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Pharmacology > Pharmacology in disease and altered physiology > Flashcards

Pharmacology in disease and altered physiology Flashcards

1
Q

What drug factors affect drug concentration at the site of action?

A

Drug composition

Soluability

Routes of administration

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2
Q

What liver factors influence drug concentration at the site of action?

A

Not relevant in parental administration

First pass effect/metabolism

Conversion of pro-drugs to drugs

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3
Q

What plasma factors influence drug concentration at the site of action?

A

Free drug vs. protein bound drugs

Metabolites

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4
Q

What tissue factors influence drug concentration at its site of action?

A

Penetration & distribution

Bound vs. free drug

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5
Q

What kidney factors influence drug concentration at the site of action?

A

Excretion vs. absorption

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6
Q

Name five routes of drug excretion

A

Urine

Bile

Saliva

Milk

Air

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7
Q

List two major ways in which a disease process can alter pharmacological processes

A

Pharmacokinetics (the way the body handles the drug)

Pharmacodynamics (the way the drug alters function)

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8
Q

What is an important consideration when applying the APVMA guidelines to patients?

A

Prior to registration by the APVMA for therapeutic use, efficacy and safety of drugs are determined by testing them in health experimental animals and healthy example of the target species. In clinical practice, patients are not generally healthy

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9
Q

What are some considerations when prescribing drugs to patients with enteric disorders?

A

Reduction in SI length (esp > 70%): Sx, inflammation

Alteration of the gastric pH

Reduced GIT transit time/malabsorption (IBD, diarrhoea)

(also consider heart and liver function)

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10
Q

What are the considerations when administering medication to patients with cardiovascular disease?

A

Reduced tissue perfusion

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11
Q

What considerations are important when administering medicine to a patient with hepatic disorders?

A

Bile needed for fat absorption

Enterohepatic recycling

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12
Q

Briefly describe the elimination of drugs from the renal system

A

Passive elimination of small drug molecules (ionized and unionized)

Plasma protein bound drugs cannot be filtered

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13
Q

What percentage of renal plasma flow goes to the glomerulus?

A

10%

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14
Q

What portion of the renal plasma flow goes to the peritubular capillaries of the kidney?

A

90%

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15
Q

Briefly describe active tubular secretion

A

Active secretion occurs in the proximal tubule, against gradient and protein binding

Can be competition between drugs for the same transporters

Basic carriers e.g. cimetidine, neostigmine

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16
Q

Briefly describe active tubular reabsorption

A

Active tubular reabsorption also occurs mainly in the proximal tubule

Primarily endogenous compounds, e.g. Na+, K+, uric acid, glucose

Also drugs with similar structure to amino acids, e.g. alpha-methyl-dopa, aminoglycerides

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17
Q

Briefly describe passive tubular reabsorption

A

Non-ionised (lipophilic) drugs move from renal tubule back to blood stream along concentration gradient

Urine pH will affect reabsorption of weak acids/bases (ion trapping)

Increased urine flow (e.g. forced diuresis) can reduce passive resorption by reducing concentration gradient

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18
Q

What could be given to increase renal elimination of asprin (weak acid) or phenobarbitone (pKa 7.2)?

A

Bicarbonate

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19
Q

What could be given to increase renal elimination of amphetamine (pKa 5)?

A

Ammonium chloride

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20
Q

When might increasing urine flow (forced diuresis) may be useful in drug intoxications?

A

When kidney is the main route of elimination

AND the drug is normally extensively reabsorbed

Especially irritant drugs

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21
Q

Are drugs that are excreted changed or unchanged most signficantly affected by reduced renal function?

A

Unchanged

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22
Q

When might kidney disease not affect excretion or function of a drug?

A

When kidney disease is not especially severe (large physiological reserve)

When other routes of elimination also occur

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23
Q

What is a useful indicator of the renal clearance of most drugs?

