Kidney and Liver Flashcards
(220 cards)
1
Q
What are the three main functions of the nephron?
A
Filtration, tubular reabsorption, and tubular secretion.
2
Q
Which part of the nephron reabsorbs the majority of sodium, water, and glucose?
A
The proximal convoluted tubule (PCT).
3
Q
What hormone increases water reabsorption in the collecting duct?
A
Antidiuretic hormone (ADH).
4
Q
What does a low GFR typically result in regarding potassium levels?
A
Hyperkalaemia (↑ K⁺ in blood).
5
Q
How do the kidneys respond to low blood pressure?
A
Release renin → activates RAAS → vasoconstriction + aldosterone release → ↑ Na⁺ and water retention → ↑ BP.
6
Q
Which hormone stimulates red blood cell production and is produced by the kidneys?
A
Erythropoietin (EPO).
7
Q
Which substances are reabsorbed by sodium symporters in the PCT?
A
Glucose, amino acids, and other solutes with sodium.
8
Q
What is the Cockcroft-Gault formula used for?
A
Estimating creatinine clearance (CrCl) for drug dosing.
9
Q
Why is eGFR a better indicator of renal function than serum creatinine alone?
A
It adjusts for age, sex, and ethnicity, providing a more accurate estimate of filtration.
10
Q
What happens to ADH levels when blood osmolality increases?
A
ADH increases → more water reabsorbed → urine becomes concentrated.
11
Q
Which renal transporters are responsible for secreting drugs like NSAIDs and methotrexate?
A
Organic anion transporters (OATs).
12
Q
Name a class of drugs that is both nephrotoxic and cleared renally, requiring close monitoring.
A
Aminoglycosides (e.g., gentamicin).
13
Q
What are the three types of causes of Acute Kidney Injury (AKI)?
A
Prerenal (reduced blood supply), Intrinsic (damage within the kidney), Postrenal (obstruction to urine flow).
14
Q
Name two common drugs that can cause prerenal AKI.
A
NSAIDs and ACE inhibitors.
15
Q
What is the earliest ECG change seen in severe hyperkalaemia?
A
Peaked T waves.
16
Q
How does calcium gluconate help in hyperkalaemia?
A
It stabilises cardiac membranes but does not lower potassium levels.
17
Q
What is the most effective treatment for removing potassium in hyperkalaemia?
A
Haemodialysis.
18
Q
What are key signs of fluid overload in AKI?
A
Peripheral oedema, pulmonary oedema, and raised jugular venous pressure.
19
Q
What hormone deficiency causes renal anaemia in CKD?
A
Erythropoietin (EPO) deficiency.
20
Q
Why does CKD lead to renal osteodystrophy?
A
Due to reduced activation of vitamin D and hypocalcaemia, leading to secondary hyperparathyroidism.
21
Q
Which drug class is first-line for slowing CKD progression?
A
ACE inhibitors (e.g., ramipril).
22
Q
How do SGLT2 inhibitors protect kidneys in CKD?
A
They reduce glucose reabsorption in the PCT, lower glomerular pressure, and slow kidney damage.
23
Q
What metabolic complication is common in both AKI and CKD?
A
Metabolic acidosis.
24
Q
List three symptoms of uraemia in CKD.
A
Itchy skin, muscle cramps, nausea, fatigue, or headache.
25
Front
Back
26
What is the primary goal of diuretic drugs?
To increase sodium (Na⁺) excretion (natriuresis), leading to water loss (diuresis).
27
Which part of the nephron do loop diuretics act on?
The thick ascending limb of the loop of Henle.
28
Which diuretic class is considered the most potent?
Loop diuretics (e.g., furosemide).
29
What is the mechanism of action of thiazide diuretics?
They block the Na⁺/Cl⁻ symporter in the distal convoluted tubule.
30
Which diuretic is used to treat cerebral oedema?
Mannitol (an osmotic diuretic).
