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CP1 revision > Liver diseases oxford > Flashcards

Liver diseases oxford Flashcards

1
Q

Fulminant liver failure

A

Massive necrosis of liver cells

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2
Q

signs of liver failure

A

jaundice, encephalopathy, aterixis, apraxia (5 pointed star drawing), fetor hepaticus (pear drop breath)

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3
Q

Effects of warfarin in liver failure

A

enhanced

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4
Q

Causes of liver cirrhosis

A

Chronic alcohol, chronic HBV or HCV, autoimmune (PBS, PSC, AIH), genetic disorder (haematomachrosis, alpha 1 antitrypsin deficiency, wilson’s disease), vascular (Budd chiari, hepatic vein thrombosis), drugs (amiodarone, methyldopa, methotrexate)

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5
Q

Imaging for cirrhosis

A

USS and duplex
Ascitic tap
Can do MRI
Liver biopsy (if not CI)

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6
Q

Hereditary haemochromatosis

A

Increased iron absorption gives deposition in joints, livre, heart, pancreas, pituitary, adrenal and skin

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7
Q

Hereditary haemochromatosis presentation

A

Typically presents 10 years later in women due to protection via menstruation.
Asymptomatic early on, but leads to tiredness and arthalgia (esp MCP and large joints), then slate grey skin, DM (bronze diabetes), chronic liver disease, hepatomegaly, cirrhosis, cardiac failure (dilated cardiomyopathy), hypogonadism (pituitary deposits), osteoporosis

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8
Q

hereditary haemochromatosis testing

A

LFT increase, increase serum ferritin, increase serum iron, decrease TIBC, transferrin sat >80%, may have hyperglycaemia

Chondrocarcinosis in xray
Perl stain in liver biopsy shows iron loading
ECG/echo for cardiomyopathy

Managed by venesection

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9
Q

Secondary haemochromatosis

A

Can occur in recurrent blood transfusions

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10
Q

PBC

A

Interlobular bile duct damage by chronic granulomatous inflammation causing progressive cholestasis

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11
Q

Typical PBC presentation

A

9:1 F:M
Associated with thyroid disease, RA, sjogren’s syndrome, keratoconjunctivitis, systemic sclerosis, renal tubular acidosis, membranous glomerulonephririts

Peak age is 50
Often found at raised ALP on LFT. Lethargy, pruritis, jaundice, xanthalasma, xanthomata, hepatomegaly, splenomegaly

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12
Q

PBC complications

A

oesoporosis is common (malabsorption of ADEK), also coagulopaty, portal HTN, ascites, varicoeal haemorrhage, hepatic encephalopathy, HCC

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13
Q

Investigations for PBC

A

Raised ALP, GGT, mildly raised AST and ALT. AMA positive. raised IgM, may have raised TSH and cholesterol
Late disease has raised bilirubin, low albumin, raised PT time

USS and ERCP used to exclude extrahepatic cholestasis.

Biopsy shows granulomas

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14
Q

PSC

A

Inflammation, fibrosis and strictures of intra and extrehaptic bile ducts. May have immunological cause

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15
Q

Typical PSC presetation

A

More common in men
Associated with UC, HLA A1/B8/DR3, (rarely) Crohn’s disease), HIV infection

Chronic biliary gives cirrhosis and liver failure. Patient may be asymptomatic, often found with raised ALP on LFT.
Hepatomegaly, portal HTN, pruritis, jaundice, abdominal pain, fatigue

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16
Q

PSC investigations

A

raised ALP, raised bilirubin, hypergammaglobulinaemia, AMA negative , ANA/SMA/ANCA may be positive.
ERCP/MRCP shows strictures of biliary tree with beading.

