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Posters > Review of posters 13/05/2016 > Flashcards

Review of posters 13/05/2016 Flashcards

1
Q

Primary biliary cholangitis (cirrhosis)

A

Autoimmune disorder where the T cells attack the cells lining the bile duct.

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2
Q

Pathology of PBC

A

T cells attack the cells lining the bile duct. They become damaged and start to leak out bile into the interstitial space. This bile eventually gets into the bloodstream.

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3
Q

Why does the immune system only target bile duct cells?

A

Patients with autoimmune PBC have high levels of anti-microbial antibodies (antibodies that attack the mitochondria) which are specific to bile ductule cells.

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4
Q

Symptoms and clinical signs of PBC

A

Jaundice
Pruiritis (itchy skin)
Joint pain
Xanthomas

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5
Q

What will blood tests show?

A

Raised ALP and GGT. Probably raised serum bilirubin in later stages of disease.

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6
Q

Treatment of PBC

A

ursodeoxycholic acid

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7
Q

What organism causes TB?

A

Mycobacterium tuberculosis

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8
Q

How does TB spread?

A

Via airborne droplets

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9
Q

Pathology of TB

A

Droplets inhaled- get into the lungs. Alveolar macrophages then ingest them. Inside the alveolar macrophages the bacilli proliferate and cause them to release neutrophil attracting chemokines and cytokines. This causes an inflammatory response and granulomas form. In the middle of the granuloma is a caseous necrotic centre.

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10
Q

Describe the differences in findings between latent TB and primary TB.

A

Latent TB- bacilli present in ghon focus
Primary TB- bacilli present in lung tissues and secretions aswell as in the ghon focus

Latent TB- non infectious
Primary TB- highly infectious

Latent TB- no symptoms
Primary TB- symptoms

Latent TB- Sputum smear and culture negative
Primary TB- sputum smear and culture positive

Latent TB- CXR normal
Primary TB- CXR showing consolidation and effusi

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11
Q

Symptoms of TB

A 
Night sweats
Fever
Haemoptysis 
Cough
Tiredness and fatigue
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12
Q

What is latent TB?

A

Generally- people who develop TB are immunocompromised in some way which allows it to take over. However if TB infects a normal individual the body will form an immune response against it and will remember it.

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13
Q

Treatment of TB

A 
2 months of:
Rifampicin- yellow body fluids
Isoniazid- yellow skin
Ethambutol - blurred vision
Pyraxinamide - gout exacerbation

4 months of
Rifampicin
Isoniazid

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14
Q

Tests for TB

A

Ziehl Neelson test- stains bacilli yellow orange
Culture- 6 weeks
Smear and sputum sample

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15
Q

Define a hernia

A

An abnormal protrusion of a viscera out with its normal body cavity

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16
Q

Name hernias coming from natural openings

A

Inguinal, femoral, umbilical, splegian, obtrurator, oesophageal hiatus

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17
Q

Name hernias coming from weak areas

A

Incisional, epigastric, paraumbilical, parastornal

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18
Q

Predisposing factors to hernias

A

Obesity, heavy lifting, pregnancy, physical debility

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19
Q

Paraumbilical hernia

A

Fat adult-

Hernia coming out of the umbilical region

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20
Q

Umbilical hernia

A

Congenital defect- weakness

Usually resolves by the time they are 3, if not surgically remove

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21
Q

Epigastric hernia

A

Arise from congenital weakness in the linea alba. Usually contains extraperitoneal fat.
Asymptomatic/local symptoms (treat with surgery)

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22
Q

Femoral hernia

A

Defect in the femoral canal.

Below and lateral to the pubic tubercle. Loss of groin crease. Typically elderly, thin female.

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23
Q

Paediatric inguinal hernia

A

Processes vaginalis- This is the hole in the peritoneal cavity where the testes descend through. Usually closes but sometimes it doesnt and areas of bowel can come through.

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24
Q

Inguinal hernia

A

Two types- indirect and direct
Indirect- lateral to inferior epigastric vessels
Direct- medial to inferior epigastric vessels.

