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SJ Phase 2a > Liver + friends > Flashcards

Liver + friends Flashcards

1
Q

Define acute liver failure

A

Rapid decline in hepatic function

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2
Q

Clinical presentation of acute liver failure

A
  1. Jaundice
  2. Abdominal pain
  3. Hepatic encephalopathy (confusion,insomnia)
  4. N+V
  5. Right upper quadrant tenderness
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3
Q

Diagnosis of acute liver failure

A
  1. LFT
    • Hyperbilirubinemia
    • Raised ALT
    • Raised AST
  2. PT/INR (coagulation test)
    • INR>1.5
  3. U&E
  4. Hepatitis screen (ABCE)
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4
Q

Treatment of acute liver failure

A
  1. ITU support
  2. Monitor and correct glucose + electrolytes
  3. Liver transplant
  4. N-acetylcisteine (paracetamol OD)
  5. Viral hepatitis - ACICLOVIR
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5
Q

Clinical presentation of chronic liver failure

A
  1. Oedema
  2. Gynaecomastia
  3. Anorexia
  4. Clubbing
  5. Easy bleeding + bruising
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6
Q

Aetiology of acute liver failure

A
  1. Paracetamol overdose
  2. Alcohol
  3. Viral hepatitis
  4. Drugs
  5. Obstruction
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7
Q

Aetiology of chronic liver failure

A
  1. Alcohol
  2. Viral hepatitis
  3. autoimmune
  4. Metabolic
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8
Q

Define liver cirrhosis

A
  1. Fibrosis and conversion of normal liver architecture
  2. To structurally abnormal nodules (regen nodules)
  3. Final stage of any chronic liver disease
  4. Irreversible
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9
Q

Aetiology of liver cirrhosis

A
  1. Alcohol abuse
  2. Hep B and C
  3. Fatty liver disease
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10
Q

Clinical presentation of liver cirrhosis

A
  1. Palmar erythema
  2. Dupuytren’s contracture
  3. Jaundice
  4. Ascites
  5. Spider naevi
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11
Q

Diagnosis of liver cirrhosis

A
  • serum albumin and PT (INR/PT = high)
    • Platelets
    • Thrombocytopenia
    • U+E
    • Biopsy
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12
Q

Treatment of liver cirrhosis

A
  1. LIVER TRANSPLANT
  2. Ascites = diuretics = SPIRONOLACTONE
  3. Cerebral oedema = MANNITOL
  4. Bleeding = VIT K
  5. Encephalopathy = decrease ammonia = LACTULOSE, ANTIBIOTICS, ENEMA
  6. Hep B - TENOFOVIR
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13
Q

Define ascites

A

Fluid in peritoneal cavity

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14
Q

Aetiology of ascites

A

Cirrhosis

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15
Q

pathophysiology of ascites

A
  1. Peritonitis = more leaky
  2. Raised capillary hydrostatic pressure
  3. Reduced colloid oncotic pressure
  4. Peritoneal lymphatic draining
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16
Q

How do you distinguish between transudate and exudate ascites

A
  1. Transudate = protein<25g/L
  2. Exudate = protein>25g/L
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17
Q

Aetiology of transudate ascites

A
  1. Portal hypertension
  2. Low plasma protein
  3. Heart failure
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18
Q

Aetiology of exudate ascites

A
  1. Peritonitis
  2. Peritoneal malignancy
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19
Q

Clinical presentation of ascites

A
  1. Shifting dullness - fluid = buoyancy -> tympanic sound on front where air filled bowel loops are, when patient lying supine but dullness on flanks
  2. Abdominal disetension
  3. Resp. distress
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20
Q

Diagnosis of ascites

A
  1. Physical examination of abdomen
  2. Diagnostic aspiration (needle for fluid check in abdomen)
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21
Q

Treatment of ascites

A
  1. salt restriction
  2. Diureitcs = FUROSEMIDE
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22
Q

What is SAAG

A
  1. Serum-Ascites Albumin Gradient
  2. Used to determine cause of ascites
  3. SAAG = (serum albumin) - (albumin level of ascitic fluid)
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23
Q

Aetiology of portal vein hypertension

A
  1. Prehepatic = portal vein thrombosis
  2. Intrahepatic = schistosomiasis, cirrhosis
  3. Posthepatic = right side heart failure
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24
Q

