Liver diseases oxford Flashcards
Fulminant liver failure
Massive necrosis of liver cells
signs of liver failure
jaundice, encephalopathy, aterixis, apraxia (5 pointed star drawing), fetor hepaticus (pear drop breath)
Effects of warfarin in liver failure
enhanced
Causes of liver cirrhosis
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)
Imaging for cirrhosis
USS and duplex
Ascitic tap
Can do MRI
Liver biopsy (if not CI)
Hereditary haemochromatosis
Increased iron absorption gives deposition in joints, livre, heart, pancreas, pituitary, adrenal and skin
Hereditary haemochromatosis presentation
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
hereditary haemochromatosis testing
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
Secondary haemochromatosis
Can occur in recurrent blood transfusions
PBC
Interlobular bile duct damage by chronic granulomatous inflammation causing progressive cholestasis
Typical PBC presentation
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
PBC complications
oesoporosis is common (malabsorption of ADEK), also coagulopaty, portal HTN, ascites, varicoeal haemorrhage, hepatic encephalopathy, HCC
Investigations for PBC
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
PSC
Inflammation, fibrosis and strictures of intra and extrehaptic bile ducts. May have immunological cause
Typical PSC presetation
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
PSC investigations
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
PSC complications
Bacterial cholangitis, cholangiocarcinoma, increased risk of colorectal cancer
Autoimmune hepatitis
Inflammatory disease. Autoantiodies directed against hepatocytes. Has Type 1 and Type 2 (Type 2 generally just affects children)
Autoimmine hepatitis typical presentation
Young female
Acute hepatitis and features of autoimmune disease (fever, malaise, urticarial rash, polyartritis, pleurisy, pulmonary infiltration or glomerulonephritis).
Amenorrhoea is common
Autoimmune hepatitis diagnosis
raised AST, hypergammaglobulinaemia (esp IgG), positive ANA, SMA, LKM1
Biopsy shows mononuclear infiltrate of portal/periportal areas, necrosis, fibrosis.
Risk factors for HCC
Viral hepatitis (B or C), cirrhosis (alcohol induced, haemachromotosis), parasites, anabolic/contraceptive steroids, PBC
Risk factors for Cholangiocarcinoma
Flukes, PSC, congenital biliary cysts
Haemangiomas
Most common benign liver tumour, often incidental finding.
Whipples procedure
Removes masses from head of pancreas by resecting lower portion of stomach, head of pancreas, upper duodenum cystic duct.
Causes of chronic pancreatitis
Alcohol, familial, CF, haemochromatosis, pancreatic duct obstruction, Hyperparathyroidism, congenital
Thiamine
B1. Absorbed in small intestine. Causes Wenicke’s in deficiency
Riboflavin
B2. Absorbed in proximal small intestine. Defieincy causes angular stomatis and cheilitis
B12
Absorbed in terminal ileum. Deficiency causes macrocytic anaemia, neuropathy and glossitis
Vitamin D absorbed
Jejunum. Defieicny causes rickets/osteomalacia
Folic acid
Absorbed in jejunum. Deficiency causes macrocytic anaemia
Nicotinamide
Absorbed in jejunum. Deficiency causes pellagra.
Berger’s disease (IgA nephropathy)
Most common glomerulonephritis. Episoding haematuria, often associated with viral infection. Secondary causes are alcoholic liver disease, ankylosing spondilitis, coeliac disease
Baker’s cyst
Popliteal cyst. Causes pain and swelling. DDx is DVT can can distinguish with USS duplex
Buerger’s disease
Thromboangiitis obliterans. Inflammation of arteries, veins and nerves with thrombosis. Often in heavy smokers. Can cause gangrene.
Budd Chiari syndrome
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
Dubin Johnson syndrome
Autosomal recessive. Defective excretion of conjugated bilirubin, intermittent jaundice with RUQ pain and no hepatomegaly.
Felty’s syndrome
RA, splenomegaly and neutropoenia. See low platelets
Gilbert’s syndrome
Intermittent failure of bilirubin conjugation
Henoch schonlein purpura
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
T1 Weighting MRI
Water is hypo, bone and fat are white
T2 Weighting MRI
Water is white, bone is black (TWO - The white ocean)
Diabetes insipidus biochemistry
Hypernatraemia, increased plasma osmolarity, decreased urine osmolarity
SIADH biochemistry
hyponatraemia, low/normal urea/creatinine, reduced plasma osmolarity, urine osmolarity raised and higher than plasma osmolarity.
Conn’s vs Cushing’s biochemistry
In conns, hypokalaemia, increased bicarb, HTN. Normal/raised sodium
In Cushing’s, hypokalaemia, raised bicarb, raised sodium
False positive urobilinogen
Seen if urine is not resh.
