European Pharma Exam Flashcards
1
Q
Which of the 3 effects is not attributable to paracetamol: antipyretic, anti-inflammatory, analgesic
A
anti-inflammatory
2
Q
At which dose does liver toxicity from pcm occur?
A
150 mg/kg
3
Q
What are the risk factor for developing liver damage due to pcm (over)use? Name 3
A
1.alcoholism
2.preexisting liver disease
3.poor nutritional status
4
Q
What is the antidote for pcm?
A
N-acetylcysteine
5
Q
Why does malnutrition predispose to liver toxicity in pcm (over)use?
A
malnutrition results in lowerlevels of glutathion (antioxidant that detoxifies the pcm hazardous metabolite NAPQ1)
6
Q
What is the mechanism of action of NSAIDs?
A
inhibiton of prostaglandin synthesis by inhibiting cyclooxygenase
7
Q
What are the 2 isoforms of the COX enzyme and what are their functions? Name 3 for each
A
COX1: autoregulation of renal perfusion, gastric protection, thrmbocyte function
COX2: inflammation, closure ofductus arteriosus, pain perception
7
Q
What are the 4 main serious side effects of NSAIDs?
A
1.peptic ulcer
2.renal failure
3.thrombocytopathy (prevention of platelet aggregation)
4.worsening of heart failure
7
Q
What is 1 advantage and 1 disadvantage of COX-2 selective NSAIDs?
A
+: fewer GI side effects
-: some have been reported tocause severe cardiovascular events
8
Q
What are factors that increase the risk of a peptic ulcer in NSAID users? Name 8
A
- history of peptic ulcer
- RA
- DM
- heart failure
- use of corticosteroids
- use of SSRIs
- use of OAC
- H. pylori
8
Q
How do NSAIDs cause renal impairment
A
blocking prostaglandin production which are responsible for dilation of afferent arteriole –> constriction of afferent arteriole –> decreased renal blood flow & fluid retention
8
Q
Which NSAID inhibits platelet aggregation irreversibly?
A
acetysalylic acid
9
Q
What are the absolute inications for a PPI in NSAID use?
A
- age >70
- history of peptic ulcer
- untreated H. pylori
9
Q
What are factors that increase the risk of renal failure in NSAID users? Name 5
A
1.heart failure
2.dehydration
3.sepsis
4. pre-existing renal failure
5. use of RAAS inhibitors
10
Q
When is renal blood flow more prostglandin dependant?
A
when renal perfusion is low
11
Q
What are the 6 main absolute contraindications for NSAID use?
A
- active GI issue with bleeding risk (M. Crohn, perforated ulcus)
- history of perforated ulcus
- severe dehydration
- severe heart failure (NYHA 4)
- severe renal failure (eGFR <30)
- 3rd trimester pregnancy
12
Q
What are the 3 main side effects of opioids?
A
- Sedation
- Constipation
- Respiratory depression
13
Q
What is the risk of using opioids in patients with COPD?
A
respiratory depression
14
Q
What are the 3 laxative options when using opioids?
A
- Movicolon/lactulose
- Bisacodyl
- Enema
15
Q
Which 3 classes of medications increase therisk of contipation when using opioids?
A
- anticholinergics
- antidepressants
- diuretics
16
Q
Which class of medication increases the riskofrepsiratory depresion whe used in combination with opioids?
A
benzodiazepines
17
Q
What are the 3 phases of hemostasis?
A
- Platelet adhesion
- Fibrin formation (via coagulation cascade)
- Fibrinolysis (via plasmin)
18
Q
What is the cause of arterial thrombi? Venous thrombi?
A
arterial - interruption in endothelial layer –> leads to platelet aggregation
venous - circulatory stasis –> hypercoagulation
19
Q
What is the mechanism of action of aspirin (as anticoagulant)?
A
inhibits COX –> inhibition of thromboxane A2 –> inhibition of primary hemostasis
20
What is teh mechanism of action of clopidogrel/prasugrel/ticagrelor?
Inhibition of ADP receptor on platelets --> prevents platelet aggregation
21
What is the mechanism of action of dypiridamol?
Inhibits phosphodiesterase --> less phosphdiesterase activity --> prevents degradation of cAMP --> cAMP inhibits platlet aggregation
22
Which antiplatelet agents bind irriversibly?
aspirin & P2Y12 inhibitors
23
What is the duration of action of aspirin & P2Y12 inhibitors?