31
What side effect is common with loop and thiazide diuretics but not potassium-sparing diuretics?
Hypokalaemia (low potassium).
32
How do potassium-sparing diuretics like spironolactone work?
They antagonize aldosterone receptors, preventing Na⁺ reabsorption and K⁺ excretion in the collecting duct.
33
Why might NSAIDs reduce the effectiveness of loop diuretics?
NSAIDs reduce renal blood flow and inhibit prostaglandin synthesis, blunting diuretic effect.
34
What condition can thiazides help prevent by reducing calcium excretion?
Kidney stones.
35
What are key side effects of loop diuretics?
Hypokalaemia, hypocalcaemia, hypomagnesaemia, and metabolic alkalosis.
36
Which class of diuretics is best for treating resistant hypertension?
Thiazide diuretics, especially thiazide-like ones like indapamide.
37
Why are potassium-sparing diuretics often combined with thiazides?
To prevent hypokalaemia caused by thiazides.
38
What is the role of the kidneys in ion homeostasis?
Regulate water, Na⁺, K⁺, H⁺, Ca²⁺, and HCO₃⁻ levels in plasma.
39
What is hyperkalaemia and what causes it?
High potassium in the blood; often caused by AKI or CKD due to impaired K⁺ excretion.
40
What is the function of Sodium Zirconium Cyclosilicate (SZC)?
Exchanges Na⁺ and H⁺ for K⁺ in the gut to reduce blood potassium levels.
41
Why is SZC selective for potassium?
Its 3Å pore size matches the unhydrated K⁺ ion, allowing selective exchange.
42
What is a chelate?
A complex where a polydentate ligand forms multiple bonds to a metal ion, creating a stable ring.
43
Why are chelate complexes more stable than those with monodentate ligands?
They are entropically favoured and thermodynamically more stable.
44
What does a high formation constant (Kf) indicate?
A more stable metal-ligand complex.
45
How do phosphate binders work?
They bind dietary phosphate in the GI tract to form insoluble compounds that are excreted.
46
Give two examples of phosphate binding agents.
Calcium carbonate and sevelamer.
47
What are calcimimetics like cinacalcet used for?
Treat hyperparathyroidism by activating CaSR, reducing PTH secretion.
48
Why is alfacalcidol used in renal failure?
It bypasses kidney-dependent 1α-hydroxylation needed to activate vitamin D.
49
How do thiazide diuretics work?
Block Na⁺/Cl⁻ transporter in the DCT, increasing Na⁺ and water excretion.
50
What is the main benefit of sustained/controlled release formulations?
They maintain drug levels in the therapeutic range, reduce dose frequency, and minimise side effects.
51
What is the difference between sustained and controlled release?
Sustained release maintains drug release over time, while controlled release delivers the drug at a nearly constant rate.
52
What is delayed release?
A formulation that releases the drug at a time other than immediately after administration, e.g., enteric coated tablets.
53
What type of release mechanism is used in enteric coated tablets?
Delayed release to protect the drug from gastric acid or to avoid gastric irritation.
54
What are the main diffusion-based delivery systems?
Matrix systems and reservoir systems.
55
What is the mechanism of drug release in reservoir systems?
Drug diffuses through a polymer membrane at a constant rate (zero-order).
56
Give an example of a matrix diffusion system.
NuvaRing — delivers hormones through a polymer matrix over 21 days.
57
How does osmotic-controlled drug delivery work?
Water enters through a semi-permeable membrane, swelling a polymer that pushes drug out through an orifice.
58
What is a GLIADEL wafer used for?
It is a biodegradable implant that delivers carmustine directly to brain tumors.
59
What are examples of stimuli-responsive drug delivery?
Systems that respond to pH, temperature, magnetic fields, or enzymes.
60
What is a mucoadhesive gastroretentive system?
It uses polymers that stick to the mucosa, prolonging stomach retention time.
61
What is the purpose of magnetic gastroretentive systems?