Transmission of Hep A

A

Faecal-oral

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25
Q

Epidemiology of Hep A

A
  1. Rare
  2. Poor ends
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26
Q

Pathophysiology of Hep A

A
  1. Acute infection
  2. Usually cleared by host immune system
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27
Q

Clinical presentation of Hep A

A

NON SPECIFIC SYMPTOMS
1. Nausea
2. Anorexia
3. Malaise
LIVER SYMPTOMS
1. Jaundice
2. Hepatomegaly
3. Skin rash

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28
Q

Diagnosis of Hep A

A

LFTs
1. Raised ALT (alanine transaminase)
2. Raised bilirubin
3. Serology

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29
Q

Treatment of Hep A

A

Vaccine

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30
Q

Transmission of Hep B (HBV)

A
  1. Blood products (IVDU)
  2. Sex (MSM)
  3. Vertical transmission (across generations)
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31
Q

Pathophysiology of Hep B

A
  1. Acute infection infects hepatocyte
  2. Cellular response usually suffices
  3. Chronic HBV if HbsAg >6months
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32
Q

Clinical presentation of Hep B

A
  1. Acute infection symptoms
  2. chronic -> cirrhosis symptoms
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33
Q

Diagnosis of Hep B

A

LFTs
Serology
Ag (Antigen) after 6 months = chronic Hep B

34
Q

Treatment of Hep B

A
  1. Vaccine
  2. Antiviral treatment TENOFOVIR
35
Q

Transmission of Hep C

A
  1. Blood/blood products - IVDU
  2. More common in UK
36
Q

Pathophysiology of Hep C

A
  1. Acute infection often asymptomatic .˙. can become chronic
  2. Chronic -> slow progressive fibrosis over years
37
Q

Clinical presentation of Hep C

A

Acute = asymptomatic
Chronic = chronic liver disease

38
Q

Diagnosis of Hep C

A

LFTs
Serology
If Ag after 6m = chronic HCV

39
Q

Treatment of Hep C

A

Interferon based regimens

40
Q

Transmission of Hep D

A

Blood borne
- Sex
- IVDU

41
Q

Pathophysiology of Hep D

A
  1. Requires concurrent HBV infection to replicate
  2. Progression to cirrhosis more likely
42
Q

Clinical presentation of Hep D

A
  1. Vaccine
  2. Antiviral treatment TENOFOVIR
43
Q

Transmission of Hep E

A

Faeco-oral transmission (undercooked meat)
Common in UK

44
Q

Clinical presentation of Hep E

A

Asymptomatic

45
Q

Diagnosis of Hep E

A

Serology

46
Q

Treatment of Hep E

A

Not required but supportive

47
Q

Define haemochromatosis

A
  1. Multi-system disorder
  2. Dysregulated dietary iron absorption
  3. Increased iron release from macrophages
48
Q

Aetiology of haemochromatosis

A
  1. Autosomal recessive
  2. Secondary iron overload by multiple transfusion
49
Q

Pathophysiology haemochromatosis

A

Iron accumulates in:
- liver
- joints
- pancreas
- heart
- skin
- gonads

50
Q

Clinical presentation of haemochromatosis

A
  1. Slate grey skin
  2. Hypogonadism
51
Q

Diagnosis of haemochromatosis

A
  1. Bloods
    • Iron
    • LFTs
  2. Liver biopsy
52
Q

Treatment of haemochromatosis

A
  1. Venesection
  2. Iron chelation
  3. liver transplant
53
Q

Define Wilson’s disease

A
  1. Excessive copper
  2. Build up in liver and CNS
54
Q

Aetiology of Wilson’s disease

A
  1. Autosomal recessive
  2. Defective enzyme involved in biliary excretion of excess copper
55
Q

Pathophysiology of Wilson’s disease

A
  1. Cu2+ accumulates in liver -> liver symptoms
  2. Cu2+ accumulates in basal ganglia -> Parkinson’s symptoms
  3. Cu2+ accumulates in cornea -> Kayser-Fleischer rings)
56
Q

Clinical presentation of Wilson’s disease

A
  1. Parkinson
  2. Depression
  3. Neurotic behaviour
  4. Kayser-Fleischer ring
57
Q

