PSA data interpretation Flashcards

1
Q

Most drugs are metabolised by which enzyme system?

A

Most drugs are metabolised to inactive metabolites by the cytochrome P450 enzyme system in the liver, preventing them from exerting infinite effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How can enzyme inducers and inhibitors affect P450 enzyme activity?

A

An enzyme inducer will increase P450 enzyme activity, hastening metabolism of other drugs with the result that they exert a reduced effect.

An enzyme inhibitor will decrease P450 enzyme activity and there will be increased levels of other drugs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can the addition of erythromycin to a patient on warfarin affect their INR?

A

Erythromycin is an enzyme inhibitor and can sometimes unpredictably cause a dangerous rise in INR if the warfarin dose is not decreased.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the common enzyme inducers?

A

PC BRAS

Phenytoin

Carbmazeine

Barbiturates

Rifampicin

Alcohol (chronic excess)

Sulphonylureas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the common enzymes inhibitors?

A

AODEVICES

Allopurinol

Omeprazole

Disulfiram

Erythromycin

Valproate

Isoniazid

Ciprofloxacin

Ethanol (acute intoxication)

Sulphonamides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Drugs to stop before surgery

A

I LACK OP

Insulin

Lithum

Anticoagulants/antiplatelets

COCP/HRT

K-sparing diuretics

Oral hypoglycaemic

Perindoril and other ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How should oral hypoglycaemia drugs and insulin be managed pre-operatively?

A

Patients are nil by mouth before surgery, thus metformin should be stopped as it will cause lactic acidosis. The other oral hypoglycaemic and insulin will cause hypoglycaemia unless stopped.

A sliding scale should be started instead where hourly blood glucose monitoring adjusts the hourly dose of insulin given to provide much tighter control.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Contraindications to drugs that increase bleeding (aspirin, heparin and warfarin):

A

Patients who are:

Bleeding

At risk of bleeding (eg prolonged prothrombin time due to liver disease)

Remember prophylactic heparin is contraindicated in acute ischaemia stroke due to the risk of bleeding into the stroke.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Contraindications for steroids:

A

STEROIDS

Stomach ulcers

Thin skin

Edema

Right and left heart failure

Osteoporosis

Infection

Diabetes (commonly causes hyperglycaemia)

Cushing’s Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

NSAIDs cautions and contraindications

A

NSAID

No urine (ie renal failure)

Systolic dysfunction (ie heart failure)

Asthma

Indigestion (any cause)

Dyscrasia (clotting abnormality)

While aspirin is technically an NSAID, it is not contradicted in renal or heart failure, or in asthma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Side effects of anti hypertensives

A
  • Hypotension (including postural hypotension)
  • Bradycardia may occur with beta blockers and some calcium channel blockers
  • Electrolyte disturbance can occur with ACE inhibitors and diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Specific side effect of ACE inhibitors

A

Dry cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Specific side effects of beta blockers

A
  • Wheeze in asthmatics
  • Worsening of acute heart failure (but helps chronic heart failure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Specific side effects of calcium channel blockers:

A

Calcium channel blockers can cause peripheral oedema and flushing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Contraindications to compression stockings

A

Peripheral arterial disease (as this may cause limb ischaemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Contraindications to metoclopramide

A
  • Parkinson’s disease due to risk of exacerbating symptoms
  • Young women due to the risk of dyskinesia, ie unwanted movements especially acute dystonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

First line treatment for neuropathic pain

A

Amitriptyline (10mg oral nightly) or pregabalin (75mg oral 12 hourly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Managment of painful diabetic neuropathy

A

Duloxetine (60mg oral daily)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Causes of microcytic anaemia (low MCV)

A
  • Iron deficiency anaemia
  • Thalassaemia
  • Sideroblastic anaemia
20
Q

Causes of normocytic anaemia (normal MCV)

A
  • Anaemia of chronic disease
  • Acute blood loss
  • Haemolytic anaemia
  • Renal failure (chronic)
21
Q

Causes of macrocytic anaemia (high MCV)

A
  • B12/folate deficiency (‘megaloblastic anaemia’)
  • Excess alcohol
  • Liver disease (including nonalcoholic causes)
  • Hypothyroidism
  • Haematological diseases beginning with ‘M’: myeloproliferative, myelodysplastic, multiple myeloma
22
Q

Causes of high neutrophils (neutrophila)

A
  • Bacterial infection
  • Tissue damage (inflammation/infarct/ malignancy)
  • Steroids
23
Q

Causes of low neutrophils (neutropenia)

A
  • Viral infection
  • Chemotherapy or radiotherapy*
  • Clozapine (antipsychotic)
  • Carbimazole (antithyroid)
24
Q

Causes of high lymphocytes (lymphocytosis)

A
  • Viral infection
  • Lymphoma
  • Chronic lymphocytic leukaemia
25
Q

Causes of low platelets

A
  • Reduced production:
    • infection (usually viral)
    • drugs (esp. penicillamine (e.g. in rheumatoid arthritis treatment))
    • myelodysplasia, myelofibrosis, myeloma
  • Increased destruction:
    • heparin
    • hypersplenism
    • disseminated intravascular coagulation (DIC)
    • idiopathic thrombocythaemia purpura (ITP)
    • haemolytic thrombocytopenic purpura
26
Q

Causes of high platelets (thrombocytosis)

A
  • Reactive:
    • Bleeding
    • Tissue damage (infection/inflamation/malignancy)
    • Post-splenectomy
  • Primary
    • Myeloprolifertive disorders
27
Q