To localise drug delivery using an internal magnet controlled by an external field.
62
What are the advantages of targeted drug delivery?
Optimises drug action at the target site, reduces required dose, and minimises side effects.
63
What is the main route of clearance for particles <10 nm in the body?
Renal clearance via glomerular filtration.
64
What is the size cutoff for particles to avoid liver sinusoidal clearance?
Particles larger than 100–150 nm may avoid liver sinusoidal clearance.
65
How do liposomes work in drug delivery?
They encapsulate hydrophilic drugs in the core and lipophilic drugs in the bilayer, protecting and targeting delivery.
66
What is PEGylation in liposomes?
Addition of PEG polymers to prevent immune recognition and clearance (stealth effect).
67
What are exosomes used for in drug delivery?
Naturally derived vesicles that can evade immune detection and deliver therapeutic molecules.
68
What is a key limitation of micelles in drug delivery?
They can disassemble on dilution, leading to premature drug release.
69
What is the core structure of dendrimers used for?
To encapsulate or conjugate drugs; allows for high drug loading and targeted delivery.
70
What makes albumin nanoparticles suitable for drug delivery?
They are biocompatible, non-toxic, and can bind to receptors overexpressed in diseased tissues.
71
What are metallic nanoparticles used for?
Drug delivery, targeting, and imaging due to their high stability and functional surface.
72
How do silica nanoparticles carry drugs?
Via porous structures for hydrophilic drugs and hydrophobic cores for hydrophobic drugs.
73
What are the concerns with carbon-based nanoparticles like graphene or nanotubes?
Hydrophobicity, insolubility, and potential for aggregation or toxicity.
74
What is nephrotoxicity?
A rapid deterioration in kidney function caused by medications or chemicals.
75
Name two antimicrobial classes associated with nephrotoxicity.
Aminoglycosides and vancomycin.
76
Why are aminoglycosides nephrotoxic?
Their positive charge facilitates uptake in the proximal tubule via the megalin/cubilin complex.
77
What structural drug factor increases risk of nephrotoxicity?
Insolubility in urine, leading to crystal formation (e.g., methotrexate, acyclovir).
78
How do patient factors like age or CKD affect nephrotoxicity risk?
They reduce kidney resilience, making damage more likely from nephrotoxic drugs.
79
What type of nephropathy results from drug accumulation in lysosomes?
Osmotic nephropathy.
80
Which common diagnostic agents can cause nephrotoxicity?
Radiocontrast agents and gadolinium (in high doses).
81
Name a nephrotoxic herbal substance.
Aristolochic acid.
82
What role do transporters like hOAT and hOCT play in nephrotoxicity?
They mediate drug uptake and accumulation in tubular cells.
83
Which biomarker is commonly used for detecting kidney injury?
Kidney Injury Molecule-1 (KIM-1).
84
What is a key prevention strategy for nephrotoxic drugs?
Dose adjustment, monitoring, and ensuring hydration.
85
What are common signs of nephrotoxicity in labs?
↓GFR, ↑creatinine, ↓urine output, ↑K⁺, ↓Na⁺.
86
What are the four main stages of alcoholic liver disease?
1) Fatty liver, 2) Alcoholic hepatitis, 3) Fibrosis, 4) Cirrhosis.
87
Which liver disease stage is still reversible with alcohol abstinence?
Fatty liver and mild alcoholic hepatitis.
88
What is the purpose of the CIWA-Ar protocol?
To assess severity of alcohol withdrawal and guide diazepam dosing.
89
What vitamin is deficient in Wernicke's encephalopathy?
Thiamine (Vitamin B1).
90
What drug is used for acute management of Wernicke's encephalopathy?
Pabrinex IV or IM.
91
What drug is used long-term to prevent hepatic encephalopathy?
Lactulose (± Rifaximin if recurrent).
92
How does lactulose help in hepatic encephalopathy?
Reduces ammonia absorption by acidifying gut contents and increasing stool frequency.
