Q

T/F- a recent Cochrane review found evidence for an increased incidence of thrombotic events with the use of EACA or TXA?

A

false

172
Q

What is the concern re: antifibrinolytic use in cats?

A

can cause seizures and myocardial injury- their use is not recommended (at least use caution)

173
Q

what is the MOA of EACA?

A

competitively inhibits plasminogen activation; at higher doses may directly inhibit plasmin

174
Q

what is the half life of EACA? how is it excreted?

A

1-2 hrs, renal 65% and 30% hepatic metabolism then urinary excretion

175
Q

adverse effects of EACA?

A

hypotension, nausea, vomiting, diarrhea, weakness, myonecrosis, rhabdomyolysis

176
Q

MOA of tranexamic acid (TXA)?

A

competitive inhibitor of plasminogen activation and at higher concentrations is noncompetitive inhibitor of plasmin
Also competitively inhibits the activation of trypsinogen by enterokinases and noncompetitively inhibits trypsin and thrombin

177
Q

half life of tranexamic acid? excreted via what route?

A

2-3 hours; 95% excreted unchanged in kidneys

178
Q

T/F- tranexamic acid, TXA, is 6-10x more potent than EACA?

A

true

179
Q

t/f- TXA increased mortality when given early (within 3 hours) to trauma patients with significant risks of bleeding?

A

false- it decreases mortality if given within 3 hours but after 3 hours increases risk of death due to bleeding

180
Q

adverse effects of TXA?

A

hypotension after rapid administration, GI side effects, seizures after high doses, care in patients with renal disease

181
Q

t/f- a recent Cochrane review did not support concerns stating that TXA causes thrombosis?

A

true

182
Q

what are some other names for desmopressin acetate?

A

1-desamino-8-d-arginine vasopressin, DDAVP

183
Q

what is the MOA of DDAVP?

A

it has no vasopressor activity (v1 receptor); it enhances antidiuretic activity and stimulation of endothelial release of factor VIII and vWF (v2 receptors); it is an altered form of vasopressin

184
Q

what is the half life of DDAVP after IV administration?

A

2.5-4.4 hrs

185
Q

t/f- the absorption of DDAVP after oral administration is reliable?

A

false- it is destroyed in GI tract

186
Q

what types of veterinary patients would benefit from receiving DDAVP?

A 
hemophilia A (deficiency of factor VIII), type I vWD
Does not work for type II or III vWD, uremic thrombocytopathia, congenital platelet function defects, chronic liver disease, diabetes insipidus
187
Q

t/f- a recent cochrane review concluded that use of DDAVP did not reduce the need for blood transfusion in patients that do not have congenital bleeding disorders

A

true

188
Q

adverse effects of DDAVP?

A

hypotension (rapid administration), water retention, hyponatremia, tachyphylaxis, thrombotic events, transient thrombocytopenia in dogs with type II vWD (GSP and wirehaired pointers)

189
Q

what is the indication for use of protamine?

A

treatment or prevention of of bleeding due to administration of UFH or LMWH

190
Q

MOA of protamine?

A

it is positively charged and combines with the negatively charged heparin, forming a protamine-heparin complex that is devoid of anticoagulant activity; it competes with ATIII for binding with heparin

191
Q

adverse effects of protamine?

A

systemic hypotension (histamine release via mast cells), anaphylactic rxns (antibody and Ag-Ab complexes), severe pulmonary hypertension (complement activation and TXA2 and endothelin release), NCPE, thrombocytopenia

192
Q

t/f- protamine dose should be doubled if some time has elapsed since administration of heparin?

A

false- protamine should be halved because heparin has an extremely low half life

193
Q

what is the MOA of conjugated estrongens for shortening prolonged bleeding times?

A

unknown, but may increase the levels of vWF and factors VII and XII

194
Q

what patients should be considered for treatment with conjugated estrogens?

A

patients with acute and subacute renal failure in combination with DDAVP

195
Q

In what patients is recombinant factor VIIa used?