A

Renal clearance of most drugs is proportional to creatinine clearance

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24
Q

Define renal clearance

A

The volume of plasma “cleared” by a substace that is removed by the kidney per unit time (e.g. ml/min)

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25
What is the formula for renal clearance?
CLr = (Cu x Vu)/Cp Where CLr = renal clearance Cu = urinary drug concentration Vu = urine volume Cp = plasma drug concentration
26
What factors determine the rate of glomerular filtration?
Rate of glomerular filtration + Rate of active tubular secretion - Rate of passive reabsorption
27
What effects will renal disease cause on pharmacokinetics of drugs?
Halflife increases (especially if excreted unchanged) Distribution may change (especially if protein-bound in plasma) Nephrotic syndrome can resultin in proteinurea and uraemia: altered protein binidng my increase drug effects across the BBB (e.g. propafol) Intestinal oedema may decrease absoprtion Nephrotoxic drugs should be avoided if renal failure
28
List four nephrotoxic drugs
Aminoglycosides (especially if dehydrated) Amphotericin B Polymixin NSAIDs
29
What could be used instead of Enalapril in a patient with renal disease?
Enalapril = 95% renal Beazepril = 45% renal, 55% hepatic
30
Should NSAIDs be used if there is decreased renal function or hypotension?
No, NSAIDs = counterindicated
31
What is a consideration when using COX-1 inhibitors in patients with renal impairment?
COX-1 inhibitors can significanly decreased renal perfusion
32
What is a consideration when using COX-2 inhibitors in a patient with decreased renal function
COX-2 is constitutively expressed in kidney and regulates intravascular volume (via renin release and regulating Na+ excreation, mainting renal blood flow)
33
What are some of the effects of nonselective NSAIDS or COX2 inihibitors in patients with decreased renal function?
Oedema and modest increased in blood pressure (beware pre-existing hypertension or patients on anti-hypertensive e.g. ACEI)
34
What three factors are important in reducing the dose of a drug in patients with chronic renal disease?
Therapeutic index Renal clearance / total clearance Severity of renal impairment
35
How should dosing be changed in response to renal disease?
In most cases, can estimate change in dosing from change in GFR Increase dosing interval and/or decrease dose rate Therapeutic drug monitoring ideal
36
How much must renal function be reduced before affecting plasma urea and creatinine?
75% (functional reserve)
37
How can glomerular filtration rate (GFR) be estimated using creatining clearance?
Clcr = (Urine [Cr] x volume)/(plasma [Cr] x collection time) Where Clcr = creatinine clearence Cr = creatinine
38
How dose plasma [Cr] relate to GFR?
Creatinine is produced at a constant rate by muscle metabolism Plasma [Cr] is inversely proportional to GFR
39
How may age affect the relationship betwee plasma creatinine and glomerular filtration rate?
Renal function, GFR, and muscle mass (and therefore creatinine) may all be reduced to varying degrees in the elderly. Since [Cr] is used to estimate GFR, a value considered "normal" may actually be abnormal
40
What is the hepatic arterial buffer response?
Decreased blood flow to/from GIT decreases portal blood flow. There is a compensatory increase in hepatic arterial blood flow
41
What effect do volatile anaesthetics have on total hepatic blood flow?
Increased by desflurane and isoflurane Decreased by halothane (disrupts hepatic arterial buffer response)
42
Describe the pathophysiology of liver disease?
Hypoproteinaemia, decreased destriction of renin, portal hypertension \> ascites, oedema, pulmonary oedema Decreased urea synthesis \> polyuria Decreased RBC production, possible effects on EPO \> anaemia Decreased albumin-bound Ca++ and Vit D conversion \> hypocalcemia \> Hypoglycaemia, hypothermia, decreased blood clotting, jaundice \> Increased blood ammonia, bile acids \> acid base and electrolyte abnormalities \> Hepatic encephalopathy \> Autonomic dysnfucntion, increased circulating vasodilators, increased response to vasoconstrictors
43
How does hepatic dysfunction effect pharmacokinetics?
Decreased albumin and other proteins \> change in plasma protein binding Ascites and increased total body water compartments \> change in volume of distribution Decreased metabolims
44
Name one drug that should be avoided in patients with liver disease
Thiopentone
45
Name two drugs that are well tolerated by patients with hepatic dysfunction
Alfaxalone and propofol
46
Name three drug classes that may have exaggerated effects in patients with advanced liver disease, and that may induce or worsen hepatic encephalopathy.
Anaesthetics, sedatives, opioids NB the synthetic opioid Remifentanil is hydrolysed by blood and tissue esterases independently of the liver
47
Name some effects of advanced liver disease on pharmacology