Biopsy shows fibrous, obliterative cholangitis

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17
Q

PSC complications

A

Bacterial cholangitis, cholangiocarcinoma, increased risk of colorectal cancer

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18
Q

Autoimmune hepatitis

A

Inflammatory disease. Autoantiodies directed against hepatocytes. Has Type 1 and Type 2 (Type 2 generally just affects children)

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19
Q

Autoimmine hepatitis typical presentation

A

Young female
Acute hepatitis and features of autoimmune disease (fever, malaise, urticarial rash, polyartritis, pleurisy, pulmonary infiltration or glomerulonephritis).
Amenorrhoea is common

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20
Q

Autoimmune hepatitis diagnosis

A

raised AST, hypergammaglobulinaemia (esp IgG), positive ANA, SMA, LKM1
Biopsy shows mononuclear infiltrate of portal/periportal areas, necrosis, fibrosis.

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21
Q

Risk factors for HCC

A

Viral hepatitis (B or C), cirrhosis (alcohol induced, haemachromotosis), parasites, anabolic/contraceptive steroids, PBC

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22
Q

Risk factors for Cholangiocarcinoma

A

Flukes, PSC, congenital biliary cysts

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23
Q

Haemangiomas

A

Most common benign liver tumour, often incidental finding.

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24
Q

Whipples procedure

A

Removes masses from head of pancreas by resecting lower portion of stomach, head of pancreas, upper duodenum cystic duct.

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25
Q

Causes of chronic pancreatitis

A

Alcohol, familial, CF, haemochromatosis, pancreatic duct obstruction, Hyperparathyroidism, congenital

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26
Q

Thiamine

A

B1. Absorbed in small intestine. Causes Wenicke’s in deficiency

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27
Q

Riboflavin

A

B2. Absorbed in proximal small intestine. Defieincy causes angular stomatis and cheilitis

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28
Q

B12

A

Absorbed in terminal ileum. Deficiency causes macrocytic anaemia, neuropathy and glossitis

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29
Q

Vitamin D absorbed

A

Jejunum. Defieicny causes rickets/osteomalacia

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30
Q

Folic acid

A

Absorbed in jejunum. Deficiency causes macrocytic anaemia

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31
Q

Nicotinamide

A

Absorbed in jejunum. Deficiency causes pellagra.

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32
Q

Berger’s disease (IgA nephropathy)

A

Most common glomerulonephritis. Episoding haematuria, often associated with viral infection. Secondary causes are alcoholic liver disease, ankylosing spondilitis, coeliac disease

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33
Q

Baker’s cyst

A

Popliteal cyst. Causes pain and swelling. DDx is DVT can can distinguish with USS duplex

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34
Q

Buerger’s disease

A

Thromboangiitis obliterans. Inflammation of arteries, veins and nerves with thrombosis. Often in heavy smokers. Can cause gangrene.

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35
Q

Budd Chiari syndrome

A

Hepatic vein obstruction by thrombosis/tumour. Causes ischaemia, hepatocyte damage. Can be liver failure or cirrhosis.
See abdo pain, ascites, raised ALT. Can be hypercoagulable state (coc, pregnancy, malignancy, paroxysmal noctural haemoglobinuria, polycythemia rubra vera, thrombophilia), liver/renal/adrenal tumour.
Diagnosis: USS doppler, CT, MRI

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36
Q

Dubin Johnson syndrome

A

Autosomal recessive. Defective excretion of conjugated bilirubin, intermittent jaundice with RUQ pain and no hepatomegaly.

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37
Q

Felty’s syndrome

A

RA, splenomegaly and neutropoenia. See low platelets

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38
Q

Gilbert’s syndrome

A

Intermittent failure of bilirubin conjugation

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39
Q

Henoch schonlein purpura

A

Small vessel vasculitis with purpura (purple non blanching nodules) over buttocks and extensor surface. More common in young men. Often glomerulonephritis, joint involvement, abdo pain

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40
Q

T1 Weighting MRI

A

Water is hypo, bone and fat are white

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41
Q

T2 Weighting MRI

A

Water is white, bone is black (TWO - The white ocean)

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42
Q

Diabetes insipidus biochemistry

A

Hypernatraemia, increased plasma osmolarity, decreased urine osmolarity

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43
Q

SIADH biochemistry

A

hyponatraemia, low/normal urea/creatinine, reduced plasma osmolarity, urine osmolarity raised and higher than plasma osmolarity.

