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CP1 revision > Deck 5 > Flashcards

Deck 5 Flashcards

1
Q

Pancreatisis causes

A 
Idiopathic
gallstones (lodged at sphincter of oddi)
alcohol (increases zymogen secretion and decreases fluid and bicarb, causing obstruction)
Trauma
Steroids
Mumps
Autoimmune
Spider/scorpion bite
Hypercalcaemia/hypertriglyceridaemia
ERCP
Drugs (azathioprine, furosemide, immunosuppressants, thiazides, ACEi, NSAIDs, sulphonamides)
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2
Q

Pancreatitis general

A

Can range from mild to severe. 20% are mild and resolve spontaneously.
Males affected more than females. Gallstones and alcohol are biggest causes

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3
Q

Pancreatitis S+S

A

N&V, epigastric pain, radiating to back, relieves on sitting forward.
Cullen’s sign
Grey turner sign
Hypercalcaemia (due to fat necrosis)
Signs of sepsis (tachycardia, fever, rigid abdomen, shock)
ileus

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4
Q

Pancreatitis investigations

A

Amylase, lipase (more specific and better after initial phase when amylase decreases), bone profile (hypercalaemia), triglycerides, FBC, U&E, CRP, ABG, lactate and o2

Clinical diagnosis, imaging not needed but may do:
AXR to show ileus
CXR to exclude other cause
USS to exclude gallstones
CT abdo if uncertainty
MRCP to visualise ductal system
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5
Q

Scoring system for pancreatitis

A 
Glasgow scoring system
P (aO2<8)
Age (>55)
Neutrophils/WCC>15
Calcium <2mmol
Renal, urea (>16)
Enzymes (LDH >600, AST>200)
Albumin (<32)
Sugar (glucose >10)
3 or more is severe -HDU/ITU

Can also use Apache II (clinical features, age and comorbidities to give score. >9 is severe)

Randon criteria uses age, lab score on admission and38h to give mortality risk

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6
Q

periductal pancreatitis

A

Necrosis of acinar cells adjacent to duct- obstruction cause

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7
Q

panlobular pancreatitis

A

whole acinar lobule necrosis. Drugs, toxins, viruses, metbolic insult

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8
Q

Perilobular pancreatitis

A

necrosis of peripheries. shock/hypothermia

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9
Q

Pancreatitis management

A

Fluids (3rd space loss), analgesia (caution with morphine, can spasm sphincter of oddi), NG tube, adeqaute oxygenation, ERCP if gallstones, broad spec Abx

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10
Q

Pancreatitis complications

A 
Pancreatitis necrosis (liquifactive haemorrhagic necrosis), pseudocyst (can be infected and form abscess), abscess formation (pain, anorexia, palpable tender mass - CT visible)
Can also lead to hypovolaemic shock (blood vessels rupture), , DIC, ARDS (inflammation causes leaky blood vessels), thrombosis of splenic/gastroduodenal arteries (bowel necrosis), hyperglycaemia, hypokalaemia, hypoalbuminaemia, vitamin deficiency
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11
Q

Primary haemostasis

A

Platelet mediated.
Injury causes vasoconstriction to allow platelet adhesion to exposed collagen.
VWF binds collagen, Gp2b on platelets bind vWF.
Platelets release ADP/TXA2
Collagen activated platelets expose fibrinogen receptors.
Soft, weak plug formed

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12
Q

Primary haemostasis impairment

A

Bruising, epistaxis, gum bleeding, menorrhagia, intra/immediate post op bleed

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13
Q

Primary haemostasis impairment cauaes

A

Thrombocytopoenia, lack of GP1b (Bernard Soullier syndrome), lack of GP2b/a (Glanzmann’s thrombasthaenia), antiplatelet drugs, VWF impairment

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14
Q

Thrombocytopoeania causes

A

Overuse (septicaemia, DIC, TTP), immune reaction (autoimmune, drug induced), decreased production (alcohol, cytotoxic drugs, bone marrow failure), hyperplenism

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15
Q

Aspirin/NSAIDs block`

A

COX1 (TXA2), but also COX2

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16
Q

Clopidogrel/tricagrelor block

A

ADP binding P2Y12

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17
Q

Abciximab/eptifibatide block

A

Gp2b3b

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18
Q

Secondary haemostasis

A

Clotting cascade and fibrin mesh (needs tissue factor).

