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1
Q

Cytochrome P450 inducers

A 
CRAP GPs
Carbemazepines
Rifampicin
Alcohol
Phenytoin
Griseofulvin
Phenobarbitone
Sulphonylureas
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2
Q

Cytochrome P450 inhibitors

A 
SICKFACES.COM
Sodium valproate
Isoniazid
Cimetidine
Ketoconazole
Fluconazole
Alcohol & Grapefruit juice
Chloramphenicol
Erythromycin
Sulfonamides
Ciprofloxacin
Omeprazole
Metronidazole

AODEVICES
Allopurinol
Omeprazole
Disulfiram
Erythromycin
Valproate
Isoniazid
Ciprofloxacin
Ethanol (acute)
Sulphonamides
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3
Q

Steroids side effects

A 
STEROIDS
Stomach ulcers
Thin skin
oEdema
Right and left heart failure
Osteoporosis
Infection (including Candida)
Diabetes (commonly causes hyperglycaemia and uncommonly progresses to diabetes)
Syndrome - cushing's
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4
Q

NSAID cautions and contraindications

A 
NSAID
No urine (i.e. renal failure)
Systolic dysfunction (i.e. heart failure)
Asthma
Indigestion (any cause)
Dyscrasia (clotting abnormality)
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5
Q

ACE-inhibitor main side effects (x2), how and an example

A

1) Dry cough through accumulation of bradykinin via reduced degradation by ACE
2) Hyperkalaemia through reduced aldosterone production and thus reduced potassium excretion in the kidneys
E.g. lisinopril

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6
Q

What electrolyte disturbance do loop and thiazide diuretics (inc bendroflumethiazide) cause?

A

Hypokalaemia

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7
Q

What electrolyte disturbance do aldosterone antagonists and ACE-inhibitors cause?

A

Hyperkalaemia

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8
Q

What drugs contribute to indigestion?

A

Ibuprofen inhibits prostaglandin synthesis needed for gastric mucosal protection from acid. It is therefore at risk of influencing inflammation and ulceration.

Oral steroids inhibit gastric epithelial renewal thus predisposing to ulceration.

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9
Q

Drugs responsible for renal failure

A

Ibuprofen inhibits prostaglandin synthesis which reduces renal artery diameter (and blood flow) and thereby reducing kidney perfusion and function.

Ramipril, an ACE-inhibitor, reduces angiotensin-II production necessary for preserving glomerular filtration when the renal blood flow is reduced.

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10
Q

To what sort of pt shouldn’t you give ibuprofen to

A

Asthmatics
NSAIDs can cause bronchoconstriction in asthmatics and are therefore avoided unless strictly necessary and under close supervision (i.e. not at home).

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11
Q

Trimethoprim shouldn’t be used along side ….

and why?

A

Methotrexate

Trimethoprim is a folate antagonist, and is a direct contraindication to patients taking methotrexate (another folate antagonist) due to the risk of bone marrow toxicity. This can lead to pancytopenia and neutropenic sepsis.

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12
Q

When should methotrexate be withheld?

A

If a patient has sepsis. Need to exclude neutropenic sepsis

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13
Q

All diuretics cause what sort of electrolyte disturbance?

A

Hyponatraemia, although when they contribute to dehydration the sodium can increase too

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14
Q

Loop diuretic e.g.

A

Furosemide

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15
Q

Calcium-channel blocker: e.g. and side effect

A

Amlodipine, verapamil

Peripheral oedema

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16
Q

What should not be taken after an acute stroke for 2 months (duration varies)

A

Heparin thromboprophylaxis e.g. enoxaparin

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17
Q

Cardioprotective dose of aspirin; dose in tx of acute coronary syndromes and stroke