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44
Q

Conn’s vs Cushing’s biochemistry

A

In conns, hypokalaemia, increased bicarb, HTN. Normal/raised sodium

In Cushing’s, hypokalaemia, raised bicarb, raised sodium

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45
Q

False positive urobilinogen

A

Seen if urine is not resh.

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46
Q

Anion gap

A

Increase is acidosis

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47
Q

Metabolic acidosis with increased anion gap

A

Seen with increased organic acids (bicarb falls). Lactic acid, urate (renal failure), ketones (DM, alcohol), drugs/toxins (includes methanol)

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48
Q

Causes of metabolic acidosis with normal anion gap

A

Loss of bicarb, or ingestion of H+ .

Seen in renal tubular acidosis, diarrhoea, drugs, addison’s disease, pancreatic fistulae, ammonium chloride ingestion.

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49
Q

Hyperuricaemia causes

A

Drugs (cytotoxics, thoazies, pyrazinamide), increased cell turnover (lymphoma, leukaemia, psoriasis, haemolysis, muscle death), hout, chronic renal failure, lead nephropathy, hyperparathyroidism, pre eclapsia)

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50
Q

Hyponatraemia S+S

A

Confusion, seizure, HTN, cardiac failure, oedema, anorexia, nausea, muscle weakness

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51
Q

Hyponatraemia diagnosis

A

Check on patient volume status

If dehydrated, check urinary sodium. If >20mmol/L then sodium is lost through kidney (addison’s, renal failure, diuretics, osmolar diuresis)
If urinary sodium is <20mmol/L then sodium and water is lost extra renal (Diarrhoea, vomit, fistulae, burn, villous adenoma, SBO, CF, heat exposure)

If not dehydrated and oedematous, then think nephrotic, cardiac failure, liver cirrhosis, renal failure

If not dehydrated and not oedematous, check urine osmolarity. If >500 then SIADH. If <500 then water overload, severe hypothyroid, glucocorticoid insuffieincy)

52
Q

Hyponatraemia, dehydrated with high urine sodium

A

Think kidney loss (addison’s, diuretics, renal disease, osmolar diuresis (high glucose and urea)

53
Q

Hyponatraemia with dehydration and low urine sodium

A

Think extra renal loss such as vomiting, diarrhoea, burns, distulae, villous adenoma, trauma, CD, SBO

54
Q

Hyponatraemia qith no dehydration and no oedema

A

If urine osmolarity >500 then SIADH, if now then water overload, severe hypothyroidism or glucocorticoid insufficiency

55
Q

Hyponatraemia with no dehydration but does have oedema

A

Nephrotic, cardiac failure, liver failure, renal failure

56
Q

Hypernatraemia symptoms and signs

A

Thirst, confusion, coma, fits, dehydration signs, postural hypotension, oliguria

57
Q

Causes of hypernatraemia

A

Think water loss beyond sodium loss.

Can be diarrhoea, vomit, burns, excess IV saline, Diabetes insipidus, osmotic diuresis, primary aldosteronism

58
Q

Hyperkalaemia S+S

A

Cardiac arrythmias, sudden death, ECG (Tall T, small P, wide QRS - > VF)

59
Q

Causes of hyperkalaemia

A

oliguric renal failure, K sparing diuretics, rhabdomyolysis, metabolic acidosis, excess potassium therapy, Addison’s disease, massive blood transfusion, ACEi, suxamethonium, pseudohyperkalaemia (artefact)

60
Q

Causes of hypokalaemia

A

Diuretics, vomiting, diarrhoea, pyloric stenosis, vilous adenoma rectum, intestinal fistulae, Cushging’s (/steroids/ACTH), conn’s, alkalosis, purgative and liquorice abuse, renal tubular failure.