A

hemophilia A & B patients with antibodies against factor VIII & IX, respectively; uremia, vWD, liver disease, trauma, surgical procedures

196
Q

what is the MOA of rFVIIa?

A

formation of TF-factor VIIa complex at the site of endothelial damage, which initiates coagulation & binding directly to the phospholipid membrane of activated platelets

197
Q

what is the half life of rFVIIa?

A

2.7 hours

198
Q

adverse effects of rFVIIa?

A

rare; thromboembolic states, type I hypersensitivity reactions

199
Q

t/f- yunnan paiyao has been shown to markedly shorten bleeding and clotting times in experimental states in rabbits, rats, and humans?

A

true

200
Q

what are some concerns about giving yunnan paiyao?

A

not overseen by FDA; ingredients not known; contamination with mycotoxins, heavy metals, microbial agents, pesticides

201
Q 
Give examples of each of the following:
alkylating agents
antibiotic chemo drugs
antimetabolites
nsaids
hormones
enzymes
platinum products
vinca alkaloids
tyrosine kinase inhibitors
A

alkylating agents - cyclophosphamide, chlorambucil, CCNU, carmustine

antibiotic chemo drugs - doxorubicin, actinomycin

antimetabolites - methotrexate, cytosine arabinoside

nsaids - piroxicam, meloxicam, deracoxib

hormones - prednisone

enzymes - L-aspariginase

platinum products - cisplatin, carboplatin

vinca alkaloids - vincristine, vinblastine

tyrosine kinase inhibitors - toceranib phosphate, masitinib

202
Q

What is acute tumor lysis syndrome?

A

Complication of chemotherapy that occurs in patients with chemotherapy or radiation responsive tumors. Destruction of tumor cells leads to release of intracellular electrolytes as well as toxic by products of cell necrosis into circulation. May see renal failure, metabolic acidosis, cardiovascular collapse, vomiting, diarrhea, hyperkalemia, hyperphosphatemia, hypocalcemia, and azotemia.

203
Q 
When does the nadir occur for each of the following drugs?
doxorubicin
cyclophosphamide
cisplatin
carboplatin
A

doxorubicin 7-10 days
cyclophosphamide 7-10 days
cisplatin 7 and 16 days
carboplatin 11 and possibly 21 days

204
Q

Below what neutrophil count are prophylactic antibiotics warranted?

A

Below 1,000 cells/ul

205
Q

What chemotherapy drugs most commonly extravasate? What are the clinical signs and when do they occur?

A

Doxorubicin is the most common. Other ones that are irritating are vinca alkaloids and anthracyclines.

Clinical signs include pain, pruritus, erythema, moist dermatitis and necrosis

Signs may occur for 7-10 days with doxo, and up to 7 days with vinca alkaloids.

206
Q

What drug can be given if doxorubicin extravasates?

A

Dexrazoxane

207
Q

To what specific colitis are chemotherapy patients predisposed? What is the treatment?

A

Clostridial colitis

Treatment: sulfasalazine, metronidazole, ampicillin, tylosin, increased fiber content

Doxorubicin can cause hemorrhagic colitis that is responsive to metronidazole or sulfsalazine

208
Q

Cyclophosphamide administration can result in which specific toxicity?

A

sterile hemorrhagic cystitis

209
Q

What neurologic signs can be seen with each of the following drugs?
vinca alkaloids
cisplatin
5-fluorouracil

A

vinca alkaloids: Peripheral neuropathies such as hind limb weakness, partial paralysis, and ileus leading to abdominal pain and constipation

cisplatin: cortical blindness

5-fluorouracil: excitability, blindness, tremors, dysmetria, and death. In dogs, it can also result in excitation, seizures, and ataxia

210
Q

What are the reported toxocities for alkylating agents?

A 
Alopecia
Bone marrow suppression
Gastrointestinal toxicity
Nausea
Inappetence
Vomiting
Diarrhea
211
Q

What are the reported toxocities for antibiotics that are used for chemotherapy?