93
Which beta-blockers are used for portal hypertension?
Propranolol and Carvedilol.
94
What is the mechanism of action of Terlipressin in variceal bleeding?
Vasoconstriction via vasopressin receptor agonism.
95
What diuretic is first-line for managing ascites in liver disease?
Spironolactone.
96
What lab signs are typical of liver dysfunction?
↑ ALT/AST, ↑ bilirubin, ↓ albumin, ↑ INR, ↓ platelets.
97
What medication is used to manage coagulopathy in liver disease?
Vitamin K (10mg OD stat, max 5 days).
98
What drug is used to treat spontaneous bacterial peritonitis (SBP)?
Tazocin (Piperacillin/Tazobactam).
99
Which medications should be avoided in alcoholic liver disease?
NSAIDs, benzodiazepines (unless for withdrawal), and hepatotoxic drugs.
100
What pharmacological treatment is used off-label for NAFLD?
Pioglitazone or Vitamin E in advanced fibrosis.
101
What condition is lactulose used to treat in liver disease?
Portal-Systemic Encephalopathy (PSE) / Hepatic Encephalopathy (HE).
102
What is the mechanism of lactulose in reducing ammonia levels?
Lactulose is broken down in the colon into organic acids, lowering pH and converting NH₃ to NH₄⁺, which is excreted.
103
Where in the GI tract does lactulose act?
The large intestine (colon).
104
What type of compound is lactulose?
A synthetic disaccharide of galactose and fructose.
105
What are the three main forms of Vitamin K?
Vitamin K1 (phylloquinone), K2 (menaquinone), K3 (menadione).
106
What causes Vitamin K deficiency?
Poor fat absorption due to liver disease or bile duct obstruction.
107
What is the role of Vitamin K in blood clotting?
It is a cofactor for γ-glutamylcarboxylase, enabling carboxylation of clotting factors.
108
What is the Vitamin K–epoxide cycle?
A recycling mechanism where oxidised Vitamin K is converted back to its active hydroquinone form.
109
What enzyme reduces Vitamin K epoxide to Vitamin K?
Vitamin K epoxide reductase (VKOR).
110
Why is Vitamin K stored in small amounts in the body?
Despite being fat-soluble, it is rapidly depleted without regular intake.
111
What happens to protons near electronegative atoms in NMR?
They are deshielded and appear downfield (lower field strength).
112
What does the chemical shift (δ) indicate in NMR?
The position where a proton resonates relative to TMS, measured in ppm.
113
How can NMR distinguish between Vitamin K1 and K3?
K1 shows more aliphatic peaks due to its long side chain; K3 has fewer.
114
What effect does multiple electron-withdrawing groups have on NMR?
They increase deshielding and shift peaks further downfield.
115
What does integration in NMR tell you?
The ratio of protons in different environments (not absolute number).
116
What is hepatitis?
Inflammation of the liver, caused by alcohol, drugs, autoimmune/metabolic diseases, or viral infections.
117
Which hepatitis viruses can lead to chronic infection?
Hepatitis B (HBV), C (HCV), and D (HDV with HBV).
118
How is hepatitis A transmitted and treated?
Feco-oral route; treated with supportive care; vaccine available.
119
What are the three phases of acute viral hepatitis?
Prodromal, icteric, and resolution phases.
120
What serological marker indicates acute HBV infection?
Anti-HBc IgM.
121
What is the significance of HBeAg in HBV infection?
Indicates active viral replication and high infectivity.
122
Which type of viral genome does HBV have?
Partially double-stranded DNA (dsDNA).
123
What is the mechanism of nucleos(t)ide analogues in HBV treatment?
They inhibit reverse transcriptase, halting viral DNA replication.
124
Which virus requires HBV co-infection to cause disease?
Hepatitis D virus (HDV).
125
What are the most common transmission routes for HBV?
Sexual, perinatal, and parenteral (blood exposure).