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19
Q

Vitamin K dependent clotting factors

A

2,7,9,10

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20
Q

Extrinsic pathway

A

Activation of VII and X
Use PT to measure.
INR is PT corrected - normal is 0.9-1.1

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21
Q

Intrinsic pathway

A

12->11->9–>8 and 10

APTT meausres.

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22
Q

Measure for unfractionated heparin

A

APTT

Intrinsic pathway

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23
Q

Symptoms of secondary haemostasis disorder

A

Haemarthrosis, muscular/soft tissue bleed, extensive bruising, delayed post op bleed/poor wound healing

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24
Q

Causes of secondary haemostasis disorder

A

Reduced coagulation factors (congenital is haemophilias, acquired through warfarin, liver dysfunction, DIC)

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25
Q

To investigate primary haemostasis disorders

A

FBC (platelet number), blood film (morphology), platelet function test, vWF assays (specialist

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26
Q

To investigate secondary haemostasis

A

Clotting screen:
- PT time (extrinsic. Needs tissue factor and calcium. Prolonged is VII issue)
APTT (intrinsic. Add kalolin, phospholipid and calcium. Prolonged is VIII, IX, XI or XII).
If prolonged APTT then mixing stud used to see if correctable factor deficiency or inhibitory protein.

Can also look at D dimers/fibrinogen degredation products, or individual clotting factor (specialist).

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27
Q

Prolonged PT and APTT`

A

Likely mixed clotting deficiency, but rarely can be II, V or X

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28
Q

Fibrinolysis

A

Plasminogen - > tPA to plasmin. Degrades fibrin (products include D dimer)

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29
Q

Haemophilia A

A

More common, larger gene.
Severity based on VIII levels.
<1% is severe, >5% is mild and can be asymptomatic

Mild may respond to desmopressin as this increases VWF in blood (and VWF carries factor VIII)

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30
Q

Acute hepatitis

A

Fever, nausea, arthalgia, jaundice, develops over several days.
Typical pre-icteric phase beforehand - often has cigarette smoke aversion and RUQ pain.
Hepatocytes swell, then necrose (esp zone 3 as less blood)

Jaundice, pale stoole and dark urine as intrahepatic cholestatic jaundice. Get pruritus and rash

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31
Q

Hep A

A

A is faeco-oral. 2-6 week incubation. Notifiable disease. 80% asymptomatic. Not chronic. No specific treatment. Typically affects age extremes.

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32
Q

Hep B

A

B is in blood/semen/saliva. But vertical transmission is most common worldwide. 1-6 month incubation. Has core antigen (HBcAg) and surface (HBsAg). 10% of those infected get chronic disease, 1% get fulminant disease. Only DNA Hepatitis.

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33
Q

HEP B markers

A

○ HBsAg shows at 6 weeks, but disappears by 3 months
○ HBsAB marks previous cleared infection or vaccination
○ HBeAg shows infectivity (viral replication)
○ HBeAb is natural immunity marker
○ HBcAb IgG is non specific marker of infection (current/previous)
○ HBcAbIgM marks infection within last 6 months
○ HBVPCR is best viraemia marker
Summary is that surface antigen shows recent infection. No core antibody is vaccination only. Lack of HBeAb can be chronic infection.

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34
Q

Hep C

A

C causes chronic infection, transmitted in body fluids. V common in IVDU. Vertical and sexual transmission uncommon. 85% become chronic, 30% get cirrhosis in 20 years. No vaccine.

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35
Q

Hep D

A

D is dependent on B. Can be acquired simultaneously, but subsequent hep D infection has worse outcome.

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36
Q

Hep E

A

Hep E is feco-oral. Similar picture to hep A. More common in indo-china. Can cause severe disease in pregnant women. No vaccine?

