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Flashcards in Review of posters 13/05/2016 Deck (74):
1

Primary biliary cholangitis (cirrhosis)

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

2

Pathology of PBC

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.

3

Why does the immune system only target bile duct cells?

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

4

Symptoms and clinical signs of PBC

Jaundice
Pruiritis (itchy skin)
Joint pain
Xanthomas

5

What will blood tests show?

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

6

Treatment of PBC

ursodeoxycholic acid

7

What organism causes TB?

Mycobacterium tuberculosis

8

How does TB spread?

Via airborne droplets

9

Pathology of TB

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.

10

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

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

11

Symptoms of TB

Night sweats
Fever
Haemoptysis
Cough
Tiredness and fatigue

12

What is latent TB?

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.

13

Treatment of TB

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

4 months of
Rifampicin
Isoniazid

14

Tests for TB

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

15

Define a hernia

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

16

Name hernias coming from natural openings

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

17

Name hernias coming from weak areas

Incisional, epigastric, paraumbilical, parastornal

18

Predisposing factors to hernias

Obesity, heavy lifting, pregnancy, physical debility

19

Paraumbilical hernia

Fat adult-
Hernia coming out of the umbilical region

20

Umbilical hernia

Congenital defect- weakness
Usually resolves by the time they are 3, if not surgically remove

21

Epigastric hernia

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

22

Femoral hernia

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

23

Paediatric inguinal hernia

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.

24

Inguinal hernia

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

25

Indirect inguinal hernia

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

26

Direct inguinal hernia

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

27

Complications of hernias

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

28

Operations performed on hernias

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

29

Post op advice for people with hernias

No driving for a week
Avoid heavy lifting.

30

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

Hep B or Hep C

31

Lab tests for hep B

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

Children and acute hep B

Child is more likely to develop chronic Hep B

33

Which Hepatitis virus is most likely to become chronic?

Hep C

34

Which peiple are at risk of developing Hep B?

Densely populated areas
Muiltiple sexual partners
IV Drug use

35

Labs for Hep C

Screen for Hep C IgG antibodies
Hep C virus RNA test- positive will mean viral RNA present

36

Hepatitis D

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

How is Hepatitis A spread?

Faecal- oral route

38

Who is most likely to get infected with Hep A?

Children/young adults
Densely populated and poor hygienic areas

39

Describe Hep A infection?

ACUTE

40

Labs for Hep A

IgM hep A present

41

How is hepatitis E spread?

Faecal oral route

42

Who is hepatitis E most common in?

Travellers (more common in tropical areas)

43

How does Hep E present?

Acute- similarly to hep A.
SERIOUS IN PREGNANT WOMEN

44

Management of acute hepatitis

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

45

Management of chronic hepatitis

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

46

Drug treatment of hepatitis

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

47

Describe the formation of bilirubin.

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

What does an increase in unconjugated bilirubin do?

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

What does an increase in conjugated bilirubin do?

Pigmented gall stones
Darker urine

50

Physiologic jaundice of the newborn

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

Gilberts syndrome

Decreased UGT- infection, stress and starvation exacerbate this.

52

Crigler Naff syndrome

No UGT- fatal

53

Dubin Johnson Syndrome

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

54

Obstructive jaundice

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

55

Acute cholecystitis

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

56

Symptoms of acute cholecystitis

Biliary colic pain
Pain becomes more localised and causes severe RUQ pain

57

Biliary colic

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

Common bile duct stones

Stones in the common bile duct
Presents as biliary colic, fever, jaundice.

59

Investigations into common bile duct stones

Increased serum bilirubin
Increased WCC
Increased CRP
Increased ALP and GGT

60

Investigations into acute cholecystitis

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

61

Management of acute cholecystitis

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

62

Cholangiocarcinoma

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

Investigations into cholangiocarcinoma

CT
MRCP
Ultrasound

64

Treatment of cholangiocarcinoma

Resection or radical chemotherapy

65

Cancer of the gallbladder

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

Symptoms of acute pancreatitis

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

67

Causes of acute pancreatitis

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

68

Basic pathogenesis

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

Blood tests and investigations

Serum amylase
Urinary amylase
X-ray
Ultrasound

70

Causes of chronic pancreatitis

Autoimmune pancreatitis
Chronic alchohol consumption

71

Symptoms of chronic pancreatitis

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

72

Treatment of chronic pancreatitis

Opiate analgesia and NSAIDs for the pain.

73

Describe autoimmune pancreatitis

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

74

Basic pathogenesis of chronic pancreatitis

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