GI Defences Flashcards

0
Q

What are the innate physical defences of the GI?

A
Sight, smell and memory
Saliva which contains lactoperoxidase, IgA, complement, polymorphs and washes toxins into the stomach
Gastric acid
Small intestine secretions including bile, proteolytic enzymes, lack of nutrients
Anaerobic environment
Shedding of epithelial cells
Rapid transit - peristalsis 
Mucus to protect colonic epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What toxins can the GI tract be exposed to?

A
Chemicals
Bacetrial
Viruses
Protozoa
Nematodes (round worms)
Cestodes (tapeworm)
Trematodes (flukes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What innate cellular defences are there in the GI tract?

A
Neutrophils
Macrophages 
Kupffer cells
Natural killer cells
Tissue mast cells
Eosinophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are Kupffer cells and why do we need them?

A

Specialised macrophages in the liver

All venous blood from the GI tract passes through the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the adaptive defences of the GI tract?

A

B lymphocytes - produce antibodies including IgA and IgE. Effective against extracellular microbes
T lymphocytes - directed against intracellular organisms
Gut-associated lymphoid tissue (GALT) - diffusely distributed. Found in tonsils, appendix and Peyer’s patches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is infection if the salivary glands called?

A

Parotitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What infectious consequences are there of xerostomia?

A

Parotitis caused by Staph aureus

Hairy tongue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can cause achlorydia? (Lack of gastric acid)

A

Pernicious anaemia
H2 antagonists
Proton pump inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What infections are patients at a higher risk of if they have achlorydia?

A

Shigellosis
Cholera
Salmonella
Hospital patients on PPIs - C. difficile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which bacteria are resistant to gastric acid?

A

H pylori

Mycobacterium tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which viruses are resistant to stomach acid?

A

Enteroviruses

  • hep A
  • polio
  • coxsackie
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What causes recruitment of mast cells in the gut and what do they cause?

A
Gut infections which activate complement
Recruit mast cells
Release histamine
Causes vasodilation and increased capillary permeability
Massive fluid loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the mortality of cholera if left untreated?

A

60%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What infection of the gut can cause right iliac fossa pain?

A

Mesenteric adenitis caused by adenovirus or coxsackie virus. Affects ileocaecal GALT
Appendicitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What can cause appendicitis?

A

Lymphoid hyperplasia of the appendix base leading to obstructed outflow. Stasis and infection

Faecolith (calcified faecal matter)

Worm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What complication in the gut can typhoid fever lead to?

A

Inflamed Peyer’s path in the terminal ileum which can perforate and kill the patient.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What infectious complication occurs if blood supply to the GI tract is compromised?

A

Cannot carry out defence mechanisms

Overwhelming sepsis and rapid death within hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What can compromise blood flow to the gut?

A

Arterial disease
Systemic hypotension
Intestinal venous thrombosis

18
Q

Causes of liver failure?

A
Viral hepatitis
Alcohol
Drugs eg paracetemol, halothane
Industrial solvents
Mushroom poisoning
19
Q

What can you be more susceptible to with liver failure?

A

Infections
Toxins
Drugs
Hormones

20
Q

What is hepatic encephalopathy?

A

High blood concentration of ammonia

21
Q

How is ammonia produced?

A

Colonic bacteria

Deamination of amino acids

22
Q

How do oesophageal varices occur?

A

Vein? drains into hepatic portal vein
If there is cirrhosis, can cause portal hypertension
Blood backs up in the oesophageal veins and causes them to dilate

23
Q

What is caput medusae caused by?

A

Portal hypertension

Ligamentum teres opens up and blood radiates out from the umbilicus

24
Q

How do haemorrhoids develop?

A

Portal hypertension
At anorectal junction, vein? joins with hepatic portal vein. If pressure is increased in portal vein, can cause the junction to open up and causes haemorrhoids

25
Q

How does the liver handle bile pigments?