126
What is the first-line treatment for chronic HCV?
Direct-acting antivirals (DAAs) targeting NS3/4A, NS5A, and NS5B.
127
Is there a vaccine for HCV?
No, there is currently no vaccine for hepatitis C.
128
How is HCV primarily diagnosed?
Detection of HCV antibodies and confirmation with HCV RNA PCR.
129
Why is chronic HCV a concern?
It can lead to liver fibrosis, cirrhosis, and hepatocellular carcinoma.
130
What is the goal of HCV therapy?
Eradication of the virus (cure), preventing progression and transmission.
131
What are the two main blood supplies to the liver?
Portal vein (75%) and hepatic artery (25%).
132
What is the functional unit of the liver?
The hepatic lobule.
133
Name three zones of hepatocytes based on function and perfusion.
Zone 1 (periportal), Zone 2 (midzonal), Zone 3 (pericentral).
134
Which enzyme primarily metabolises ethanol in the liver?
Alcohol dehydrogenase (ADH).
135
What is the main site of fatty acid and cholesterol metabolism in the body?
The liver.
136
How does the liver contribute to carbohydrate metabolism?
Through glycogenesis, glycogenolysis, and gluconeogenesis.
137
What are Phase I drug metabolism reactions catalysed by?
Cytochrome P450 enzymes.
138
What is the purpose of Phase II drug metabolism reactions?
To conjugate Phase I products, making them more water-soluble for excretion.
139
Which proteins involved in coagulation are synthesised by the liver?
Factors II, VII, IX, X, fibrinogen, and anticoagulants like antithrombin III.
140
What is the urea cycle’s role in the liver?
To convert toxic ammonia into urea for renal excretion.
141
Which hormone is activated in the liver by deiodination?
Thyroid hormone T4 is converted to active T3.
142
What does the liver produce from old red blood cells?
Conjugated bilirubin for bile production.
143
Which fat-soluble vitamins are stored in the liver?
Vitamins A, D, E, and K.
144
What is albumin's function and where is it made?
Maintains osmotic pressure and transports substances; synthesised in the liver.
145
What liver structure allows exchange of substances between blood and hepatocytes?
Liver sinusoids (porous capillaries).
146
What is the difference between compensated and decompensated cirrhosis?
Compensated: liver still functions with few symptoms; Decompensated: severe damage with symptoms like jaundice, ascites, and encephalopathy.
147
Name three common complications of cirrhosis.
Ascites, hepatic encephalopathy, oesophageal variceal bleeding.
148
What is the main cause of portal hypertension?
Increased resistance to blood flow through the liver due to fibrosis and cirrhosis.
149
How is portal hypertension defined?
Portal venous pressure >5 mmHg; significant if >10 mmHg.
150
What are signs of portal hypertension?
Bloated abdomen, vomiting blood, black stools, oedema, mental confusion.
151
What causes hepatic encephalopathy?
Build-up of ammonia and other toxins due to reduced liver detoxification capacity.
152
How is hepatic encephalopathy treated?
Lactulose to reduce ammonia; Rifaximin to reduce gut bacteria producing toxins.
153
What is ascites and what causes it?
Fluid accumulation in the peritoneal cavity due to portal hypertension and sodium/water retention.
154
How is ascites managed?
Low-salt diet, diuretics (spironolactone, furosemide), paracentesis, or TIPS.
155
What are oesophageal varices and why are they dangerous?
Dilated veins due to portal HTN that can rupture and cause life-threatening bleeding.
156
What is the first-line prevention for variceal bleeding?
Non-selective beta-blockers (e.g., propranolol).
157
What is hepatorenal syndrome (HRS)?
Renal failure due to severe vasoconstriction in the kidneys caused by advanced liver disease.
158
Why does cirrhosis cause coagulopathy?
Impaired synthesis of clotting factors and anticoagulants by the liver.
159
What are signs of impaired liver protein synthesis?
Oedema, bleeding/bruising, low platelets, anaemia.
