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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
Q

What is the formula for renal clearance?

A

CLr = (Cu x Vu)/Cp

Where

CLr = renal clearance

Cu = urinary drug concentration

Vu = urine volume

Cp = plasma drug concentration

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26
Q

What factors determine the rate of glomerular filtration?

A

Rate of glomerular filtration + Rate of active tubular secretion - Rate of passive reabsorption

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27
Q

What effects will renal disease cause on pharmacokinetics of drugs?

A

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
Q

List four nephrotoxic drugs

A

Aminoglycosides (especially if dehydrated)

Amphotericin B

Polymixin

NSAIDs

29
Q

What could be used instead of Enalapril in a patient with renal disease?

A

Enalapril = 95% renal

Beazepril = 45% renal, 55% hepatic

30
Q

Should NSAIDs be used if there is decreased renal function or hypotension?

A

No, NSAIDs = counterindicated

31
Q

What is a consideration when using COX-1 inhibitors in patients with renal impairment?

A

COX-1 inhibitors can significanly decreased renal perfusion

32
Q

What is a consideration when using COX-2 inhibitors in a patient with decreased renal function

A

COX-2 is constitutively expressed in kidney and regulates intravascular volume (via renin release and regulating Na+ excreation, mainting renal blood flow)

33
Q

What are some of the effects of nonselective NSAIDS or COX2 inihibitors in patients with decreased renal function?

A

Oedema and modest increased in blood pressure (beware pre-existing hypertension or patients on anti-hypertensive e.g. ACEI)

34
Q

What three factors are important in reducing the dose of a drug in patients with chronic renal disease?

A

Therapeutic index

Renal clearance / total clearance

Severity of renal impairment

35
Q

How should dosing be changed in response to renal disease?

A

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
Q

How much must renal function be reduced before affecting plasma urea and creatinine?

A

75% (functional reserve)

37
Q

How can glomerular filtration rate (GFR) be estimated using creatining clearance?

A

Clcr = (Urine [Cr] x volume)/(plasma [Cr] x collection time)

Where

Clcr = creatinine clearence

Cr = creatinine

38
Q

How dose plasma [Cr] relate to GFR?

A

Creatinine is produced at a constant rate by muscle metabolism

Plasma [Cr] is inversely proportional to GFR

39
Q

How may age affect the relationship betwee plasma creatinine and glomerular filtration rate?

A

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
Q

What is the hepatic arterial buffer response?

A

Decreased blood flow to/from GIT decreases portal blood flow. There is a compensatory increase in hepatic arterial blood flow

41
Q

What effect do volatile anaesthetics have on total hepatic blood flow?

A

Increased by desflurane and isoflurane

Decreased by halothane (disrupts hepatic arterial buffer response)

42
Q

Describe the pathophysiology of liver disease?

A

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
Q

How does hepatic dysfunction effect pharmacokinetics?

A

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
Q

Name one drug that should be avoided in patients with liver disease

A

Thiopentone

45
Q

Name two drugs that are well tolerated by patients with hepatic dysfunction

A

Alfaxalone and propofol

46
Q

Name three drug classes that may have exaggerated effects in patients with advanced liver disease, and that may induce or worsen hepatic encephalopathy.

A

Anaesthetics, sedatives, opioids

NB the synthetic opioid Remifentanil is hydrolysed by blood and tissue esterases independently of the liver

47
Q

Name some effects of advanced liver disease on pharmacology

A

Impaired elimination

Prolonged the half life

Potentiate the clincial effects of many drugs

48
Q

List four considerations in the jaundiced patient

A

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
Q

How does chronic heart failure/shock alter pharmacokinetics?

A

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
Q

Describe how cerebral autoregulation effects pharmacokinetics in congestive heart failure with intravenous drug delivery

A

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
Q

What are the cardiovascular changes that occur during pregnancy?

A

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
Q

What are the pulmonary changes that occur during pregnancy?

A

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
Q

What are some of the effects on altered pulmonary changes during pregnancy on the pharmacokinetics of drugs?

A

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
Q

What are the renal changes that occur during pregnancy?

A

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
Q

What are the changes of the gastrointestinal system during pregnancy?

A

Decreased GIT transit time, Increased intestinal blood flow

Gastric compression

Change in GIT absorption of drugs

Reduction in lower oesophageal pressure > increased reflux

56
Q

What factors should be considered when administering general anaesthetics during pregnancy?

A

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
Q

Which agents cross the placenta?

A

All GA inhalational agents, most IV agents

Benzodiazapine (significant and prolonged foetal effects)

Opiates (Fentanyl may be safe, epidural with minimal effects)

58
Q

Name four drugs that do not cross the placenta

A

All NMJ blockers

Glycopyrrolate

Insulin

Heparin

59
Q

Which drugs/classes cross the placenta and may be potentially dangerous?

A

Opiates

Benzodiazapines

Ephedrine

Local anaesthetics

Atropine

Beta-blockers

Vasodilators

Thiopentone

60
Q

Which drugs cross the placenta and may be potentially safe?

A

Alfaxalone

Propofol

Ketamine

Fentayl < 1 mu g /kg

Epidural opiates (morphine, fentanyl, sufentanil)

metoclopramide

61
Q

Which andimicrobial drugs are safe to use during pregnancy

A

Beta lactams (1st choice)

Macrolides, lincosamides

62
Q

What antimicrobial drugs are unsafe to use during pregancny

A

Nitrofurantoin

Streptomycine, gentamicin, amikacin?

Tetracyclines

Sulphonamides, trimethoprim

Metronidazole

Fluroquinolones?

63
Q

Which drugs can affect lactation?

A

Atropine

Bromocriptine (Prolactin antagonist, may also decrease false preganancy, cause abortion)

64
Q

Which drugs will pass into milk?

A

Lipid soluable drugs

65
Q

What are some considerations of drug dosing in the neonate?

A

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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