A 
Alopecia
Bone marrow suppression
Gastrointestinal toxicity
Nausea
Inappetence
Vomiting
Diarrhea
Necrosis, ischemia, and severe soft tissue
reaction if given perivascularly
212
Q

What are the reported toxocities for antimetabolites?

A 
Alopecia
Bone marrow suppression
Gastrointestinal toxicity
Nausea
Inappetence
Vomiting
Diarrhea
213
Q

What are the reported toxocities for enzymes used for chemotherapy?

A

Anaphylaxis

214
Q

What are the reported toxocities for platinum products?

A 
Bone marrow suppression
Gastrointestinal toxicity
Inappetence
Nausea
Vomiting
Diarrhea
215
Q

What are the reported toxocities for protein tyrosine kinase inhibitors
(toceranib phosphate, masitinib)?

A 
Bone marrow suppression
Gastrointestinal toxicity
Inappetence
Nausea
Vomiting
Diarrhea
216
Q

What are the reported toxocities for vinca alkaloids?

A 
Alopecia
Bone marrow suppression
Gastrointestinal toxicity
Ileus
Peripheral neuropathies
217
Q

What specific toxicity do we worry about with cisplatin?

A

Pulmonary edema and death in cats, nephrotoxicity in dogs

218
Q

What specific toxicities do we worry about with doxorubicin?

A

Cumulative dose–related risk of
dilated cardiomyopathy in dogs, possible renal
toxicity in cats, allergic reactions in both
species, hemorrhagic colitis

219
Q

What specific toxicity do we worry about with CCNU?

A

Cumulative dose–related risk of hepatotoxicity

220
Q

What specific toxicities do we worry about with L-Asparaginase?

A

Pain on injection, pancreatitis,

insulin resistance, anaphylaxis

221
Q

How can acute tumor lysis syndome cause renal failure?

A

Nucleic acids released from cellular necrosis include purines, which are metabolized to uric acid. Increased levels of uric acid exacerbate metabolic acidosis and renal impairment or failure. Deposition of calcium phosphate salts in the renal tubules in addition
to the aforementioned biochemical alterations, intraluminal tubular obstruction, intravascular volume depletion, and release of malignancy-associated nephrotoxins can result in oliguric renal
failure.

222
Q

When can we see signs of acute tumor lysis syndrome occur?

A

Hours to days after therapy has been administered.

223
Q

what is the mechanism of action of beta lactam antimicrobials?

A

interfere with bacterial cell wall synthesis via binding to and inhibiting the transpeptidases and peptidoglycan-active enzymes (collectively referred to as penicillin-binding proteins (PBPs)

224
Q

what is the role of penicillin binding proteins?

A

they catalyze the cross-linking of the glycopeptides that form the bacterial cell wall

225
Q

t/f: beta lactams are bactericidal?

A

true

226
Q

are beta lactam antimicrobials lipid soluble or insoluble?

A

insoluble

227
Q

which organs do not get high concentrations of beta lactams b/c of their lack of crossing biological membranes?

A

testes, eyes, brain, prostate

228
Q

how are most beta lactams excreted?

A

via the kidney into the urine- urine levels can be many times higher than those seen in serum

229
Q

how are the cephalosporins classified according to Ch 176 in Hopperstein?

A

five generations (1-5); more gram negative specific with increasing generation among the first 3 generations

230
Q

which types of bacteria have been known to produce a beta lactamase enzyme that inactivates the beta lactams?

A

staph bacteria; many gram negative rods

231
Q

What is ESBL?

A

extended spectrum beta lactamase- it can hydrolyze penicillins, cephalosporins and aztreonam; many gram negative bacteria produce ESBL; it does not confer resistance to the carbapenems

232
Q

methicillin resistant staphylococci are resistant to all beta lactam antimicrobials except ______?

A

the fifth generation cephalosporins

233
Q

describe the spectrum of activity of penicillin G

A

gram positive, anaerobic except Staph; synergistic with aminoglycosides, drug of choice for strep, clostridial, and actinomyces infection

234
Q

spectrum of activity of extended spectrum penicillins (amoxi and ampicillin)?