61
Q

Hypokalaemia S+S

A

Muscle weakness, hypotonia, cardiac arrythmias, cramps, tetany. on ECG, small/inverted T wave, prominent u wave, prolonged PR, depressed ST

Hypokalaemia worsens digoxin toxicity

62
Q

Hypocalcaemia S+S

A

tetany, depression, perioral praesthesiae, carpo-pedal spasm, neuromuscular excitability . Prolonged QT. Cataracts if chronic

63
Q

Hypercalcaemia S+S

A

Bone pain, weakness, tiredness, renal stones, renal failure, abdominal pain, polyuria, polydipsia, constipation, vomiting, depression, anorexia, weight loss, confusion, pyrexia. Cardiac arrest.. Short WT interval

64
Q

Howell Jolley bodies

A

DNA nuclear remnants in RBCs (normally removed by the spleen). Seen in post splenectomy or hyposplenism (e.g. sickle cell disease, coeliac disease, UC/crohns, myeloproliferative disease, amyloid)

65
Q

Target cells

A

RBC with central staining, pallour rim and outside staining. Seen in liver disease, hyposplenism, thalassaemia and IDA

66
Q

Neutrophilia causes

A

Steroids, bacterial infection, inflammation (including MI), disseminated malignancy, stress, surgery, trauma, myeloproliferative disorders

67
Q

Neutropoenia causes

A

Viral infection, chemi, cytotoxic agents, carbimazole, severe sepsis, neutrophil antibodies (SLE, haemolytic anaemia), Hypersplenism, Felty’s, bone marrow failure

68
Q

Lymphocytosis

A

Acute viral infection, chronic infection (TB, brucella, hepatitis, syphillis), leukaemia, lymphoma, EBV

69
Q

Lymphocytopoenia

A

Steroid therapy, SLE, uraemia, legionnaire’s disease, HIV infection marrow infiltration, post chemo/radio, HIV

70
Q

myeloma

A

Malignant clonal proliferation of B lymphocyte derived plasma cells. Detected as monoclonal band on serum/urine electrophoresis. Classed based on Ig product (can be IgG in 60%, IgA in 30%). Often has Bence Jones protein.

Causes osteolytic bone lesions (back, vertebrae, ribs. Back pain. Punched out on imaging), anaemia, neutropoenia, thrombocytopoenia, recurrent bacterial infections, renal impairment, systemic amyloidosis.

71
Q

Inherited thrombophilia (most common)

A

Most common cause is activated protein C resistance/Factor V Leiden. Clotting factor V mutation means wont be broken down by protein C. Thrombotic risk further increased in pregnancy or oestrogens

72
Q

LEss common inherited thrombophilia

A

Prothrombin gene mutation (causes high prothrombin levels), protein C and S deficiency (needed to neutralise factor V and VIII), antithrombin deficiency

73
Q

TTP

A

Thrombotic thrombocytopoenic purpura.
Pentad: fever, fluctuating CNS signs, haemolytic anaemia (may have jaundice), thrombocytopoenia, renal failure (haematuria/proteinuria)

Typically affects adult females. Lack of protease leads to aggregates of VWF and large scale platelet aggregation and deposition in small vessels, giving microthrombi. Often idiopathic, but associated with SLE, clopidogrel, cyclosporin, pregnancy, HIV.

74
Q

HUS

A

Haemolyitic uraemic syndrome. Microangiopathic haemolytic anaemia.

Endothelial damage leads to platelet aggregation, thrombosis and fibrin deposition. Fibrin damages RBCs.
Leads to thrombocytopoenia and acute renal failure.
Commonly after E coli.

75
Q

ITP

A

Idiopathic thrombocytopoenia purpura.