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37
Q

Other viral hepatitis

A

CMV, yellow fever, HSV in immunocompromise

38
Q

Bacterial hepatitis causes

A

Leptospirosis, Q fever, syphilis

39
Q

Parasitic hepatitis causes

A

malaria

40
Q

Non infective hepatisis

A

○ Autoimmune
○ Alcoholic (shows fatty changes, necrosis, ballooned cells and hyaline deposits)
○ NAFLD
○ Toxins
○ Metabolic (haemochromatosis, Wilson’s)
Drug induced (paracetamol, aspirin, diclofenac, co-amox)

41
Q

Hepatitis classed as hepatic or cholestatic or steatosis

A

Hepatocellular (AST/ALT rise), or cholestatic(bilirubin/ALP/GGT rise)
Histologically, if inflammatory change then hepatitis, if bile block then cholestasis and fatty is steatosis

42
Q

Chronic hepatitis

A

Last longer than 6 months. Can be HepB/C/D but also autoimmune

43
Q

Autoimmune hepatitis may present

A

Jaundice, fatigue, deranged LFTs, urticaria, polyarthritis, glomerulonephritis, amenorrhoea

44
Q

Cirrhosis

A

Fibrosis, loss of normal architecture and nodule development. Kupffer cells and hepatocytes cause fibrosis, stellate cells become myoofibroblasts and secrete collagen

45
Q

Micronodular disease

A

<3mm - tends to be alcoholic liver damage or biliary tract disease

46
Q

Macronodular

A

> 3mm, tends to be previous hepatitis

47
Q

Cirrhosis S+S

A

Fatigue, Hx of liver disease, weight loss, anorexia, ascites, jaundice, peripheral oedema, bleeding/bruising, pruritis (tx with cholestyramine), leukonychia, palmar erythema, clubbing, liver flap, duyputren’s contracture, pigmentation, spider nevi, striae, portal HTN signs,

48
Q

Cirrhosis causes

A

Hep B and C, Alcoholism, NAFLD, haemochromatosis, wilson’s, PBC, PSC, autoimmune hepatitis, Drugs (e.g. amiodarone)

49
Q

Cirrhosis complications

A

hypoproteinuria (ascites and odema)
oesophageal varices
Secondary hyperaldosteronism (hypoalbuminaemia and portal HTN cause renal hypoperfusion - hepatorenal syndrome
Ascites (portal HTN, low protein and salt/water ret - Transudate)
Hepatic encephalopathy (ammonia, glutamine, use lactulose)
Venous distension (haemorrhages, paraumbilical vein, osesophageal varices)

50
Q

Cirrhosis decompensation

A

Can be stable, but deterioration can occur in:
- Dehydration
- Constipation (ammonia builds up in bowel)
- Alcohol binge
- Sepsis (spontaneous bacterial peritonitis)
- Excessive opioid use (metabolised in liver, also gives constipation)
GI bleed (extra protein in bowel - > ammonia production)

51
Q

Portal HTN varices

A

Varices at left gastric vein (gastric/oesophageal varices), rectal vein, retroperitoneal organs, paraumbilical

52
Q

Portal HTN causes

A

Pre hepatic (portal vein thrombosis), hepatic(cirrhosis/hepatitis), post hepatic (Budd Chairi syndrome - hepatic veins obstructed).

53
Q

PBC

A

Primary biliary cirrhosis.
Autoimmnune against small/medium IH ducts.
normally AMA positive
More females>males.
40s and 50s
FHx and IBD association
T cell mediated, leads to bile and salt retention, hepatocyte injury and cirrhosis
Increased HCC risk
Tx by slowing progression with ursodeoxycholic acid

S+S
See fatigue, pruritus, hypercholesterolaemia (+/- skin hyperpigmentation, xanthalasma, steatorrhoea, vit D malabsorption). In advanced disease, splenomegaly, jaundice.