A

75mg; 300mg

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18
Q

Co-amoxiclav is a combination of …

A

amoxicillin and clavulanic acid

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19
Q

Who shouldn’t take COCP and eg

A

Pts who have migraine with aura as it increases their risk of stroke; microgynon

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20
Q

Paracetamol max dose

A

4g/ 24h: 2g from co-codamol and up to 2g from PRN paracetamol

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21
Q

Sodium normal range

A

135-145mmol/L

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22
Q

What should you assess to help narrow differential for hyPOnatraemia

A

Pt’s fluid status - hypovolaemic, euvolaemic, hypervolaemic

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23
Q

Hypernatraemia causes

A

All being with ‘D’
Dehydration
Drips i.e. too much IV saline
Drugs e.g. effevescent tablet preps or IV preps with a high sodium content
Diabetes insipidus - effectively the opposite of SIADH

24
Q

Potassium normal range

A

3.5-5mmol/L

25
Q

Hypokalaemia causes

A

DIRE
Drugs (loop and thiazide diuretics)
Inadequate intake or intestinal loss (diarrhoea/vomiting)
Renal tubular acidosis
Endocrine (Cushing’s and Conn’s syndromes)

26
Q

Hyperkalaemia causes

A

DREAD
Drugs (potassium-sparing diuretics and ACE-inhibitors)
Renal failure
Endocrine (Addison’s disease)
Artefact (very common, due to clotted sample)
DKA (note that when insulin is given to treat DKA the potassium drops requiring regular (hourly) monitoring +/− replacement)

27
Q

Microcytic anaemia causes

A

Iron deficiency anaemia
Thalassaemia
Sideroblastic anaemia

28
Q

Normocytic anaemia causes

A

Anaemia of chronic disease
Acute blood loss
Haemolytic anaemia
Renal failure (chronic)

29
Q

Macrocytic anaemia causes

A

B12*/folate deficiency (‘megaloblastic anaemia’)
Excess alcohol
Liver disease (including nonalcoholic causes)
Hypothyroidism
Haematological diseases beginning with ‘M’: myeloproliferative, myelodysplastic, multiple myeloma

30
Q

High neutrophils (neutrophilia) causes

A

Bacterial infection
Tissue damage (inflammation/infarct/ malignancy)
Steroids

31
Q

Low neutrophils (neutropenia) causes

A

Viral infection
Chemotherapy or radiotherapy (give urgent IV broad-spec abx)
Clozapine (antipsychotic)
Carbimazole (antithyroid)

32
Q

High lymphocytes (lymphocytosis) causes

A

Viral infection
Lymphoma
Chronic lymphocytic leukaemia

33
Q

Low platelets (thrombocytopenia) causes

A 
Reduced production:
- infection
 - drugs (esp. penicillamine (e.g. in
rheumatoid arthritis treatment))
- myelodysplasia, myelofibrosis, myeloma

Increased destruction:

  • heparin
  • hypersplenism
  • DIC
  • ITP
  • Haemolytic uraemic syndrome/ thrombotic thrombocytopenic purpura
34
Q

High platelets (thrombocytosis) causes

A

Reactive:

  • bleeding
  • tissue damage (infection/inflammation/malignancy)
  • post-splenectomy

Primary:
- myeloproliferative disorders

35
Q

Causes of hyponatraemia if hypovolaemic

A 
Fluid loss (especially diarrhoea/ vomiting)
Addison’s disease
Diuretics (any type)
36
Q

Causes of hyponatraemia if euvolaemic

A

SIADH
Psychogenic polydipsia
Hypothyroidism

37
Q

Causes of hyponatraemia if hypERvolaemic

A

Heart failure
Renal failure
Liver failure (causing hypoalbuminaemia)
Nutritional failure (causing hypoalbuminaemia)
Thyroid failure (hypothyroidism; can be euvolaemic too)

38
Q

SIADH causes

A

SIADH
small cell lung tumours, Infection,
Abscess,
Drugs (especially carbamazepine and antipsychotics), and Head injury.