Antiplatelet autoantibodies, leading to phagocytic destruction. . Can be acute (typically in children) or chronic (in adult women).
Chronic has indefinite fluctuating coarse of bleeding, purpura, epistacis, menorrhagia

76
Q

LEft sided valvular disease with displaced apex

A

Mitral regurgitation, aortic regurgitation

77
Q

Cardiac catheterisation indications

A

Coronary artery disease (diagnosis to assess vessels, therapeutic for angioplasty and stent insertion)
Valvular disease (diagnostic to assess severity, therapeutic for valvuloplasty if not able for valve surgery)
Congenital heart disease (diagnostic and therapeutic)

78
Q

Cardiac catheterisation uses

A

Sample blood to assess oxygen saturation, inject radiocontrast dye to image heart and blood vessels, perform angioplasty, valvuloplasty and biopsies, to perform intravascular USS

79
Q

Cluster headache

A

Unilateral severe headache.
Has autonomic features (tearing of eyes, rhinorrhoea, sweating, tachycardia). Associated with alcohol consumption. Happens frequently.

80
Q

MRI angiography

A

Can be done with or without gandolinium, and therefore can be used for patients with renal impairment and also means no need for femoral puncture.

81
Q

SMA

A

Anti smooth muscle antibodies, associated with AIH, PBC, idiopathic cirrhosis

82
Q

Anti Ro

A

SLE, Sjogren’s, systemic sclerosis

83
Q

AMA

A

Anti mitrochondrial antibody. PBC, but also AIH and idiopathic sclerosis

84
Q

Pernicious anaemia Abs

A

Best is anti IF antibody (specific for pernicious anaemia) but can also do anti gastric parietal cell antibody (highly sensitive, but not as specific as also seen in atrophic gastritis)

85
Q

Best testing for RA

A

Anti CCP is highly specific.
Anti RF is sensitive (70%) but not as specific.
ANA is positive in 30%
ESR and CPR are general inflammatory indicators

86
Q

Best testing for coeliac disease

A

total immunoglobulin A (IgA) and IgA tissue transglutaminase (tTG) as the first choice

use IgA endomysial antibodies (EMA) if IgA tTG is weakly positive

consider using IgG EMA, IgG deamidated gliadin peptide (DGP) or IgG tTG if IgA is deficient

Biopsy if positive

87
Q

Best testing for SLE

A

Anti DSDNA and anti smith antibodies are most specific - can also correlate to severity

Anti RF may be present

Anti Ro can be present (esp with Sjogren’s syndrome)
ANA nearly always present but seen in other diseases too so not specific.

88
Q

Thallium and cardiolite scintigraphy cardiac imaging

A

Used to assess myocardial perfusion (looks at capillary filling, rather than large vessel flow)

89
Q

Cardiac catheterisation

A

Used to measure pressure in the heart as well as the shape of chambers

90
Q

High resolution cardiac imaging

A

SPECT (loewr cost), PET is higher cost but even higher resolution

91
Q

FL imaging for renal colic

A

USe CTKUB in adults

USS if pregnant woman or children

92
Q

Renal stone features

A

Oval/geometric (as opposed to phleboliths - round (rarely oval) but never goeometric). Central lucency also suggests phlebolith

93
Q

Rim sign

A

Seen in KUB for renal colic. See oedematous tissue surrounding stone

94
Q

Initial imaging for bowel obstruction

A

Plain AXR.

95
Q

AAA imaging

A

URgent CT, or CT angiogram if tolerated by the patient

96
Q

Appendicitis imaging

A

Clinical diagnosis, doesn’t need imaging. CT or MRI are also useful

97
Q

Appendicitis imaging

A

Best investigated in young patient with USS, CT also useful

98
Q

Hydronephrosis diagnostic imaging

A

USS, but CTKUB can diagnose

99
Q

Plain CT in neuro imaging

A

Most common neuro imaging, good for haemorrhage and acute issues

100
Q

CT contrast in neuro imaging

A

Highlights tumours and abscesses

101
Q

Cytotoxic oedema

A

Diffuse oedema seen in white and grey matter - think strokes

102
Q

Vasogenic oedema

A

Localised oedema that’s restricted to white matter - associated more with tumours