Anion gap
Increase is acidosis
Metabolic acidosis with increased anion gap
Seen with increased organic acids (bicarb falls). Lactic acid, urate (renal failure), ketones (DM, alcohol), drugs/toxins (includes methanol)
Causes of metabolic acidosis with normal anion gap
Loss of bicarb, or ingestion of H+ .
Seen in renal tubular acidosis, diarrhoea, drugs, addison’s disease, pancreatic fistulae, ammonium chloride ingestion.
Hyperuricaemia causes
Drugs (cytotoxics, thoazies, pyrazinamide), increased cell turnover (lymphoma, leukaemia, psoriasis, haemolysis, muscle death), hout, chronic renal failure, lead nephropathy, hyperparathyroidism, pre eclapsia)
Hyponatraemia S+S
Confusion, seizure, HTN, cardiac failure, oedema, anorexia, nausea, muscle weakness
Hyponatraemia diagnosis
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)
Hyponatraemia, dehydrated with high urine sodium
Think kidney loss (addison’s, diuretics, renal disease, osmolar diuresis (high glucose and urea)
Hyponatraemia with dehydration and low urine sodium
Think extra renal loss such as vomiting, diarrhoea, burns, distulae, villous adenoma, trauma, CD, SBO
Hyponatraemia qith no dehydration and no oedema
If urine osmolarity >500 then SIADH, if now then water overload, severe hypothyroidism or glucocorticoid insufficiency
Hyponatraemia with no dehydration but does have oedema
Nephrotic, cardiac failure, liver failure, renal failure
Hypernatraemia symptoms and signs
Thirst, confusion, coma, fits, dehydration signs, postural hypotension, oliguria
Causes of hypernatraemia
Think water loss beyond sodium loss.
Can be diarrhoea, vomit, burns, excess IV saline, Diabetes insipidus, osmotic diuresis, primary aldosteronism
Hyperkalaemia S+S
Cardiac arrythmias, sudden death, ECG (Tall T, small P, wide QRS - > VF)
Causes of hyperkalaemia
oliguric renal failure, K sparing diuretics, rhabdomyolysis, metabolic acidosis, excess potassium therapy, Addison’s disease, massive blood transfusion, ACEi, suxamethonium, pseudohyperkalaemia (artefact)
Causes of hypokalaemia
Diuretics, vomiting, diarrhoea, pyloric stenosis, vilous adenoma rectum, intestinal fistulae, Cushging’s (/steroids/ACTH), conn’s, alkalosis, purgative and liquorice abuse, renal tubular failure.
Hypokalaemia S+S
Muscle weakness, hypotonia, cardiac arrythmias, cramps, tetany. on ECG, small/inverted T wave, prominent u wave, prolonged PR, depressed ST
Hypokalaemia worsens digoxin toxicity
Hypocalcaemia S+S
tetany, depression, perioral praesthesiae, carpo-pedal spasm, neuromuscular excitability . Prolonged QT. Cataracts if chronic
Hypercalcaemia S+S
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
Howell Jolley bodies
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)
Target cells
RBC with central staining, pallour rim and outside staining. Seen in liver disease, hyposplenism, thalassaemia and IDA
Neutrophilia causes
Steroids, bacterial infection, inflammation (including MI), disseminated malignancy, stress, surgery, trauma, myeloproliferative disorders
Neutropoenia causes
Viral infection, chemi, cytotoxic agents, carbimazole, severe sepsis, neutrophil antibodies (SLE, haemolytic anaemia), Hypersplenism, Felty’s, bone marrow failure
Lymphocytosis
Acute viral infection, chronic infection (TB, brucella, hepatitis, syphillis), leukaemia, lymphoma, EBV
Lymphocytopoenia
Steroid therapy, SLE, uraemia, legionnaire’s disease, HIV infection marrow infiltration, post chemo/radio, HIV
myeloma
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.
Inherited thrombophilia (most common)
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
LEss common inherited thrombophilia
Prothrombin gene mutation (causes high prothrombin levels), protein C and S deficiency (needed to neutralise factor V and VIII), antithrombin deficiency
TTP
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.
HUS
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.
ITP
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
LEft sided valvular disease with displaced apex
Mitral regurgitation, aortic regurgitation
Cardiac catheterisation indications
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)
Cardiac catheterisation uses
Sample blood to assess oxygen saturation, inject radiocontrast dye to image heart and blood vessels, perform angioplasty, valvuloplasty and biopsies, to perform intravascular USS
Cluster headache
Unilateral severe headache.