A

less active against gram + and anaerobic than pen G; greater effect against gram negatives
addition of beta lactamase inhibitor results in greater activity against gram negative, some gram positive anaerobes

235
Q

spectrum of activity of antipseudomonal penicillins (ticarcillin, piperacillin)?

A

pseudomonas and proteus inhibition; otherwise similar to other penicillins

236
Q

describe the activity of 1st gen cephalosporins?

A

cefazolin, cephalothin, cephalexin.. increased activity against some beta lactamase producing organisms; good gram positive, moderate gram negative, minimal anaerobe

237
Q

describe the activity of 2nd gen cephalosporins?

A

cefoxitin, cefaclor, cefotetan, cefuroxime….. moderate gram positive, greater gram negative

238
Q

describe the activity of 3rd gen cephalosporins?

A

cefotaxime, ceftriaxone, ceftiofur, cefpodoxime, cefovecin….. good gram negative, good for CNS disease

239
Q

describe the activity of carbapenems?

A

broad spectrum when used as sole agent; resistance is rare

240
Q

what is an adverse effect of the carbapenems?

A

nephrotoxic (imipenem >meropenem)

241
Q

What types of bacteria are most commonly isolated from critically ill patients?

A

Staph pseudintermedius, other staph, E coli, Klebsiella, Pasteurella, beta hemolytic strep, Pseudomonas, Proteus, Enterobacter, Enteroccocus

242
Q

Name a good first choice abx (empirical treatment) for Pasteurella, Strep, Actinomyces

A

penicillin or aminopenicillin

243
Q

Name a good first choice abx (empirical treatment) for Enterobacgteriaceae

A

aminoglycosides, cephalosporins (cefotaxime, ceftazidime), ticarcillin, ampicillin-sulbactam

244
Q

Name a good first choice abx (empirical treatment) for blood borne pathogens (Ricketssia, Ehrlichia, Hemoplasma)

A

doxycycline hyclate or monohydrate; fluoroquinolone as alternative

245
Q

T/F: the treatment duration for antimicrobials should be as long as possible?

A

false

246
Q

T/F: It is easier to escalate an antimicrobial rather than to de-escalate after receiving C&S results?

A

false- easier to de-escalate to a less expensive agent

247
Q

In urinary tract infections, how many E coli organisms are resistant to cephalexin and enrofloxacin?

A

50% to cephalexin, 22% to enrofloxacin

248
Q

Which antimicrobials are potentially effective against Pseudomonas?

A

fluoroquinolones, aminoglycosides, extended spectrum penicillin (ticarcillin); resistance is more likely if pt has been previously exposed to that abx

249
Q

When you have a suspect MSRP infection, which abx may be needed?

A

chloramphenicol, rifampin, aminoglycosides, tetracycline

250
Q

Diffusion of abx into tissues is usually limited by what?

A

Perfusion/tissue blood flow (perfusion rate-limited drug diffusion)

251
Q

What is it called when penetration of abx into the tissue is limited by the cell’s lipid membrane?

A

permeability rate-limited drug diffusion

252
Q

When a drug is limited by permeability of the cell, what are the options for the drug to get into the cell?

A

must be lipid soluble or actively carried across the membrane to attain effective concentrations in the tissues

253
Q

Name some examples of cells that cause permeability rate-limited drug diffusion

A

CNS, eye, prostate

254
Q

T/F: modest doses of abx are often sufficient to attain high abx concentrations in renal tubules and lower urinary tract?

A

true; urine concentration of abx may be 100x greater than plasma concentration

255
Q

What is a breakpoint?

A

The highest MIC achievable (usually a serum concentration of antimicrobial given at routine doses) that still inhibits growth of that microorganism

256
Q

What are the three types of bacterial resistance?