103
Q

Intrahepatic dilatation on abdo USS only

A

Intrahepatic or hilar cholangiocarcinoma, intrahepatic gallstones (rare), Caroli’s disease (rare and congenital)

104
Q

Extrahepatic dilation on abdo USS only

A

Early distal CBD obstruction, sphincter of oddi dysfunction, choledochal cyst

105
Q

Both intra and extrahepatic dilatation on abdo USS

A

Pancreatic/ampullary mass (doubt duct sign), distal CBD obstruction (gallstone, cholangiocarcinoma, lymph node, pseudocyst), minizzi syndrome, chronic pancreatitis

106
Q

Can biliary strictures be visualised on CT?

A

No, so stricture based obstruction would be missed

107
Q

Double duct sign on USS/CT

A

Dilated common bile duct and dilated pancreatic duct - head of pancreas tumours.

108
Q

MRI gallstones

A

Stones appear dark on MRI

109
Q

PTC

A

Percutaneous transhepatic cholaniopgraphy. Insert subcut into dilated hepatic duct and into common bile duct and duodenum (useful if blockage prevents duodenal access). Stent can be deployed and brushings can be taken)

110
Q

which vessel supplies the basal ganglia

A

MCA (perforating)

111
Q

CT contrast in A&E for stroke imaging?

A

Not useful as CT contast is bright and can mimic clots - use plain.
Contrast should be used to further visualise abnormalities already seen on CT (abscess or tumour), or can do CTA for vascular anatomy

112
Q

Contrast reaching brain?

A

Not readily available, but if BBB breached then can cshow

113
Q

Mnemonic for examining head CT with low GCS

A

Blood
Cisterns (present? squashed? haemorrhage?)
Brain tissue (colour? Sulci present? Gyri present?)
Ventricles (shape? squashed? haemorrhage? enlarged?)
ones and air spaces within

114
Q

Possible causes of low GCS on CT

A 
Haemorrhage
Loss of grey-white differentiation (stroke)
swelling (/mass effect/hydrocephalus)
Infection
Trauma
115
Q

Extra axial haemorrhage

A

outside parenchyma, so can be extra dural, sub dural or subarachnoid

116
Q

Intra axial haemorrhage

A

cerebral (trauma, tumous, post infarct, spontaneous)
Deep cerebral (HTN bleed)
Cerebellar (HTN bleed)
Intraventricular (spontaneous or secondary)

117
Q

CT blood visualisation

A

Clotted blood bright, active bleed is grey. Old blood is darker

Note that EDH is arterial, SDH is venous and blood in intergemispheric fissure indicates SA

118
Q

Abscess on contast CT head

A

Enhances, but centre dark due to lack of vasculature. Oedema surrounds abscess

119
Q

Red flag features suggesting IC abscess

A

immunocompromised, IVDU, infective endocarditis, TB

120
Q

IC haemorrhage complications

A

Oedema, mass effect, intraventricular extension, hydrocephalus, vasospasm (blood irritating causing new focal neurology and rebleed)

121
Q

Stroke on CT scan

A

Loss of grey/white matter differentiation. Infarcts tend to be dark in CT. Hyperdense clot signs are also a clue

122
Q

Pseudosubarachnoid haemorrhage

A

Cortices compressed together, gives hyperdense area looking like SAH star. May be seen in generalised swelling

123
Q

Causes of generalised IC swelling

A

metabolic issue (toxins, electrolytes, endocrine, organ failure, DKA)
Infection (sepsis)
Global cerebral insult (could be bilateral stroke, but might be diffuse axonal injury)

124
Q

NICE criteria for CT scan

A 
GCS<13 on ED presentation
GCS<15 at 2h from injury
Suspected skull fracture
Signs of basal skull fracture
Post traumatic seizure
Focal neurological deficit
more than 1 episode of vomiting

But also elderly adults on anticoagulation with head injury

125
Q

Fluid level in air spaces on imaging

A

Could be inflammation, but straight fluid level indicates fracture.

CP1 revision (16 decks)

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