Has autonomic features (tearing of eyes, rhinorrhoea, sweating, tachycardia). Associated with alcohol consumption. Happens frequently.
MRI angiography
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.
SMA
Anti smooth muscle antibodies, associated with AIH, PBC, idiopathic cirrhosis
Anti Ro
SLE, Sjogren’s, systemic sclerosis
AMA
Anti mitrochondrial antibody. PBC, but also AIH and idiopathic sclerosis
Pernicious anaemia Abs
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)
Best testing for RA
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
Best testing for coeliac disease
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
Best testing for SLE
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.
Thallium and cardiolite scintigraphy cardiac imaging
Used to assess myocardial perfusion (looks at capillary filling, rather than large vessel flow)
Cardiac catheterisation
Used to measure pressure in the heart as well as the shape of chambers
High resolution cardiac imaging
SPECT (loewr cost), PET is higher cost but even higher resolution
FL imaging for renal colic
USe CTKUB in adults
USS if pregnant woman or children
Renal stone features
Oval/geometric (as opposed to phleboliths - round (rarely oval) but never goeometric). Central lucency also suggests phlebolith
Rim sign
Seen in KUB for renal colic. See oedematous tissue surrounding stone
Initial imaging for bowel obstruction
Plain AXR.
AAA imaging
URgent CT, or CT angiogram if tolerated by the patient
Appendicitis imaging
Clinical diagnosis, doesn’t need imaging. CT or MRI are also useful
Appendicitis imaging
Best investigated in young patient with USS, CT also useful
Hydronephrosis diagnostic imaging
USS, but CTKUB can diagnose
Plain CT in neuro imaging
Most common neuro imaging, good for haemorrhage and acute issues
CT contrast in neuro imaging
Highlights tumours and abscesses
Cytotoxic oedema
Diffuse oedema seen in white and grey matter - think strokes
Vasogenic oedema
Localised oedema that’s restricted to white matter - associated more with tumours
Intrahepatic dilatation on abdo USS only
Intrahepatic or hilar cholangiocarcinoma, intrahepatic gallstones (rare), Caroli’s disease (rare and congenital)
Extrahepatic dilation on abdo USS only
Early distal CBD obstruction, sphincter of oddi dysfunction, choledochal cyst
Both intra and extrahepatic dilatation on abdo USS
Pancreatic/ampullary mass (doubt duct sign), distal CBD obstruction (gallstone, cholangiocarcinoma, lymph node, pseudocyst), minizzi syndrome, chronic pancreatitis
Can biliary strictures be visualised on CT?
No, so stricture based obstruction would be missed
Double duct sign on USS/CT
Dilated common bile duct and dilated pancreatic duct - head of pancreas tumours.
MRI gallstones
Stones appear dark on MRI
PTC
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)
which vessel supplies the basal ganglia
MCA (perforating)
CT contrast in A&E for stroke imaging?
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
Contrast reaching brain?
Not readily available, but if BBB breached then can cshow
Mnemonic for examining head CT with low GCS
Blood
Cisterns (present? squashed? haemorrhage?)
Brain tissue (colour? Sulci present? Gyri present?)
Ventricles (shape? squashed? haemorrhage? enlarged?)
ones and air spaces within
Possible causes of low GCS on CT
Haemorrhage Loss of grey-white differentiation (stroke) swelling (/mass effect/hydrocephalus) Infection Trauma
Extra axial haemorrhage
outside parenchyma, so can be extra dural, sub dural or subarachnoid
Intra axial haemorrhage
cerebral (trauma, tumous, post infarct, spontaneous)
Deep cerebral (HTN bleed)
Cerebellar (HTN bleed)
Intraventricular (spontaneous or secondary)
CT blood visualisation
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
Abscess on contast CT head
Enhances, but centre dark due to lack of vasculature. Oedema surrounds abscess
Red flag features suggesting IC abscess
immunocompromised, IVDU, infective endocarditis, TB
IC haemorrhage complications
Oedema, mass effect, intraventricular extension, hydrocephalus, vasospasm (blood irritating causing new focal neurology and rebleed)
Stroke on CT scan
Loss of grey/white matter differentiation. Infarcts tend to be dark in CT. Hyperdense clot signs are also a clue
Pseudosubarachnoid haemorrhage
Cortices compressed together, gives hyperdense area looking like SAH star. May be seen in generalised swelling
Causes of generalised IC swelling
metabolic issue (toxins, electrolytes, endocrine, organ failure, DKA)
Infection (sepsis)
Global cerebral insult (could be bilateral stroke, but might be diffuse axonal injury)
NICE criteria for CT scan
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
Fluid level in air spaces on imaging
Could be inflammation, but straight fluid level indicates fracture.