A
  1. Intrinsic: inherent feature of a microorganism that results in lack of activity of an antimicrobial drug or class of drugs. Example is pseudomonas resistance to beta lactams
  2. Circumstantial: when an in vitro test predicts susceptibility but in vivo the antimicrobial lacks efficacy.
  3. Acquired: change in the phenotypic characteristics of a microorganism, compared with the wild type, which confers decreased effectiveness of am antimicrobial against that microorgamism
257
Q

Define MDR, XDR, and PDR

A

MDR: multidrug resistant, those not susceptible to at least one agent in three or more class of antimicrobials to which they are usually susceptible

XDR: extensively drug resistant, susceptible to only one or two classes or antimicrobials

PDR: pandrug resistant, not susceptible to all known or licensed antimicrobials

258
Q

What is the difference between escalation and de-escalation therapy?

A

Escalation therapy involves selecting an antimicrobial with a narrow spectrum of activity that likely covers the pathogen causing the suspected infection

De-escalation therapy consists of the empiric administration of broad-spectrum antimicrobials aimed to cover all pathogens most frequently related to the infection

259
Q

What is the mechanism of resistance for methicillin-resistant staphylococcus?

A

Acquisition of the mecA gene, which encodes an altered penicillin-binding protein, making it resistant to all beta lactams

260
Q

For methicillin-resistant staphylococcus what is the drug of choice?

A

Vancomycin, or the aminoglycosides

261
Q

What is the mechanism of resistance of enterococcus species?

A

Acquisition of aminoglycoside-modifying enzymes (AME) or alterations in penicillin-binding proteins (PBP5)

262
Q

What is the drug of choice for MDR enterococcus?

A

It may not need to be treated if the patient is asymptomatic

If symptomatic, use either 1) combination of ampicillin and gentamicin, or 2) vancomycin

263
Q

What are the mechanisms of acquired resistance for pseudomonas?

A
  1. Decrease in intracellular drug entry from efflux pumps or altered membrane structure
  2. Enzymes that modify or destroy antimicrobials
  3. Modification of the target of the antimicrobials (DNA gyrase mutation)
264
Q

What is the drug of choice for MDR pseudomonas?

A

Amikacin or a carbapenem

Combination therapy is unlikely to be effective

265
Q

In what bacteria are extended spectrum beta lactamases most commonly found?

A

E. coli
Klebsiella pneumoniae
Enterobacter

266
Q

Enterococci have a high level of intrinsic resistance to which antimicrobials?

A 
cephalosporins
clindamycin
aminoglycosides
possibly fluorquinolones
TMS
267
Q

Pseudomonas has a high level of intrinsic resistance to which antimicrobials?

A

Beta lactams (except ticarcillin, piperacillin, ceftazidime, and the carbapenems)

268
Q

What is the MOA of dexmedetomidine?

A

Highly selective α2-adrenergic agonist.
Induces sedation by decreasing activity of noradrenergic neurons in the locus ceruleus in the brain stem, thereby increasing the activity of inhibitory gamma-aminobutyric acid neurons in the ventrolateral preoptic nucleus.
Twice as potent as medetomidine.

269
Q

What are contraindications to dexmedetomidine use?

A

Cardiovascular disease, respiratory disorders, liver or kidney disease, shock, severe debilitation, or stress due to extreme heat, cold, or fatigue.

Has not been evaluated in dogs less than 16 weeks old and in cats less than 12 weeks old.

270
Q

What are the side effects of dexmedetomidine?

A

Bradycardia, vasoconstriction, muscle tremors, transient hypertension, reduced tear production, occasional AV block, decreased respiration, hypothermia, urination, vomiting, hyperglycemia, and pain on IM injection.

Rare effects include prolonged sedation, paradoxical excitation, hypersensitivity, pulmonary edema, apnea, and death from circulatory failure.

271
Q

Name some drug interactions with dexmedetomidine

A

Dose reduction may be indicated when used with anesthetics, opiates, sedatives, and hypnotics. If used with atropine or glycopyrrolate arterial blood pressure and heart may significantly increase which is not recommended.
Do not use epinephrine to reverse effects of dexmedetomidine.
Yohimbine will reverse the effects but atipamezole is preferred.

Auburn ECC (26 decks)

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