39
Q

Prerenal (70%): Biochemical disturbance

A

Urea rise&raquo_space; creatinine rise

e.g. Urea 19
3–7.5 mmol/L
Creatinine 110 (35–125 μmol/L)

40
Q

Prerenal (70%): Causes

A

Dehydration (or if severe, shock) of any cause, e.g. sepsis, blood loss.
Renal artery stenosis - AKI in RAS is often triggered by drugs (ACEI or NSAIDs) and effectively causes hypoperfusion of the kidneys and thus a prerenal picture.

41
Q

Intrinsic renal (10%): Biochemical disturbance

A 
Urea rise << creatinine rise, bladder or hydronephrosis not palpable, e.g.:
Urea 9 (3–7.5mmol/L) Creatinine 342 (35–125 μmol/L)
42
Q

Intrinsic renal (10%): Causes

A 
INTRINSIC:
Ischaemia (due to prerenal
AKI, causing acute
tubular necrosis)
Nephrotoxic antibiotics (esp. gentamicin, vancomycin, tetracyclines)
Tablets (ACEI, NSAIDs)
Radiological contrast Injury Injury (rhabdomyolysis)
Negatively birefringent crystals (gout)
Syndromes (glomerulonephridites)
Inflammation (vasculitis)
Cholesterol emboli
43
Q

Postrenal (20%) obstructive: biochemical disturbance

A

Urea rise &laquo_space;creatinine rise, bladder or hydronephrosis may be palpable depending on level of obstruction

44
Q

Postrenal (20%) obstructive: causes

A

In lumen: stone or sloughed papilla
In wall: tumour (renal cell, transitional cell), fibrosis External pressure: benign prostatic hyperplasia, prostate cancer, lymphadenopathy, aneurysm

45
Q

Raised urea indicates

A

Kidney injury or upper GI haemorrhage

A raised urea usually indicates renal failure; however, because it is a breakdown product of amino acids (such as globin chains in haemoglobin), it can also reflect an upper GI bleed where haemoglobin has been broken down by gastric acid into urea, which is subsequently absorbed into the blood. The same phenomenon occurs if you eat a big (and bloody) steak. Thus, a raised urea with normal creatinine in a patient who is not dehydrated (i.e. does not have prerenal failure) should prompt a look at the haemoglobin; if this has dropped then the patient probably has an upper GI bleed.

46
Q

Vit K-dependent clotting factors

A

2,7,9,10 measured by PT/INR

47
Q

Raised bilirubin alone indicates …

A

haemolysis

48
Q

Raised alk phos indicates

A 
ALKPHOS
Any fracture,
Liver damage (posthepatic), 
K (for kancer), 
Paget’s disease of bone and Pregnancy, Hyperparathyroidism, Osteomalacia, 
Surgery.
49
Q

Which result do you check to change a levothyroxine dose for pts with hyPOthyroidism

50
Q

tsh range <0.5 mIU/L

A

decrease thyroxine dose

51
Q

tsh range 0.5-5 mIU/L

A

nil action - keep same dose thyroxine

52
Q

tsh range >5 mIU/L

A

Increase thyroxine dose

53
Q

Prehepatic

Bilirubin ⇑

A

Haemolysis

Gilbert’s and Crigler–Najjar syndromes

54
Q

Intrahepatic

Bilirubin ⇑ and AST/ALT ⇑

A

Fatty liver
Hepatitis*
Cirrhosis*
((1) alcohol, (2) viruses (Hepatitis A–E, CMV and EBV), (3) drugs (paracetamol overdose, statins, rifampicin), and (4) autoimmune (primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune hepatitis)
Malignancy (primary or secondary)
Metabolic: Wilson’s disease/haemochromatosis
Heart failure (causing hepatic congestion)

55
Q

Posthepatic (obstructive)

Bilirubin ⇑ and ALP ⇑

A

In lumen: stone (gallstone), drugs causing cholestasis - Flucloxacillin, coamoxiclav, nitrofurantoin, steroids and sulphonylureas.
In wall: tumour (cholangiocarcinoma), primary biliary cirrhosis, sclerosing cholangitis
Extrinsic pressure: pancreatic or gastric cancer, lymph node

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