~10 days (lifespan of platelets)
24
What is the duration of action of dipyridamole?
12 hours
25
What are the 3 main indications for aspirin (as anticoagulant)?
1. AP/MI
2. TIA/stroke
3. peripheral arterial disease
26
What are the 3 main indications for P2Y12 inhibitors?
1. stent placement
2. MI
3. TIA/stroke
27
Which 3 classes of drugs increase the risk of hemorrhgae when used in combination with antiplatelet drugs?
1. corticosteroids
2. NSAIDs
3. SSRIs
28
How long before surgery with a high risk of bleeding do antiplatelet drugs need tobe stopped?
aspirin/P2Y12 inhibitors - 5 days
dipyridamole - 1 day
29
What type of surgery requires stopping antiplatelet agents?
when bleeding cannot be easily visualised and/or stopped
e.g. neurosurgery, head & neck surgery,liver/kidney biopsy
30
What are the 2 possible "antidotes" toantiplatelet agents?
1. desmopressin
2. platelet transfusion
31
Does a platelet transfusion counteract the action of dypiridamole?
No, platelets are inactive as long as the drug ispresent in the system
32
Which 4 clotting factors are dependent on vit K?
2,7,9,10
33
What is the T1/2 of acenocoumarol?
8-11 hours
34
What is the T1/2 of phenprocoumon?
160 hours
35
After how many hours does acenocoumarol reach its maximum effect?
36-48 hours
36
After how many hours does phenprocoumon reach its maximum effect?
48-72 hours
37
What are the 4 main indications of vit K antagonists?
1. atrial fibrillation
2. DVT
3. PE
4. mechanic valves
38
At which CHAD-Vasc score is a vit K antagonist indicated?
>1
39
What are 2 antidotes to vit K antagonists?
1. vit K
2. prothrombin complex concentrate
40
Which antibiotic increases risk of bleeding when used in combination with vit K antagonists?
cotrimoxazol
41
Which 3 medications are CYP2C9 inducers and therefore reduce the effectiveness of vit K antagonists?
1. phenytoin
2. carbamazepine
3. rifampicin
42
What is the genera INR target with vit K antagonists?
2.5-3.5
43
What is the target INR during active bleeding?
<1.7
44
What is the treatment for pt using vit K inhibitors with a case of non-life threatening hemorrhage? When does the effect of vit K administration start?
5 mg vit K PO or IV
Oral - after 8 hours
IV - after 6 hours
45
What is the treatment in case of life threatening hemorhage under vit K antagonist use?
5 mg vit K (PO or IV) + prothrombin complex concentrate
46
What are the components of the CHA2DS2VASC score?
C - cogestive heart failure
H - hypertension
A - age >75
D - DM
S - stroke/thromboembolism
V - vascular disease
A - age 65-74
Sc - sex
47
At which CHADSVASC score is there an indication for bridging when surgical intervention is planned for a petient with vit K antagonist use?
>4
48
What are the 3 absolute indications for bridging when surgical intervention is planned for a patient with vit K antagonist use?
1. afib with CHADSVASC >=8
2. recurrent DVT/LE or DVT/LE < 3 months ago
3. artificial valve or rheumatic valve disease
49
What is the mechanism of action of heparin?
inactivation of thrombin and factor X (via activation of antithrombin III)
50
What is the lab value that must be checked to assess the efficacy of heparin?
aPTT
51
What are the 2 main LMWHs?
nadroparin & enoxaparin
52
What is the difference in the mechanism of action of unfractinated heparin and LMWH?
LMWH has a much higher anti factor X activity and lower anti factor II activity
53
What lab value must be tested to assess the effect of LMWH?
anti factor X activity test
54
What are the 2 advantages of LMWH use as opposed to unfractionated heparin?
1. longer T1/2
2. anticoagulation activity can be much more reliably predicted
55
What is the main clearance route of LMWH?
renal
56
What are the 2 main indications for unfractionated heparin use?
1. prophylaxis
2. bridging for coumarins
57
When after a surgical procedure should prophylactic heparin be started?
6-8 hours
58
In a patient not previously using any anticoagulant, when is NO heparin propylaxis after surgery the correct choice? (3 indications)
1. active mobilisation can be achieved right after surgery
2. short surgical intervention (<30 min)
3. no risk factors for venous thrombosis present
59
In a patient not previously using any anticoagulant, when is standard heparin prophylaxis indicated? When is intensive heaparin prophylaxis indicated?
standard:
intevention >30min + ward admission
intensive:
thrombosis <6 months ago + ward admission
60
What is the dosage of standard prophylaxis with nadroparin?
