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VTS(ECC) Preparation > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Catecholamines

A

Augment arterial BP, contractility and cardiac output
They will not work without cortisol so may require glucocorticoid given simultaneously in the critically ill
Increase the metabolic O2 demand

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2
Q

Addressing hypotension

A
  1. Anticholinergic or reversal is a2
  2. Fluid bolus if Hypovolaemia
  3. Start dopamine CRI at pressor rates (lower rates will vasodilate)
  4. Give antiarrhthmics
  5. If no response to dopamine consider norepinephrine
  6. No response to catecholamines consider vasopressin and/or hydrocortisone
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3
Q

Dopamine

A

Precursor to epinephrine
B and A properties depending on dose (b at lower and a at higher)

Modest vasoconstriction and increase in BP

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4
Q

Dobutmaine

A

Synthetic analog to dopamine with primary b1 agonism
Moderately vasodilate and increases forward blood flow in the face of normal BP (increasing CO)

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5
Q

Ephedrine

A

Increases norepinephrine release from the SNS and is a bronchodilator
Modest decrease in HR whilst increasing CO, SVR and arterial BP
Can deplete norepinephrine stores

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6
Q

Norepinephrine

A

Primarily a agonism
Potent vasoconstriction to increase arterial BP
Will have varying affect on HR and CO depending on volume status
Used when ineffective to dopamine

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7
Q

Phenylephrine

A

A agonism only
Raises the BP after dopamine ruled ineffective

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8
Q

Vasopressin

A

Not technically a catecholamine but is a pure vasoconstrictor that may be useful if no response to catecholamines
Will increase SVR due to baroreceptor reflex in response to a decrease in HR/Vol

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9
Q

Epinephrine

A

Works on all receptors
Not usually a first choice unless CPR
Increases HR, SVR and CO
Increases arterial BP and pacemaker activity

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10
Q

Cardiovascular support drug choice

A
  1. Dopamine and/or dobutamine as increases heart rate and contractility and potentially CO. Modestly increases vasomotor tone; dopamine “pressure” and dobutamine “output”.
  2. Norepinephrine
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11
Q

Combining catecholamines does what?

A

Midway effects of both drugs I.e. increases in heart rate and BP without arrhythmia (norepinephrine and dopamine)

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12
Q

Which of vascular resistance and cardiac output is more powerful in determining arterial BP

A

Vascular resistance

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13
Q

Arterial vasomotor tone

A

Primary determinant of visceral and tissue perfusion

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14
Q

Vasoconstriction

A

Good thing unless affecting perfusion in which case dobutamine may be used to modestly vasodilate without affecting BP but improving the forward flow

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15
Q

Cortisol and catecholamines

A

The cardiovascular system doesn’t operate well without cortisol; low cortisol causes vasoparesis and impaired response to catecholamines (CIRCI/RAI) and so low dose hydrocortisone in the critically ill that aren’t responding to catecholamines will likely help improve catecholamine activity

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16
Q

What are some affects other than cardiovascular catecholamines can have

A

Increased glucose and lactate
Increased K uptake so Hypokalaemia
Increasing metabolic O2 demand
Impaired PLT

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17
Q

Vasopressin

A

Or known as ADH or AVP
Normally released in response to an increase in osmolality, decreased blood volume or decreased BP
G-coupled receptors that primarily induce vasoconstriction
Inhibited by glucocorticoids, opiates, natriuretic factors and GABA

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18
Q

V1 receptors

A

Smooth muscles
Vasoconstriction (vasodilation at cerebral, renal, pulmonary and mesenteric vessels)

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19
Q

V2 receptors

A

Renal collecting ducts, endothelial cells, platelets and vascular endothelium
Increased water permeability
Increased vWF release
Stimulation of aggregation
Vasodilation

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20
Q

V3 receptors

A

Posterior pituitary
ACTH release

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21
Q

Oxytocin (vasopressin receptor)

A

Mammary gland, uterus, GIT and endothelium
Contraction
Vasodilation

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22
Q

In vitro vasopressin

A

More potent vasoconstrictor compared to norepinephrine, angiotensin II, phenylephrine