160
Which liver-related deficiency is linked to spider nevi and gynecomastia?
Increased circulating oestrogens due to reduced hepatic metabolism.
161
What is Drug-Induced Liver Injury (DILI)?
Liver damage caused by medications at normal doses, often unpredictable and resembling other liver diseases.
162
What are Type A (augmented) hepatotoxic drug reactions?
Predictable, dose-related reactions like paracetamol toxicity causing centrilobular necrosis.
163
What are Type B (bizarre) hepatotoxic reactions?
Unpredictable, not dose-dependent, often idiosyncratic (e.g. methyldopa, MAOIs).
164
Which drugs are associated with hepatic fibrosis and cirrhosis (Type C)?
Methotrexate and amiodarone.
165
What toxic metabolite is responsible for paracetamol-induced liver injury?
NAPQI (N-acetyl-p-benzoquinone imine).
166
How is NAPQI normally detoxified?
Conjugated with glutathione (GSH) to prevent liver damage.
167
What increases risk of DILI?
High dose, drug interactions, liver disease, age, alcohol, obesity, and genetic factors.
168
Which enzyme systems metabolise paracetamol to NAPQI?
CYP2E1 and CYP1A2.
169
How does liver disease affect first-pass metabolism?
↓ Liver function = ↓ first-pass metabolism = ↑ oral drug bioavailability.
170
Why might lipophilic drug absorption be altered in liver disease?
↓ Bile production and altered lipoproteins reduce absorption of lipophilic drugs.
171
How is drug distribution affected in liver disease?
↓ Albumin = ↑ free drug levels = ↑ drug effect/toxicity.
172
What happens to CYP enzyme activity in cirrhosis?
CYP levels decrease, reducing drug metabolism.
173
What liver function tests assess hepatotoxicity?
ALT, AST, ALP, bilirubin, albumin, and PT.
174
What route of elimination is most affected by liver disease?
Drugs eliminated via bile or liver metabolism.
175
Why might oral doses of propranolol need reduction in cirrhosis?
Propranolol has high first-pass metabolism; in cirrhosis, bioavailability can double.
176
What is ALT and what does it indicate when elevated?
ALT (Alanine Aminotransferase) is mainly found in the liver; high levels suggest liver damage, especially hepatitis.
177
What is AST and how does it differ from ALT?
AST (Aspartate Aminotransferase) is found in liver and other tissues; rises in liver or muscle damage, not as specific as ALT.
178
What does a raised ALP level indicate?
ALP (Alkaline Phosphatase) is associated with bile ducts; elevated in liver disease or bile duct obstruction.
179
What does GGT help diagnose?
GGT (Gamma-Glutamyl Transferase) can indicate bile duct issues or alcohol-related liver damage.
180
What does low albumin suggest in a liver function test?
Low albumin indicates reduced liver protein synthesis and possible chronic liver disease.
181
What does a prolonged Prothrombin Time (PT) suggest in liver disease?
It suggests impaired synthesis of clotting factors due to liver dysfunction.
182
What liver test measures the breakdown product of haemoglobin?
Bilirubin; elevated levels suggest liver dysfunction or bile duct blockage.
183
Which LFT is most sensitive to early alcohol-related liver damage?
GGT is more sensitive than ALT/AST for detecting alcohol-related damage.
184
What is the main treatment for hepatic encephalopathy?
Lactulose, often combined with Rifaximin to reduce ammonia-producing gut bacteria.
185
What is Pabrinex used for?
To treat or prevent Wernicke’s encephalopathy in alcohol-dependent patients.
186
What is the first-line drug for ascites in liver disease?
Spironolactone, often combined with furosemide for diuresis.
187
What drugs are used to manage oesophageal varices?
Non-selective beta-blockers (e.g., propranolol) and endoscopic band ligation.
188
Which antibiotic is used in SBP (spontaneous bacterial peritonitis)?