1dd 2850 units
61
What is the dosage of intensive prophylaxis with nadroparin?
1dd 5700 units
62
When is heparin prophylaxis indicated in non-surgical patients? (2 indications)
1. obstetric/gynecologic intervention
2. immobility >4days + atleast one risk factor from the Padua score
63
Which 2 medication classes increase the risk of bledding when used in combination with heparins? (not anticoagulants)
1. nsaids
2. corticos
64
What is the antidote to heparin
protamine
65
which comorbidity increases the risk of bleeding when using heparins?
renal failure
66
What is the treatment in case of non-life threatening heamorrage when using unfractionated heparin?
stop heparin
67
What is the treatment in case of life thereatening heamorrage in a pt using unfractionated heparin?
IV 1 gram protamin, administer slowly
68
What is the T1/2 of unfractionated heparin?
1.5-2 hours
69
What is the T1/2 of LMWH?
3-4 hours
70
What are the 4 main DOACs and what do they inhibit
factor II: dabigatran
factor X: edoxaban, apixaban, rivaroxaban
71
Which DOAC is primarily cleared by the kidneys?
dabigatran
72
After how long after starting a DOAC does it reach its full effect?
2-3 days
73
Which 2 medications can raise the level of anti factor X DOACS?
1. verapamil
2. itroconazole
74
What is the antidote of dabigatran?
idarucizumab
75
What are the 3 mechanisms seen in medications used for lowering blood pressure? Which medication classes use each mechanism?
1. Promoting vasodilation --> reducing peripheral resistance: dihydropyridine Ca antagonists, RAS inhibitors, ARBs
2. Decreasing preload: nitrates, RAS inhibitors, diuretics
3. Reducing heart contractility: beta blockers, non-dihydropyridine Ca antagonists
76
What are the 3 main types of diuretics?
1. Loop diuretics
2. Thiazide diuretics
3. Potassium sparing diuretics
77
What is the mechanism of action of loop diuretics?
Inhibition of Na/K/2Cl transporter (loop of Henle) --> higher concentration of Na in urine --> water follows
78
What is the mechanism of action of thiazide diuretics?
inhibition of Na/Cl cotransporter (distal tubule) --> higher concentration of Na in urine --> water follows
79
What is the mechanism of action of potassium sparing diuretics?
Inhibition of aldosterone receptor --> Na/K transporter blocked --> Na reabsorption reduced --> more Na in urine --> water follows
80
What are the 3 potassium sparing diuretics?
spironolactone
amiloride
triamterene
81
What are the 2 primary indications for loop diuretics?
heart failure
cirrhosis
82
What is the effect of renal impairment on the action of loop diuretics? How should the dose be adjusted?
Na/K/2Cl channel is on the luminal side of the tubule
In renal impairment --> less filtration --> less filtrate reaching the channel
dose should be increased
83
What are the 2 main indications for thiazide diuretics?
hypertension
mild heart failure
84
What is the main indication for spironolactone?
NYHA 3 heart failure
85
what is the consequence of too rapid/aggressive correection of hyponatremia?
central pontine myelinosis
86
What are the 3 steps to treating hyperkalemia?
1. calcium gluconate
2. insulin (+glucose)
3. sodium polysterene sulfonate
87
What is the result of an adverse inetraction between diuretics & SSRIs?
SIADH
88
Which 3 drug categories require caution when used together with diuretics due to risk of hypotension?
1. blood pressure lowering medication
2. opiates
3. benzos
89
Which beta blockers are selective (name 3)? Which are non-selective (name 3)?
Selective:
1. atenolol
2. bisoprolol
3. metoprolol
Non-selective:
1. propranolol
2. labetalol
3. sotalol
90
Which beta blocker is also an alpha blocker?
labetalol
91
Which beta blocker is also an anti-arrythmic?
sotalol
92
What are the 4 main indications for beta blockers?
1. afib
2. angina pectoris
3. hypertension
4. heart failure (HFrEF)
93
What are the 2 factors which increase the risk of arrythmia with sotalol use?
1. hypokalemia
2. impared renal function (sotalol excreed by the kidneys)
94
Which 3 types of medications increase the risk of arrhythmia whne used in combination with beta blockers?