54
Q

PSC

A

Primary sclerosing cholangitis
Affects large intrahepatic ducts and extrahepatic ducts - although small ducts can be impacted by cholestasis.
Oedema and inflammation narrow lumen and cause strictures.
Cholestsis and fibrosis give cirrhosis.
Increased risk of cholangiocarcinoma
More males affected (30s)
Symptoms: fatigue, pruritus, jaundice, ascending cholangitis, chronic pancreatitis, chronic cholecystitis.
Associated with UC (screen by raised ALP)
May have pANCA or ANA (AMA negative)

55
Q

Difference between PBC and PSC

A

PBC tends to be older, tends to be female, associated with sjogren, thyroid, scleroderma. Often AMA or ANA. PBC is radiologically normal. PBC is loss of small ducts

PSC is younger, more male, associated with IBD, often ANCA but may be ANA (AMA negative), PSC has strictures and beading of large bile ducts and pruning of smaller ducts. PSC is inflammatory desctruction of extra and intraheptic ducts, fibrotic obliteration of small ducts

56
Q

Cholesterol supersaturation

A

Pregnancy, hypercholesterolaemia, CoC, depleted bile acids (terminal ileum disease/resection), bile stasis (fasting, TPN), increase Hb breakdown (spherycytosis, sickle cell, malaria, mech heart valves

57
Q

Stones most likely to be radioopaque

A

Pigmented

58
Q

Cholelithasis

A

Stones in gallbladder

59
Q

Choledocholithiasis

A

Stones in bile duct

60
Q

Cholestasis

A

Bile flow block

61
Q

Biliary colic

A

RUQ sudden pain, typically radiates to R shoulder. Lasts <6h as stone falls back. Normal normal O/E, apyrexial but may have N&V
Stones on USS.
Analgesia and cholecystectomy within 6 weeks

62
Q

Cholecystitis

A

Stone in hartman’s pouch or cystic duct, causes chemical irritation from bile. May have superimposed infection
Constant RUQ pain, N&V, lethargy, tachycardia, no jaundice.
Murphey’s sign
Analgesia, IVAbx and fluid, cholecystectomy within 1 week

63
Q

Chronic cholecystitis

A

Fibrosis and thickening but not distension

64
Q

choledocholithiasis

A

Stone impacted in common bile duct. May cause obstructive jaundice. Can predispose to pancreatitis or ascending cholangitis

65
Q

Mirizzi’s syndrome

A

Cholelithiasis causes external compression of common hepatic duct, gives obstructive jaundice but no dilatation of cystic/common bile duct

66
Q

Cholangitis

A

Inflammation of biliary tree. Obstruction and infection.
Charcot’s triad (RUQ pain, fever and jaundice). Peristent pain, pyrexia with rigors. May have pruritus, pale stool and dark urine. Sepsis risk.
Needs blood cultures.

ERCP is diagnostic and treatment

67
Q

Carcot’s triad

A

Cholangitis symptoms. Fever, RUQ pain and jaundice

68
Q

Gallbladder imaging

A

USS good for stones, can measure gallbladder thickness and duct dilatation. Pericholecystic fluid shows inflammation
MRCP is MRI. Diagnostic onlh. Visualises biliary tree
ERCP is GSTD for cholangitis. Ideally MRCP first to visualise. Pancreatitis risk
T tube. not recommended now, used after bile duct exploration to prevent CBD blockage through swelling

69
Q

Courvoisier’s sign

A

patient with painless jaundice and enlarged gallbladder has malignancy until proven otherwise.

70
Q

Hepatobiliary cancer types

A

90% secondaries (GI, lung - esp SCLC, breast), 10% primaries (most of these are HCC, but can get cholangiocarcinomas)
Most pancreatic cancers are ductal

71
Q

Clinical features of hepatobiliary tumours

A

RUQ pain, weight loss, nausea, fever, jaundice and liver fiailure symptoms

72
Q

Liver biopsy CI

A

prolonged PT, platelet count <80, ascites, extra hepatic cholestasis

73
Q

Primary liver cancer RF

A

Chronic hep B, hep C, alcoholic liver disease, metabolic disease, PBC, NAFLD

74
Q

primary liver cancer tumour marker

A

alpha fetoprotein. Correlates to tumour size and poor prognostic marker

75
Q

cholangiocarcinoma

presentation

A

In part of biliary tree (including hepatic). Generally adenocarcinoma.
Presents as per bile duct obstruction (RU! pain, pruritus, dark urine, pale stool)

76
Q

Cholangiocarinoma RF and management

A

PSC, anatomical liver abnormality (cyst or congenital issue), obesity, diabetes, hepolithasis (chronic hepatic stones), liver fluke, hep B and C