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23
Q

Apart from vaso effects what is AVP involved in

A

Sleep
Memory
Temperature regulation
ACTH release

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24
Q

Uses of vasopressin

A

CPR
Vasodilatory shock
Central diabetes insipidus (desmopressin) - increased ADH action
vWD (desmopressin)
GI disease
Haemorrhagic shock

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25
Q

Side effects of vasopressin

A

Local irritation
Tissue necrosis
Increased liver and TBil enzymes
Reduced platelets
Low sodium
Anaphylaxis
Bronchospasm
Water intoxication

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26
Q

What BP would warrant immediate therapy with anithypertensives

A

180/120(>140)

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27
Q

Diseases that cause hypertension that warrant therapy

A

Cushings
Hepatic diseases
DM
Chromocytomas
EPO
Anaemia

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28
Q

ACE Inhibitors

A

Inhibit the conversion of ATI > ATII increasing bradykinin and reducing plasma volume
They induce arterial and veno dilation
Reduce aldosterone release so sodium and water excretion increased
Used for all forms of hypertension but can reduce it too much

I.e. enalipril, benazipril, ramipril and lisonopril

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29
Q

ATII receptor blockers

A

May be a safer antihyprtensive for those experiencing renal insufficiency
Dose-dependant fall in BP with minimal effects on HR and CO

I.e. Losartan, irbesartan, telmisartan

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30
Q

Adrenergic receptor antagonists

A

Block A and/or B
I.e. propranolol, atenolol, prazosin
B blockade = decreased renin, decreased HR, decreased adrenergy and decreased contractility
A blockade = antagonise contriction

Used when other anti hypertensives fail or in tachydysrhythmias, may also decrease bladder sphincter tone

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31
Q

Aldosterone blockers

A

I.e spironalactone

DCT and collecting ducts and decrease sodium reabsorption and decrease K excretion
Weak diuretic effect
If used with other hypertensives may induce renal insufficiency

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32
Q

Ca blockers

A

I.e. amlodipine, diltiazem
Reduce the Ca influx into smooth muscle cells reduces peripheral VR
Used in hypertensive crisis (arterial vasodilators may also be preferable)
#1 choice in CKD

Tachycardia, constipation, vomiting and weakness not uncommon

33
Q

Arteriolar vasodilators

A

Usually used in hypertensive crisis because they are very fast acting
Dilate arteries and relax resistance

I.e. hydralazine, sodium nitroprusside and fenoldopam

34
Q

Hypertensive emergency treatment

A

Aim to reduce BP 25% in first hour
Aim to reduce BP to 160/110-100 in the next 2-6h
I.e. sodium nitroprusside, hydralazine (may elect amlopidine)
* ischaemia will occur if done too rapidly

35
Q

Diuretics

A

Correct water and electrolyte excess
Act on the nephron to block the reabsorption of water and solute I.e. Na increasing there urinary excretion

Kidneys: regulate the absorption and excretion of water and solutes and rely on ADH to do so

36
Q

ADH requires

A

A functional tubular system otherwise there is inappropriate increase in ADH that requires therapeutic diuretics for water and solute excretion

37
Q

Na and water in the nephron and how this dictates diuretic therapy

A

Na highest in the PCT and LOH therefore diuretics such as mannitol, acetazolamide and furosemide better for dieresis and spironalactone and thiazides weaker as act on the more distal convoluted tubule area

38
Q

Mannitol (diuretic)

A

Osmotic diuretic that increases the osmolality of the ECF so fluid moves into this compartment and into IVS
Freely filtered by the glomerulus
No tubular reabsorption
Increasing fluid dieresis
Decrease renal vascular resistance
Decreases cerebral oedema
0.25-1g/kg

39
Q

Acetazolamide/CA inhibitor

A

Decreases proximal reabsorption resulting in a self-limiting metabolic acidosis
Increases distal Na reabsorption
Used in glaucoma