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25
Q

Indirect inguinal hernia

A

May reach scrotum.
Congenital hernias are indirect
Can be controlled by digital pressure

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26
Q

Direct inguinal hernia

A

Posterior bulge.
Through transversalis fascia
Often bilateral
Poorly controlled by digital pressure

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27
Q

Complications of hernias

A 
Recurrence
Chronic neurogenic pain
Testicular pain and atrophy
Wound infection
Acute urinary retention
Haematoma
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28
Q

Operations performed on hernias

A

Suture, open mesh, laparoscopic
Herniotomy- excision of peritoneal sac
Herniorraphy- repair of defect in wall

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29
Q

Post op advice for people with hernias

A

No driving for a week

Avoid heavy lifting.

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30
Q

Hepatitis spread by sex, blood, or from mother to child

A

Hep B or Hep C

31
Q

Lab tests for hep B

A

Hep B surface antigen present (HBsAg)
If individual is highly infectious they will have Hep B e surface antigen (HBeAg)
More antigen will be present in more infectious individuals

32
Q

Children and acute hep B

A

Child is more likely to develop chronic Hep B

33
Q

Which Hepatitis virus is most likely to become chronic?

A

Hep C

34
Q

Which peiple are at risk of developing Hep B?

A

Densely populated areas
Muiltiple sexual partners
IV Drug use

35
Q

Labs for Hep C

A

Screen for Hep C IgG antibodies

Hep C virus RNA test- positive will mean viral RNA present

36
Q

Hepatitis D

A

Always as a co-infection or superinfection with Hep B. (co-infection when you are infected with both at the same time, super infection is affected by Hep D afterwards)
Worsens symptoms of hep B

37
Q

How is Hepatitis A spread?

A

Faecal- oral route

38
Q

Who is most likely to get infected with Hep A?

A

Children/young adults

Densely populated and poor hygienic areas

39
Q

Describe Hep A infection?

A

ACUTE

40
Q

Labs for Hep A

A

IgM hep A present

41
Q

How is hepatitis E spread?

A

Faecal oral route

42
Q

Who is hepatitis E most common in?

A

Travellers (more common in tropical areas)

43
Q

How does Hep E present?

A

Acute- similarly to hep A.

SERIOUS IN PREGNANT WOMEN

44
Q

Management of acute hepatitis

A

Monitor for encaphylopathy
Monitor for resolution
Notify public health
Test for other infections and vaccinate against these

45
Q

Management of chronic hepatitis

A

Antivirals
Vaccination against other hepatitis
Treat before established cirrhosis sets in.

46
Q

Drug treatment of hepatitis

A

Peginterferon Alpha 2a- stimulates immune system to attack virus.

47
Q

Describe the formation of bilirubin.

A

Old red blood cells are eaten by macrophages. The haemoglobin gets broken down into heme and globin. The globin goes on to form amino acids. However the haem is further broken down into iron and protoporphyrin.
This is then converted to unconjugated bilirubin (which is insoluble in water). Therefore to get to the liver it needs albumin to transport it in the blood.
When it reaches the hepatocyte, unconjugated bilirubin is converted by uridine glycorynl transferase (UGT) to conjugated bilirubin.
Conjugated bilirubin travels to the bile duct where it becomes concentrated.
On eating- bile is secreted into the duodenum where it reacts with microbes to form urobilinogen. THis becomes spontaneously oxidised to urobilin (which is excreted in faeces or recycled by the livers and kidneys).

48
Q

What does an increase in unconjugated bilirubin do?

A

Increase could be due to increased breakdown of reb blood cells prematurely (extravasculation haemolytic anaemia) or due to red blood cells not forming right (ineffective haematopoesis).
This leads to an increase in unconjugated bilirubin in the blood and therefore jaundice.

49
Q

What does an increase in conjugated bilirubin do?

A

Pigmented gall stones

Darker urine

50
Q

Physiologic jaundice of the newborn

A

Decreased UGT levels (uridine glutamyl transferase) therefore no conversion of UCB to CB
UCB is not soluble and can build up in places like the brain

51
Q

Gilberts syndrome

A

Decreased UGT- infection, stress and starvation exacerbate this.