Sodium normal range

A

135-145 mmol/L

28
Q

Causes of hypernatraemia

A

4 D’s

  • Dehydration
  • Drips (too much IV saline)
  • Drugs with high sodium content
  • Diabeties insipidus
29
Q

Causes of hyponatraemia

A
  • Hypovolaemic
    • Fluid loss (especially diarrhoea/vomiting)
    • Diuretics (any type)
    • Addison’s disease
  • Euvolaemic
    • SIADH
    • Psychogenic polydipsia
    • Hypothyroidism
  • Hypervolaemic
    • Heart failure
    • Renal failure
    • Liver failure (causing hypoalbuminaemia)
    • Nutritional failure (causing hypoalbuminaemia)
    • Thyroid failure (hypothyroidism; can be euvolaemic too)
30
Q

Causes of SIADH

A
  • Small cell lung tumours
  • Infection
  • Abscess
  • Drugs (especially carbamazepine and antipsychotics)
  • Head injury
31
Q

Causes of hypokalaemia

A

DIRE

  • Drugs (loop and thiazide diuretics)
  • Inadequate intake or Intestinal loss (diarrhoea/vomiting)
  • Renal tubular necrosis
  • Endocrine (Cushing’s and Conn’ syndromes)
32
Q

Causes of hyperkalaemia

A

DREAD

  • Drugs (potassium sparing diuretics and ACE inhibitors)
  • Renal failure
  • Endocrine (Addison’s disease)
  • Artefact (very common, due to clotted sample)
  • DKA
33
Q

Biochemical disturbance seen in prerenal AKI.

Causes of prerenal AKI.

A

Urea rise >> creatinine rise

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

  • Dehydration (or if severe, shock) of any cause, e.g. sepsis, blood loss.
  • Renal artery stenosis (RAS)
34
Q

Biochemical disturbance seen in renal AKI.

Causes of renal AKI.

A

Urea rise << creatinine rise, bladder or hydronephrosis not palpable,

e.g.: Urea 9 (3–7.5mmol/L) Creatinine 342 (35–125 μmol/L)

INTRINSIC:

  • Ischaemia (due to prenal AKI, causing acute tubular necrosis)
  • Nephrotoxic antibiotics (Especially gentamicin, vancomycin and tetracyclines.)
  • Tablets (ACEI, NSAIDs)
  • Radiological contrast
  • Injury (rhabdomyolysis)
  • Negatively birefringent crystals (gout)
  • Syndromes (glomerulonephritides)
  • Inflammation (vasculitis)
  • Cholesterol emboli
35
Q

Biochemical disturbance seen in postrenal (obstructive) AKI.

Causes of postrenal AKI.

A

Urea rise << creatinine rise, bladder or hydronephrosis may be palpable depending on level of obstruction,

e.g.: Urea 9 (3–7.5mmol/L) Creatinine 342 (35–125 μmol/L)

  • In lumen: stone or sloughed papilla
  • In wall: tumour (renal cell, transitional cell), fibrosis
  • External pressure: benign prostatic hyperplasia, prostate cancer, lymphadenopathy, aneurysm
36
Q

T4 ⇓, TSH ⇑

Interpretation

Causes

A

Primary hypothyroidism

Hashimoto’s thyroiditis, drug-induced hypothyroidism

37
Q

T4 ⇓, TSH ⇓

Interpetation

Causes

A

Secondary hypothyroidism (⇓ TSH from pituitary causing ⇓ T4)

Causes: Pituitary tumour or damage

38
Q

T4 ⇑, TSH ⇓

Interpretation

Causes

A

Primary hyperthyroidism (⇑ T4 from thyroid causing ⇓ TSH)

Causes:

  • Grave’s disease
  • Toxic nodular goiter
  • Drug-induced hyperthyroidism
39
Q

T4 ⇑, TSH ⇑

Interpretation

Causes

A

(⇑ TSH from pituitary causing ⇑ T4)

Causes:

  • Pituitary tumour
40
Q

Prehepatic pattern of LFT derangement

Causes

A

Bilirubin ⇑

  • Haemolysis
  • Gilbert’s and Crigler–Najjar syndromes
41
Q

Intrahepatic pattern LFT derangement

A

Bilirubin ⇑ and AST/ALT ⇑

  • Fatty liver
  • Hepatitis
  • Cirrhosis
  • Malignancy (primary or secondary)
  • Metabolic: Wilson’s disease/haemochromatosis
  • Heart failure (causing hepatic congestion)
42
Q

Causes of hepatitis and cirrhosis

A
  • Alcohol
  • Viruses (Hepatitis A–E, CMV and EBV)
  • Drugs (paracetamol overdose, statins, rifampicin)
  • Autoimmune (primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune hepatitis)
43
Q

Post-hepatic (obstructive) LFT derangement

Causes

A

Bilirubin ⇑ and ALP ⇑

  • In lumen: stone gallstone, drugs causing cholestasis
  • In wall: tumour (cholangiocarcinoma), primary biliary cirrhosis, sclerosing cholangitis
  • Extrinsic pressure: pancreatic or gastric cancer, lymph node
44
Q

How to interpret and change levothyroxine dose following TFT results:

A
TSH range (mIU/L) Change to thyroxine
 \<0.5 Decrease dose
 0.5–5 Nil action – same dose
 \>5 Increase dose
45
Q

Causes of raised alkaline phosphate

A

ALK PHOS:

  • Any fracture
  • Liver damage (posthepatic)
  • K (for kancer)
  • Paget’s disease of bone and Pregnancy
  • Hyperparathyroidism
  • Osteomalacia
  • Surgery