Thursday [20/4/23] Flashcards

1
Q

LFTs suggesting cholestasis

A

A greater than 10-fold increase in ALT and a less than 3-fold increase in ALP suggests a predominantly hepatocellular injury

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2
Q

LFTs suggesting hepatocellular damage

A

A less than 10-fold increase in ALT and a more than 3-fold increase in ALP suggests cholestasis.

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3
Q

is it possible to have both hepatocelular injury and cholestasis?

A

yes

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4
Q

causes of isolated rise in ALP

A

Bony metastases or primary bone tumours (e.g. sarcoma)
Vitamin D deficiency
Recent bone fractures
Renal osteodystrophy

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5
Q

what is an isolated rise in bilirubin suggestive of?

A

Gilbert’s syndrome: the most common cause.
Haemolysis: check a blood film, full blood count, reticulocyte count, haptoglobin and LDH levels to confirm.

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6
Q

when is hyperbilirubinaemia visible in patients?

A

Hyperbilirubinaemia may not always cause clinically apparent jaundice (usually visible >60 umol/l).

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7
Q

Causes of jaundice

A

Normal urine + normal stools = pre-hepatic cause
Dark urine + normal stools = hepatic cause
Dark urine + pale stools = post-hepatic cause (obstructive)

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8
Q

patients Sx and Sx indicative of conjugated/unconjugated hyperbilirubinaemia

A

The patient’s symptoms and clinical signs can help differentiate between conjugated and unconjugated hyperbilirubinaemia. Unconjugated bilirubin is not water-soluble and, therefore, doesn’t affect the colour of the patient’s urine. Conjugated bilirubin, however, can pass into the urine as urobilinogen, causing the urine to become darker

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9
Q

causes of unconjugated hyperbilirubinaemia

A

Haemolysis (e.g. haemolytic anaemia)
Impaired hepatic uptake (e.g. drugs, congestive cardiac failure)
Impaired conjugation (e.g. Gilbert’s syndrome)

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10
Q

causes of conjugated hyperbiliribnaemia

A

Hepatocellular injury
Cholestasis

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11
Q

when can albumin levels fall?

A

Liver disease resulting in a decreased production of albumin (e.g. cirrhosis).
Inflammation triggering an acute phase response which temporarily decreases the liver’s production of albumin.
Excessive loss of albumin due to protein-losing enteropathies or nephrotic syndrome

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12
Q

liver screen on some pts

A

LFTs
Coagulation screen
Hepatitis serology (A/B/C)
Epstein-Barr Virus (EBV)
Cytomegalovirus (CMV)
Anti-mitochondrial antibody (AMA)
Anti-smooth muscle antibody (ASMA)
Anti-liver/kidney microsomal antibodies (Anti-LKM)
Anti-nuclear antibody (ANA)
p-ANCA
Immunoglobulins – IgM/IgG
Alpha-1 Antitrypsin (to rule out alpha-1 antitrypsin deficiency)
Serum Copper (to rule out Wilson’s disease)
Ceruloplasmin (to rule out Wilson’s disease)
Ferritin (to rule out haemochromatosis)

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13
Q

why is PSA important? [1]

A

PSA is produced for the ejaculate, where it liquefies semen in the seminal coagulum and allows sperm to swim freely.It is also believed to be instrumental in dissolving cervical mucus, allowing the entry of sperm into the uterus.

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14
Q

tamsulosin medication type

A

alpha blocker

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15
Q

finasteride medication type

A

5-alpha reductase inhibitor

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16
Q

medications used for AF

A

beta-blockers, CCB [verapamil, diltiazem, digoxin]
rhythm control: DC cardioversion, amiodarone, flecainide

17
Q

why are steroids used in COPD

A

prevent bronchospasms

18
Q

prurigo nodularis

A

a

19
Q

bullous pemphigoid

A

aa

20
Q
A

a

21
Q

a

A

a

22
Q

a

A

a

23
Q

a

A

a

24
Q

types of AF

A

paroxysmal, persistent AF, long-term persistent AF, permnanet AF