Can resect caudate lobe. Can stent bile duct for palliative relief

77
Q

Pancreatic cancer

A

Nearly always adenocarcinoma (exocrine endothelial cells, but can get acinar and cystoadenocarcinoma

78
Q

Pancreatic cancer RG

A
  • Smoking
    • Obesity
    • Diabetes (although may be cause)
    • Alcohol
    • Chronic pancreatitis
      60+
79
Q

Presentation of pancreatic cancer

A

2/3s are head of pancreas. Compresses CBD and presents late with painless obstructive jaundice. Progresses to ascites, anaemia, fatigue and nausea
1/3 body/tail. Causes vague B symptoms and nausea. Ascites late feature. May have incessant epigastric pain (relieved on sitting forward)

80
Q

Pancreatic cancer complications

A

T3c diabetes, pancreatic exocrine insufficiency (steaorrhoea, malnutrition), DVT/PE

81
Q

Islet cell tumour

A

Rare, associated with MEN syndrome
-isletoma causes hypoglycaemia and weight gain
Glucoagonoma causes secondary diabetes
Gastrinoma causes Zollinger ellison syndrome
Somatostatinoma causes diabetes, achlorrydia, gallstones
VIPoma causes profound diarrhoea

82
Q

Benign liver tumours

A

Haemangiomas, can be incidental finding on CT/USS. Tx if >5cm

83
Q

LFT analysis

A

ALT>AST in most liver injury, but AST2:ALT1 then alcohol (esp if raised GGT)

10xAST/ALT raise is hepatocellular picture
ALP/GGT 3x raise is cholestasis

Isolated ALP in bone disease and pregnancy

84
Q

Bilirubin cycle

A

Unconjugated to conjugated, then urobilinogen and either stercobilin (stool) or urobilin (or recycled)

85
Q

Prehaptic jaundice causes

A

Normal urine, normal stool.
Severe malaria, Pernicious anaemia, sickle cell anaemia, thalasaemia, transfusion reactions, autoimmuen (e.g. SLE), Gilbert’s syndrome

86
Q

Hepatic causes of jaundice

A

Dark urine, slightly pale stool.
Hepatitis (esp A) liver tumours, alcoholic hepatitis, drug introduced (NSAIDs, antiepileptic, antibiotics), autoimmune, Wilson’s disease

87
Q

Post hepatic

A

Pale stools, dark urine

Gallstone, cholangiocarcinoma, strictures, pancreatic cancer, PSC, abdominal mass (lymphoma)

88
Q

Jaundice investigations

A

Blood film/coombs if ?haemolytic jaundice
Macrocytic anaemia in haemolytic anaemia and liver disease
Viral serology/autoantibodies (?hepatitis)
MRCP (non invasive, high res)
CT/MRI to assess itnrahepatic/pancreatic lesions
Biopsy (if clotting ok)
ERCP if ductal system dilated, or percutaneous transhepatic cholangiography if ERCP not possible. Can stent but can’t view ampulla or pancreatic duct)

89
Q

Spleen basics

A 
White pulp (B and T cells screen blood), red pulp (filters out old RBCs and stores 1/3 of platelets. 
asplenic people need lifelong abx (phenoxymethylpenicllin)
90
Q

Splenomegaly causes

A

Increased demand (removing RBc, extramedullary haematopoesis, infection (EBV/HIV)
Infiltration (leukaemia, lymphoma, haematoma, cyst, IE, sepsis)
Inflammation (RA, SLE, sarcoidosis)
Abnormal blood flow (e.g. portal/hepatic vein obstriction, hepatic schistomiasis)

91
Q

Autoimmune haemolytic anaemia

A

Do Coombs test
90% are warm
If IgG alone then warm AIHA or drug induced
If complement alone then can be cold
If IgG plus complement then warm, mixed warm and cold or drug induced (methyldopa)

Can also be seen in SLE, chronic inflammatory disesae

92
Q

Splenomegaly sequaelae

A

Any splenomegaly can cause hypersplenism with panctopoenia, increased plasma volume and haemolysis

CP1 revision (16 decks)

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