Tazocin (Piperacillin/Tazobactam).
189
What is the role of vitamin K in liver disease management?
Used to correct coagulopathy by aiding clotting factor synthesis.
190
How is rifaximin used in liver disease?
It is a non-absorbable antibiotic used to reduce ammonia-producing gut bacteria in hepatic encephalopathy.
191
What is hereditary haemochromatosis?
An autosomal recessive disorder causing excessive iron absorption and storage in tissues, especially the liver.
192
Which gene is commonly mutated in hereditary haemochromatosis?
HFE gene, most commonly the C282Y mutation.
193
What are typical lab findings in haemochromatosis?
↑ Iron, ↑ transferrin saturation, ↑ ferritin, ↓ TIBC.
194
Name two treatments for hereditary haemochromatosis.
Phlebotomy and iron chelators like deferoxamine.
195
What is a common skin sign of haemochromatosis?
Bronze pigmentation (bronze diabetes).
196
What is Alpha-1 Antitrypsin (AAT) deficiency?
A genetic disorder that increases risk of liver and lung disease due to reduced AAT, leading to unchecked elastase activity.
197
What are common symptoms of AAT deficiency in children?
Liver damage, jaundice, poor appetite, failure to thrive.
198
How is AAT deficiency diagnosed?
Low AAT protein levels and genetic testing for mutations.
199
Is there a cure for AAT deficiency?
No cure; management focuses on slowing liver and lung damage.
200
What is Wilson disease?
A recessive disorder causing copper accumulation in liver, brain, and eyes due to ATP7B gene mutation.
201
What is the classic eye finding in Wilson disease?
Kayser-Fleischer rings — brown rings around the cornea.
202
What are first-line treatments for Wilson disease?
Chelation therapy with D-penicillamine or trientine.
203
What is Gestational Alloimmune Liver Disease (GALD)?
A rare neonatal condition causing acute liver failure due to maternal antibodies attacking fetal liver.
204
What IV treatment may be given to mothers at risk of GALD?
Intravenous immunoglobulin (IVIg).
205
What is the key diagnostic feature of neonatal haemochromatosis (GALD)?
Elevated ferritin, coagulopathy, ascites, and hypoalbuminemia in neonates.
206
What is the purpose of WADA?
To promote, coordinate and monitor the fight against doping in sports worldwide.
207
What is the WADA Prohibited List?
A list of substances and methods banned in sport, updated annually and used worldwide.
208
What is a Therapeutic Use Exemption (TUE)?
Permission for an athlete to use a banned substance for medical reasons, reviewed by a panel.
209
What does S0 refer to in the WADA list?
Non-approved substances not approved for human use are banned at all times.
210
What does S1–S5 cover in the Prohibited List?
Substances prohibited at all times, including anabolic agents, hormones, and masking agents.
211
What is a masking agent in doping?
A substance used to hide the presence of performance-enhancing drugs during testing.
212
How is size exclusion chromatography used in doping tests?
To separate and analyse polymers based on molecular size, detecting high MW substances.
213
What are M1–M3 in the WADA code?
Prohibited methods, including blood doping and gene doping.
214
When are S6–S9 class substances prohibited?
Only in-competition.
215
What is the urine threshold for pseudoephedrine under WADA?
Prohibited when urine concentration exceeds 150 micrograms/mL.
216
Which sports are affected by P1 class substances?
Sports like archery, shooting, and motor sports—beta-blockers are banned.
217
Where must athletes declare their location for out-of-competition testing?
On ADAMS – Anti-Doping Administration Management System.
218
What are the rules for transgender athletes regarding testosterone levels?
Must maintain serum testosterone <2.5 nmol/L and meet puberty or legal criteria.
219
What is the key regulatory hormone used by some transgender athletes?
Oestrogen, sometimes with spironolactone (requires TUE).
220
Why is alcohol not universally banned in sport?
Only banned in certain precision sports like shooting or archery, not across all disciplines.