A

Conjugates bilirubin and secretes it into the faeces which can then be excreted.

26
Q

What is the most abundant plasma protein and what is it essential for?

A

Albumin

Maintaining osmotic pressure needed for proper distribution of body fluids.

27
Q

What coagulation factors does the liver produce?

A

Fibrinogen (I)
Prothrombin (II)
V, VII, IX, X, XI

Protein C, protein S, antithrombin

28
Q

What is thrombopoietin and what does it do?

A

A glycoprotein hormone

Regulates production of platelets by bone marrow

29
Q

What does a high level of alkaline phosphatase indicate and why?

A

When liver’s biliary ducts are obstructed

It is an enzyme in the cells of these ducts

30
Q

What does low albumin indicate?

A

Chronic liver disease

31
Q

What does an increased prothrombin time show?

A

The clotting tendency of the blood

Would show if there is liver damage?

32
Q

Signs of hyperbilirubinaemia?

A

Yellow pigmentation of skin

Yellow conjunctival membranes over the sclerae

33
Q

What should bilirubin levels in the blood be below normally and when is it an issue?

A

Normally <22mmol/L

Clinically detectable above 44mmol/L

34
Q

What is pre-hepatic jaundice caused by?

A

Excessive haemolysis

  • red cell membrane defects
  • haemoglobin abnormalities
  • metabolic defects
  • hyperbilirubinaemia
  • Gilbert’s syndrome

Acquired include

  • immune
  • mechanical (eg RBCs running across the metal heart valve)
  • membrane defects
  • infections
  • burns
35
Q

What is hepatocellular jaundice caused by?

A

Deranged hepatocyte function

Can be an element of cholestasis

36
Q

Lab findings in pre-hepatic jaundice?

A
Unconjugated hyperbilirubinaemia
Reticulocytosis
Anaemia
High LDH (contained in RBCs)
Low haptoglobin (normally bound to bilirubin)
37
Q

Lab findings in hepatocellular jaundice?

A

Mixed conjugated and unconjugated hyperbilirubinaemia
High ALT and AST
Normal/high ALP (alkaline phosphatase??)
Abnormal clotting

38
Q

Causes of hepatocellular jaundice?

A

Congenital

  • Gilbert’s syndrome
  • Crigler-Najjar syndrome

Hepatic inflammation

  • EBV
  • Hep A-E
  • autoimmune hepatitis
  • alcohol
  • haemochromatosis
  • Wilson’s disease

Drugs

Cirrhosis caused by

  • alcohol
  • hepatitis
  • metabolic disorders

Hepatic tumours: hepatocellular carcinomas, metastases

39
Q

What is post-hepatic/cholestatic jaundice?

A

Obstruction of biliary system affecting drainage of bile
Causes a back up of bile acids into the liver
Can be inta or extra hepatic
Passage of conjugated bilirubin is blocked

40
Q

Lab findings in post-hepatic jaundice?

A

Conjugated hyperbilirubinaemia
Bilirubin in urine (dark)
Increased canalicular enzymes (ALP)
Normal or raised ALT/AST due to mild hepatocyte damage from pressure

41
Q

Causes of post-hepatic jaundice?

A

Intrahepatic

  • hepatitis
  • drugs
  • cirrhosis
  • primary biliary cirrhosis

Extra-hepatic (obstruction distal to bile canaliculi)

  • gallstones
  • biliary stricture
  • carcinoma
  • pancreatitis
  • sclerosis cholangitis
42
Q

Where can carcinomas be which cause extra-hepatic jaundice?

A
Head of pancreas
Ampulla
Cholangiocarcinoma
Porta hepatis
Lymph nodes
Liver metastases
43
Q

Overall causes of pre-hepatic, hepatic and post-hepatic jaundices

A

Pre-hepatic - excessive bilirubin produced
Hepatic - reduced capacity to conjugate or excrete bilirubin
Post-hepatic - obstruction to biliary system