Diagnosis of Wilson’s disease

A
  1. 24h urine copper and blood caeruloplasmin
  2. Liver biopsy
58
Q

Treatment of Wilson’s disease

A
  1. Pencillamine (copper chelation)
  2. Liver transplant
59
Q

Define acute pancreatitis

A
  1. Sudden inflammation of pancreas
  2. Auto-digestion of the gland
  3. reversible
60
Q

Clinical presentation of acute pancreatitis

A
  1. Sever epigastric pain radiating to back
  2. N+V
  3. Fever and chills
  4. Haemodynamic instability
  5. Retroperitoneal haemorrhage
61
Q

Aetiology of acute pancreatitis

A
  1. Idiopathic
  2. Gallstones
  3. Alcohol
  4. Trauma
  5. Steroids
62
Q

Diagnosis of acute pancreatitis

A
  1. Amylase/lipase
  2. LFTs
  3. CRP
  4. CT
63
Q

Treatment of acute pancreatitis

A
  1. Nil By Mouth (NBM) - bowel rest
  2. Aggressive fluid resuss
  3. Analgesia
  4. Abx (antibiotics) if necrotising pancreatitis
64
Q

Define chronic pancreatitis

A
  1. Long standing inflammation
  2. From irreversible damage to pancreas
65
Q

Clinical presentation of chronic pancreatitis

A
  1. Epigastric pain radiating to back
  2. N+V
  3. Steatorrhea (fatty stool)
  4. Weight loss
  5. Insulin dependent DM
66
Q

Aetiology of chronic pancreatitis

A
  1. Alcohol
  2. CF
  3. Cancer
  4. Autoimmune
67
Q

Diagnosis of chronic pancreatitis

A
  1. Secretin stimulation test
  2. CT, MRI, MRCP
68
Q

Treatment of chronic pancreatitis

A
  1. Creon (pancreatic enzyme replacement therapy)
  2. Insulin
  3. Opioids
  4. Alcohol cessation
  5. Surgery
69
Q

Define biliary colic

A

Temporary blockade of cystic duct by gallstones

70
Q

Clinical presentation of biliary colic

A
  1. RUQ pain after fatty meals
  2. Referred shoulder pain
  3. N+V
71
Q

Diagnosis of biliary colic

A
  1. USG
  2. LFT
  3. FBC
  4. Lipase
72
Q

Treatment of biliary colic

A
  1. Analgesia
  2. Lap. Cholecystectomy
73
Q

Define acute cholecystitis

A
  1. Blockade of cystic duct
  2. Leading to build up of bile
  3. -> transmural inflammation of gallbladder
74
Q

Clinical presentation of acute cholecystitis

A
  1. RUQ pain after fatty meals
  2. Referred shoulder pain
  3. N+V
  4. Fever
  5. Murphy’s +ve (inspiratory arrest upon applying pressure to RUQ)
75
Q

Diagnosis of acute cholecystitis

A
  1. FBC
  2. CRP
  3. LFTs
  4. USG (ultrasonography)
76
Q

Treatment of acute cholecystitis

A
  1. Lap cholecystectomy (within 7 days)
  2. Fluids + analgesia for surgery
77
Q

Define ascending cholangitis

A
  1. Medical emergency
  2. Bacteria ascending through biliary tree
  3. -> septicaemia
78
Q

Clinical presentation of cholangitis

A
  1. Charcot’s Triad
    • RUQ pain
    • Jaundice
    • Fever + rigors
  2. Reynol’d pentad
    • Charcot’s Triad
    • Confusion
    • Septic shock
79
Q

Diagnosis of cholangitis

A
  1. Amylase/lipase
  2. LFTs
  3. CRP
  4. FBC
  5. CT, USG, MRCP, ERCP
80
Q

Treatment of cholangitis

A
  1. Aggressive fluid resuss
  2. IV Abx -> PENICILLIN & AMINOGLYCOSIDES
  3. Pressor support
  4. ERCP
  5. Cholecystectomy when improved
81
Q

Define primary biliary cirrhosis

A
  1. Progressive autoimmune destruction of liver + biliary tree
  2. -> fibrosis then cirrhosis

SJ Phase 2a (13 decks)

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