1. potasium lowering meds (e.g. diuretics)
2. meds affecting renal function (e.g. NSAIDs)
3. QT interval prolonging meds (e.g. antipsychotics)
95
What is the mechanism of action of Ca channel blockers? Which of the 2 effects is primarily seen with dihydropyridines?
blocking the inflow of Ca ions
* vascular smooth muscle --> vasodilation <== dihydropyridines
* myocardial cells --> reduced velocity of cardiac conductivity <== non-dihydropyridines
96
What does concommitant use of beta blockers and non-dihydropyridine Ca channelblockers increase the risk of?
bradycardia & AV conduction disorders
97
What are the 3 main indications for RAS inhibitors?
1. hypertension
2. heart failure
3. diabetic proteinuria
98
Which electrolyte disorder can be caused by RAS inhibitors? How?
Hyperkalemia
reduced aldosterone secretion --> reduced potassium excretion
99
What is a rare but life threatening complication of ACE inhibitors?
angioedema
100
What are the 2 main indications for digoxin?
1. heart failure
2. afib with rapid ventricular response
101
What is the mechanism of action of digoxin?
Blockade of Na/K/ATPase --> increase in intracellular sodium --> activation of Na/Ca exchnager --> increase in intracellular Ca --> positive inotropy
102
How is dogixin cleared?
kidneys
103
How should digoxin be dosed initially? Why?
initial loading with high dose
digoxin binds specifically to cardiac cells --> high concentration i cardiac cells needed for effect
104
What is the mechanism of action of nitrates?
Conversion of nitrates into nitric oxie --> vasodilation of venous system --> reduced preload
105
What are the 2 types of nitrates? How is each administered?
1. isosorbide dinitrate: mucosal (due to large first pass effect)
2. isosorbide mononitrate: orally
106
What is the mechanism of action of metformin? (3 mechanisms)
1. inhibition of glucose production in the liver
2. inhibition of glucose uptake in the ileum
3. increases peripheral insulin sensitivity
107
Can metformin result in hypoglycemia? Why (not)?
No, doesnot stimulate insulin production
108
What is the maximal dosage of insulin with a normal kidney function? What is the max dosage with areduced kidney function? What are the cut-offs of the kidney function?
eGFR >60 --> 3000 mg per day
eGFR 30-60 --> 1000 mg per day
109
Under which eGFR is metformin contraindicated?
<30
110
What is the reason metformin is contraindicated for pt with a low kidney function?
Metformin is exclusively cleared by the kidneys
Low kidney function --> low metformin clearance --> metformin accumulation --> lactic acidosis
111
How can a metformin overdose lead to lactic acidosis?
Reduced clearance --> accumulation
Metformi inhibits gluconeogenesis --> pyruvate cannot procede to the next step in gluconeogenesis (oxalate formation) --> chooses the path of lactic acid formation
112
What are the 4 important SU derivates? Which are short-acting? Which are long-acting?
Short acting: tolbutamide, gliclazide
Long acting: glibenclamide, glimepiride
113
What is the mechanism of action of SU derivates?
Stimulate releaseof insulin form beta cells, independently of glucose concentration
Blockade of K+ ATP channels --> depolarisation of beta cell --> release of insulin
114
Can SU derivates result in hypoglycemia? Why (not)?
Yes, stimulate insulin release independently of glucose concentration
115
Which SU derivate can be safely continued in patients with renal impairment? Why?
gliclazide
produces inactive metabolites which will nto result in hypoglycemia if accumulated
116
What are the 2 interactions betwen beta-blockers & SU derivates?
1. Beta blockers can mask early warning signs of hypoglycemia
2. Beta blockers can prevent hypoglycemia recovery: beta receptor activation in the liver results in hepatic glucose release; beta-blockers --> inhibit glucose release
117
What are the 2 stages of hypoglycemia symptoms?
1. Activation of adrenergic system: tachycardia, sweating, restlessness, tremors
2. Effect on the brain --> neurologic symptoms: confusion, dysartria
118
What is the mechanism of action of SGLT2 inhibitors?
inhibition of glucose reabsorption in the kidneys --> increased glucose excretion
119
What is the main side effect of SGLT2 inhibitors?
Euglycemic ketoacidosis
Loss of glucose via urine --> no insulin increase ==> euglycemia
+
Reduced glucose in blood --> conversion to lipolysis ==> ketones
120
What are the 2 intecarions between insulin & beta-blockers?