40
Q

Furosemide/loop diuretic

A

Inhibits Na-K-Cl at the loop of Henle
Marked natriuesis and dieresis and causes an osmotic gradient shift
Increases renal O2 parenchymal supply and decreases renal resistance
Increases ECF fluid removal
Used in CHF and fluid overload as well as Oliguria

41
Q

Aquaretics

A

Act in V2 receptors to promote solute free water clearance
Treat FW retention in hypervolaemic and hyponateaemic patients (HF, liver failure, SIADH)

42
Q

Diuretic therapy in renal disease

A

I.e. mannitol or furosemide
Converts Oliguria
Will increase dieresis but not improve renal function

43
Q

Diuretic therapy in heart failure

A

Combination of LOH and DCT diuretics particularly if not fully responsive to furosemide alone

44
Q

Diuretic use in liver failure

A

Try to reduce portal hypertension and oedema

45
Q

Common causes of GUE and treatment options

A

Anoxia to the gastrointestinal mucosa such as in hypovolaemic shock and drugs such as NSAIDS. Stress also (SIRS, masses etc)
H2RA, PPI, prostaglandin analogs are some options for treatment

46
Q

H2RA

A

Cimeditine, ranitidine
Work at gastric parietal cells and compete for gastric acid secretion > reduce gastric acid secretion
P450 metabolism
Work rapidly

47
Q

PPI

A

Irreversible inhibit H-K ATP in luminal parietal cells > stopping gastric secretion and reducing gastric reflux and duodenal ulcers
I.e. omeprazole, pantoprazole, esomeprazole
First pass metabolism
Peak effect after 2-5 days
More effective than H2RA

48
Q

Sucralfate

A

Viscous and binds tightly to epithelial cells creating a physical barrier whilst adhered to gastric ulcer or erosion
Signals PG to promote mucosal repair
Can absorb some drugs I.e. enro

49
Q

Misoprostal

A

PG analog that has mucosal protective and antacid properties
Acts on parietal cells to reduce gastric acid
Helpful in NSAID toxicity

50
Q

Effects of increasing gut pH

A

More susceptible to bacterial infections

51
Q

Neurokinin-1 antagonist

A

Maropitant
Reduces substance P in CNS and NK-1 in the gut
Must be over 11 weeks to avoid bone marrow suppression
Good for visceral pain
First-pass metabolism in the liver

52
Q

5HT3 antagonists

A

Ondanserron, granisetron, dolasteron
Block serotonin receptors (5HT3) both peripherally and centrally to reduce vomiting
Liver metabolism
Eliminated in urine and bile

53
Q

Metoclopramide

A

Both antidopaminergic and 5HT3 blocker reducing nausea and vomiting (block CRTZ)
Less effective in cats as lower dopaminergic receptors
Gastric prokinetic when given as CRI (increases transit time and reduces reflux)

  • don’t give if GI obstruction
54
Q

Promazine derivatives in vomiting patients

A

Centrally act
I.e. chlorpromazine and acepromazine
Travel sickness
Cardiovascular changes so caution to be used
Avoid if substantial liver disease

55
Q

Best prokinetic

A

Cisapride as stronger effects than most other prokinetics I.e. metoclopramide and erythromycin
Increases gastric emptying
Increases lower oesophageal sphincter tone
Not helpful in megaoesophagus as this is striated muscle
Good for idiopathic constipation

56
Q

Cholinomimetics as prokinetics

A

Bethanechol/ranitidine
Inhibit ACh
Increase colonic motility and gastric emptying

57
Q

Erythromycin

A

Powerful prokinetic working on motilin receptors
Increases lower oesophageal sphincter tone to reduce reflux
Increases lower bowel peristalsis
‘Gastric hunger’

58
Q

Opioids

A

Have little cardiovascular effects when given within therapeutic range
Have substantial effects on the respiratory system so care to be taken (pontine and medullary centres)
Stereospecific receptor binding throughout CNS and the peripheral system
Metabolised by the liver and excreted by the kidneys
Some can induce an excitatory response particularly if given with MAOIS and other antidepressants
Most increase ADH so cause urine retention
Decrease GI motility

59
Q

Morphine, meripidine and methadone can..