52
Q

Crigler Naff syndrome

A

No UGT- fatal

53
Q

Dubin Johnson Syndrome

A

Conjugated bilirubin can’t move into bile canniculi and therefore build up in the hepatocyte.

54
Q

Obstructive jaundice

A

Something obstructs the flow of bile- leads to back up of bile into the blood.

55
Q

Acute cholecystitis

A

Obstruction of the cystic duct (most likely due to gallstones) causing back up of bile and the gall bladder to enlarge.

56
Q

Symptoms of acute cholecystitis

A

Biliary colic pain

Pain becomes more localised and causes severe RUQ pain

57
Q

Biliary colic

A

Pain felt when gallstones temporarily obstruct the cystic duct. Pain is constant. Exacerbated by eating (especially fatty foods). Nausea and vomiting.
Pain may radiate over right shoulder or spontaneously stop. May need opiate analgesisa

58
Q

Common bile duct stones

A

Stones in the common bile duct

Presents as biliary colic, fever, jaundice.

59
Q

Investigations into common bile duct stones

A

Increased serum bilirubin
Increased WCC
Increased CRP
Increased ALP and GGT

60
Q

Investigations into acute cholecystitis

A

Raised CRP
Raised ALP and GGT
Slightly elevated serum bilirubin
Ultrasound will show thickened bile duct walls/enlarged bile duct.

61
Q

Management of acute cholecystitis

A 
Nil by mouth
IV fluids
IV antibiotics
Opiate analgesia
Wait for it to settle and then perform cholecystectomy.
62
Q

Cholangiocarcinoma

A

Cancer of the biliary tree. Could be intrahepatic (in the bile ducts inside the liver) or extra hepatic (in the cystic, hepatic, gallbladder). Associated with primary sclerosing cholangins, chronic infection.
Usually presents with jaundice

63
Q

Investigations into cholangiocarcinoma

A

CT
MRCP
Ultrasound

64
Q

Treatment of cholangiocarcinoma

A

Resection or radical chemotherapy

65
Q

Cancer of the gallbladder

A

Benign polyps- adenomas
Maligant- adenocarcinoma
Related to calcification which is the final stage in acute cholecystitis. Also polyps greater than 10mm in diameter are likely to become malignant.

66
Q

Symptoms of acute pancreatitis

A

Epigastric pain that radiates through to the back
Nausea
Vomiting
In severe cases- tachycardia, hypotension, Cullens sign and Grey Turners sign.

67
Q

Causes of acute pancreatitis

A

Alcohol, viral infection (cocksackie), gallstones, pancreatic tumours, drugs.

68
Q

Basic pathogenesis

A

Anything that leads to increased intracellular calcium. Blockage of the pancreatic duct leads to early activation of trypsinogen to form trypsin. This somehow leads to increased intrapancreatic pressure and increased calcium depositation.

69
Q

Blood tests and investigations

A

Serum amylase
Urinary amylase
X-ray
Ultrasound

70
Q

Causes of chronic pancreatitis

A

Autoimmune pancreatitis

Chronic alchohol consumption

71
Q

Symptoms of chronic pancreatitis

A 
Epigastric pain- may be episodic
Steatorrhea
Weight loss
Anorexia
Malabsorption or diabetes
Gallstone related jaundice
72
Q

Treatment of chronic pancreatitis

A

Opiate analgesia and NSAIDs for the pain.

73
Q

Describe autoimmune pancreatitis

A

Defect in the PRSS1 gene that is involved with the activation of trypsin. IgG4 related. Dense lymphoblastic infiltrate. Reversed by corticosteroids.

74
Q

Basic pathogenesis of chronic pancreatitis

A

Chronic alcohol consumption leads to premature activation of trypsinogen to form trypsin. This leads to precipitation of protiens that form plugs in the duct. This causes an increase in pancreatic pressure and therefore release of cellular calcium

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