1. Beta blockers can mask early warning signs of hypoglycemia
2. Beta blockers can prevent hypoglycemia recovery: beta receptor activation in the liver results in hepatic glucose release; beta-blockers --> inhibit glucose release
121
What is the dosage & route of administration of glucagon in hypoglycemia?
1mg
subcutaneously or IM
122
What is the mechanism of action of TCAs?
Inhibition of reuptakeof serotonin & norepinephrine
123
What are the 4 toxidromes occuring as side effects of TCAs? Which of these is most common?
1. anticholinergic <-- most common
2. antihistaminic
3. anti-noradrenergic
4. quinidine-like
124
Which TCA is preferred for elderly patients? Why?
Nortriptyline, has fewer central antichoinergic side effects (confusion, cognitive dysfunction)
125
What is the main risk of TCA overdose?
arrythmia
126
Which hormonal disorder can be a side effect of SSRIs?
SIADH
127
What is the iteraction between SSRIs & thiazide diuretics
SSRI --> SIADH --> hyponatremia
thiazides --> natrium loss
SSRI + thiazide ==> risk of severe hyponatremia
128
What are the 5 characteristics of the anti-cholinergic toxidrome?
1. "Mad as a hatter": confusion, delirium
2. "Hot as hell": hyperthermia, tachycardia
3. "Red as a beet": flushed skin
4. "Dry as a bone": dry mouth, urine retention, constipation (absent bowel sounds)
5. "Blind as a bat": visual disturbances, mydriasis
129
What are the characteristics of the anti-histaminergic toxidrome?
Sedation & drowsines
130
What is the interaction between TCAs & anti-hypertensive medication?
othostasis
131
How is lithium excreted & reabsorbed?
excreted via kidneys
75% reabsorbed in the proximal tubule in proprtion to Na & water reabsorption
132
What is the therapeutic dosage range of lithium?
0.4-1.2 mmol/L
133
What are the 4 main side effects of lithium?
1. N&V
2. renal dysucntion
3. hypothyroidism
4. diabetes insipidus
134
Which lifestyle instruction is important togive to patients using lithoum? Why?
drinking 2-3 l of water per day
dehydration & sodium loss can result in lithium accumulation & toxicity
135
Which 3 medication groups can increase blood lithium levels?
1. diuretics
2. NSAIDs
3. RAS inhibitors (ACE-inhibitors, ARBs)
136
What is the mechanism of action of benzodiazepines?
enhance activity of GABA (inhibitory neurotransmitter)
137
Which benzodiazepine has the longest T1/2?
diazepam
40-100 hours
138
What are the 5 effects of benzodiazepines?
1. sedative
2. hypnotic (sleep-promoting)
3. anxiolytic
4. anti-convulsant
5. muscle relaxing
139
Why is benzodiazepine elimination often slower in the elderly?
higher fat % --> increased volume of distribution
140
What is therisk of benzodiazepines in pt with severe COPD?
respiratory depression
141
Which pt groups can show a paradoxical reaction to benzodiazepines (agitation, aggresive behaviour)?
children & elderly
142
What is the antidote for benzodiazepine intoxication?
flumazenil
143
What is the half-life of flumazenil & why is this important?
1 hour, much shorter that T1/2 of most benzos --> may need to be administered several times
144
What is the interaction between antibiotics & coumarins?
Antibiotics can potentiate the action of coumarins --> increased risk of bleeding
145
What are the 3 classes of beta lactam antibiotics?
penicillins
cephalosporins
carbapenems
146
What is the mechanism of action of beta-lactam antibiotics?
Inhibition of bacterial transpeptidase --> prevention of synthesis of bacterial peptidoglycan wall
147
Are beta-lactams more effective against active/rapidly-growing bacteria or against slow-growing/dormant bacteria? Why?
Active/rapidly-growing
Mechanismof action is breakdown of wall synthesis --> more effective in active/rapidly growing bacteria
148
Which type of bacteria are penicillins most effective against?
G+
149
What is the treatment of choice fro MRSA?
vancomycine or teicoplanin
150
Which penicillin is effective against Pseudomonas?
Piperacillin
151
What are the 2 beta-lactamase inibitors? Whhat are the 2 most common combinations of penicillin + beta-lactamase inhibitor?
Clavulanic acid, tazobactam
1. Amoxicillin + clavulanic acid
2. Piperacillin + tazobactam
152
What is the antibiotic of choice for Enterococcus faecalis?
amoxicillin
153
What is the antibiotic of choice for beta lactamasze producing S aureus? (2)
amoxicillin + clavulanic acid
flucloxacillin
154
What are the 2 most common side effects of penicillins?