A

Release histamine inducing vasodilation and bronchoconstriction

60
Q

Strongest and weakest analgesic opioids

A

Fentanyl/remifentanil = strongest
Butorphanol = weakest

61
Q

Morphine

A

Mu opioid agonist
Sedation and analgesia
May cause histamine release, vomiting, diarrhoea, bradycardia
Lasts 4-6h

62
Q

Methadone

A

Similar to morphine
Some NMDA activity
Sedation & analgesia
Lasts 4-6h

63
Q

Fentanyl/remifentanil

A

Use to treat severe pain
Rapid onset and short duration
May induce dysphoria
Available in transdermal patches

64
Q

Butorphanol

A

Kappa agonist
Mild pain relief but good sedation
Lasts 1-2h
Partial mu reversal
Ceiling effect

65
Q

Buprenorphine

A

Partial agonist
Mild to moderate pain
Longer DOA 8-12h

66
Q

Benzodiazepines

A

Used as first line anticonvulsants in most patients unless HE/PSS
Works on inhibitory GABA receptors to potentialities GABA and may antagonise serotonin
Sedation, hypnosis, amnesia, anticonvulsant, skeletal muscle relaxation
Diazepam highly protein bound whilst midazolam is water soluble
Effects from sedative to excitatory and best given with an opioid to combat this
Midazolam at 0.005-0.4mg/kg may stimulate the appetite

67
Q

A2 agonists

A

Used for sedation and analgesia
Decrease autonomic responses by reducing norepinephrine release
Inhibit ADH/insulin (Diuresis and increased glucose)
Potentiate opioid analgesia even at low doses
Can decrease anaesthetic drug requirements <80%
Cardiovascular response is biphasic
Arrhythmia associate with bradycardia and reduced CO warrants reversal and +- anticholinergic

68
Q

A2 agonist biphasic response

A

Initially increased BP and SVR, decrease HR and CO
Then… decreased BP, HR and CO may remain reduced, variable SVR.

  • watch whole body perfusion, core organs usually remain perfused but other tissues may not
69
Q

Drugs eliminated via what body system are subject to enterohepatic recycling?
a. Renal
b. Hepatic
c. Urinary
d. Biliary

A

D

70
Q

Which of the following drugs is an example of an osmotic diuretic?
a. Furosemide
b. Mannitol
c. Atropine
d. Vasopressin

A

B

71
Q

Which of the following drugs is the best choice for a patient in congestive heart failure with hypotension?
a. Dopamine
b. Epinephrine
c. Dobutamine
d. Norepinephrine

A

C

72
Q

Mycophenolate, ciclosporin, leflunomide, and azothiaprine are examples of what type of drug?
a. Immunosuppressive agents
b. Antifungals
c. Macrolides
d. Calcium channel blockers

A

A

73
Q

What is the movement of a drug from the site of administration to the circulatory system called?
a. Absorption
b. Distribution
c. Metabolism
d. Elimination

A

A

74
Q

Which process is inefficient in the feline, which leads to their reduced ability to metabolize NSAIDs?
a. P450
b. Glucuronidation
c. Sulfonation
d. Reduction

A

B

75
Q

In the absence of an initial loading dose, a CRI will not reach steady-state plasma concentrations for how long?
a. One hour
b. One half-life
c. 3–5 hours
d. 3–5 half-lives

A

D

76
Q

A drug that binds to a receptor and blocks its response is known as what?
a. Agonist
b. Antagonist
c. Partial agonist
d. Mixed agonist/antagonist

A

B

77
Q

Which antiemetic is known to inhibit substance P in the vomiting center in the brain?
a. Metoclopramide
b. Ondansetron
c. Chlorpromazine
d. Maropitant

A

D

78
Q

Which of the following would be considered a potassium-sparing diuretic?
a. Spironolactone
b. Furosemide
c. Mannitol
d. Torsemide

A

A

VTS(ECC) Preparation (21 decks)

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