Impaired elimination Prolonged the half life Potentiate the clincial effects of many drugs
48
List four considerations in the jaundiced patient
High anaesthetic mortality rate Marked hypotension and unresponsive to vasopressors Whole blood transfusions useful (even if PCV/TP okay) Extra care maintaining hepatic perfusion and myocardial function/circulating volume
49
How does chronic heart failure/shock alter pharmacokinetics?
Decreased vascular perfusion \> altered drug absorption im, sc, po Decreased hepatic and renal blood flow \> decreased drug clearance from plasma + possible decrease in hepatic enzyme activity Change in drug distribution\> Decreased perfusion to most organs, but increased perfusion to brain and myocardium (iv) Abnormalities e.g. porto-caval shunts \> impact bioavailabilty, reduced first pass, reduced conversion of pro-drugs
50
Describe how cerebral autoregulation effects pharmacokinetics in congestive heart failure with intravenous drug delivery
Cerebral auto regulation \> ensure brain recieves constant blood flow, regardless of cardiac output Cardiac output lower than normal \> increase in "leg-brain" circulation time The brain receives higher percentage of CO \> higher dose of drug **Onset slower, effect greater**
51
What are the cardiovascular changes that occur during pregnancy?
Increased CO (\>=50%) and HR (15-25%) Increased E & P \> Increased VD and decreased PVR \> Increased RAAS \> Increased plasma volume (45%) Increased Na+ retention \> Increased total body water Increased red cell mass (20-30%) = physiological anaemia of pregnancy Changes in water compartments (placenta, amniotic fluid and foetus)
52
What are the pulmonary changes that occur during pregnancy?
Progesterone \> bronchial and tracheal sm. m relaxation \> reduced airway resistance Progesterone \> hypersensitivity to CO2 \> Increased RR and TV Decreased PaCO2 and PACO2 Compensatory decreased serum bicarbonate \> maintains pH O2 consumption and CO2 production increased by 60% Reduced functional residual capacity
53
What are some of the effects on altered pulmonary changes during pregnancy on the pharmacokinetics of drugs?
Increased O2 consumption + decreased FRC &PaO2 \> Pre-oxygenation (anaesthesia pre-med) is less effective during pregnancy Increased RR and TV speeds uptake of inhalational drugs
54
What are the renal changes that occur during pregnancy?
Increased renal plasma flow and GFR Increased clearance of urea, creatinine and HCO3- \> Decreased plasma levels Progesterone \> Increased RAAS \> Increased water retention \> Decreased plama osmolarity Change in volume of distribution and excretion of certain draigs \> dose adjustments required Polar drugs (ionised) distributed throughout body water
55
What are the changes of the gastrointestinal system during pregnancy?
Decreased GIT transit time, Increased intestinal blood flow Gastric compression Change in GIT absorption of drugs Reduction in lower oesophageal pressure \> increased reflux
56
What factors should be considered when administering general anaesthetics during pregnancy?
Induction and changes in depth of inhalational anaesthesia occur faster Increased resting ventilation \> more agent to the alveoli/min Decreased FRC \> rapid replacement of lung gas with inspired agent General decrease in anaesthetic requiremnets (also applies to injectible GA agents)
57
Which agents cross the placenta?
All GA inhalational agents, most IV agents Benzodiazapine (significant and prolonged foetal effects) Opiates (Fentanyl may be safe, epidural with minimal effects)
58
Name four drugs that do not cross the placenta
All NMJ blockers Glycopyrrolate Insulin Heparin
59
Which drugs/classes cross the placenta and may be potentially dangerous?
Opiates Benzodiazapines Ephedrine Local anaesthetics Atropine Beta-blockers Vasodilators Thiopentone
60
Which drugs cross the placenta and may be potentially safe?
Alfaxalone Propofol Ketamine Fentayl \< 1 mu g /kg Epidural opiates (morphine, fentanyl, sufentanil) metoclopramide
61
Which andimicrobial drugs are safe to use during pregnancy
Beta lactams (1st choice) Macrolides, lincosamides
62
What antimicrobial drugs are unsafe to use during pregancny
Nitrofurantoin Streptomycine, gentamicin, amikacin? Tetracyclines Sulphonamides, trimethoprim Metronidazole Fluroquinolones?
63
Which drugs can affect lactation?
Atropine Bromocriptine (Prolactin antagonist, may also decrease false preganancy, cause abortion)
64
Which drugs will pass into milk?
Lipid soluable drugs
65
What are some considerations of drug dosing in the neonate?
More efficient absorption from the GI tract Increased volume of distribution Slower elimination Increased permeability of blood brain barrier Oral administration may upset colonisation of GIT Differences in hepatic enzymes Renal excretion poorly absorbed

Pharmacology (12 decks)

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