1. drug eruption
2. diarrhea
155
Which penicillin is more strongly associatedwith the pssibility of drug eruptions as side effect?
amoxicillin
156
What is the treatment for a C. difficile infection?
metronidazole
157
What are the 2 main carbapenems? When are they typically used?
imipenem, meropenem
"last resort" antibiotics, used for ESBL
158
What is the mechanism of action of tetracyclines?
Inhibition of bacterialprotein synthesis
159
What are the 2 main contraindications for tetracyclines?
1. children <8
2. pregnancy
160
What lifestyle advice needs to be given topt taking tetracycline antibiotics?
avoid excessive sunlight exposure
161
Interaction of tetracyclines with which medication results in formation of insoluble complexes?
iron, calcium, magnesium, zinc
162
What type of bacteria are aminoglycosides effective against?
Gram neg
163
What are the 2 main aminoglycosides?
gentamicin
tobramycin
164
Are tetracyclines bacteriostatic or bactericidal?
Bacteriostatic
165
What is the mechanism ofaction of aminoglycosides?
blockinteractionbetween bacterial mRNA & ribososmes --> prevent protein synthesis
166
Which group of antibiotics cannot be absorbed by the intestines and thus can only be given via IV?
aminoglycosides
167
What are the 2 main side effects of aminoglycosides?
Ototoxicity
Nephrotoxicity
168
What are the 3 main macrolide antibiotics?
erythromycin
azithromycin
clarithromycin
169
What type of bacteria are macrolides effective against?
G+
Intracellular (legionella, chlamydia, mycobacteria)
170
What is the most important side effect of macrolides?
QTc prolongation
171
Which enzyme are macrolides metabolised by?
CYP3A4
172
What is the mechanism of action of cotrimoxazol?
blocking of folic acid synthesis --> bacteria cannot produce RNA/DNA
173
What is the interaction between cotrimoxazole & MTX?
severe folic acid depletion --> bone marrow suppression
174
What is the interaction between vit K antagonists & cotrimoxazole?
cotrimoxazol can inhibit breakdown of vit K antagonists --> risk of bleeding
175
What are the 4 main quinolones?
ciprofloxacin
levofloxacine
moxifloxacine
norfloxacine
176
What type of bacteria are quinolones effective against?
Gram neg
177
Interaction of quinolones with which medication results in formation of insoluble complexes?
aluminium, calcium, magnesium, iron
178
What is the mechanism of action of quinolones?
affect bactrial DNA synthesis
179
What is the main side effect of metronidazole?
disulfiram propeties
180
What is the interaction between metronidazol & vit K antagonists?
metronidazole can increase the effects of vit K antagonists --> risk of bleeding
181
What typeof bacteria is metronidazole used for?
anaerobic
182
What are the 3 medications most commonly associated with anaphylactic reactions?
1. beta lactams
2. NSAIDs
3. muscle relaxants
183
What are the 2 main medications associted with development of thrombocytopenia or hemolytic anemia?
1. beta lactams
2. heparins
184
What are the 3 main medications associated with the risk of developing SJS/TEN?
1. antibiotics
2. carbamazepine
3. allopurinol
185
What is the 3 step treatment for anaphylaxis?
1. adrenaline 0.5-1mg IM
2. Clemastine 2 mg IV
3. Dexamethasone 0.1 mg/kg IV
186
What is bioavailability?
fraction of drug that reaches the general circulation in unchanged form
187
What is the volume of distribution?
ratio between amount of drug taken up in the body & plasma concentration immediately after administration
188
What kind ofdrugs have a small volume of distribution? What kind of drugs have a large volume of distribution?
small - drugs with high affinity for plsma proteins
large - lipophilic drugs
189
What is the goalof phase I & phase II reaqctions?
making a drug more water soluble to prepare for excretion
190
What 4 substances/medications/medication classes are known inhibitors of CYP3A4?
1. azoles (e.g. metronidazole)
2. macrolides (e.g. erythromycin)
3. verapamil
4. grapefruit juice
191
What 3 substances/medications/medication classes are known inducers of CYP3A4?
1. rifampicin
2. anti-epileptics (e.g. phenytoin)
3. St John's wort
192
What is clearance?
volume of plasma that is cleared of a substance per unit time
193
Which pharmacokinetic value determines whether there is a need for a loading dose of a drug?
T1/2
