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ESA 3 > GI 7 > Flashcards

GI 7 Flashcards

1
Q

List the categories of toxins that may be encoutered in the GI tract

A

Chemical

Bacteria

Viruses

Protozoa

Nematodes, Cestodes, Trematodes

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2
Q

What methods of defense are used aginst these toxins?

A

Innate:

Physical

Celullar

Adaptive

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3
Q

What are the innate phyiscal defenses protecting the GI tract?

A

Sight

Smell

Memory

Saliva

Gastric Acid

Small intestine secretions

Colonic mucus peristalsis/Segmentation

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4
Q

What is the effect of slowed peristalsis on a gut infection?

A

Course of disease is prolonged (E.g. Shigellosis)

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5
Q

How is saliva protective against infection?

A

Contains Lysosyme, lactoperoxidase, complement, IgA and polymorphs

Washes toxins into the stomach (acid)

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6
Q

What effect can severe dehydration have on salivary defense?

A

Xerostomia:

Lead to microbial overgrowth in the mouth and dental caries

Parotitis:

Caused by staph aureus

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7
Q

Describe the functions of the stomach as they relate to innate protection of the gut

A

Stomach acid works to digest food, but also to sterilise it

The 2.5L of gastric juice per day can have a pH as low as 0.87, killing all but a few bacteria and viruses

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8
Q

What might reduce the protective effect of stomach acid?

What is the effect of this?

A

Pts who have achlorhydria (Lack of stomach acid) due to anaemia, H2 antagonists and PPIs

This increases susceptibility to Shigellosis, cholera, salmonella and C. difficle infections

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9
Q

Give examples of bacteria and viruses resistant to stomach acid

A

Mycobacterium tuberculosis

Enteroviruses:

Hep A, Polio, Coxsackie

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10
Q

List the protective mechanisms of the small intestine

A

Bile

Proteolytic enzymes

Lack of nutrients

Anaerobic environment

Shedding of epithelial cells

Rapid transit (Peristalsis)

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11
Q

What is the normal bacterial load in the small intestine?

A

Normally sterile

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12
Q

What are the main protective mechanisms of the colon

Why are the important?

A

Mechanism:

Mucus layer covering epithelium

Anaerobic environment

Importance:

Faeces are 40% bacteria by weight and so the colon wall must be isolated from this

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13
Q

What are the cells involved in the innate cellular defense of the GI tract?

A

Neutrophils

Macrophages

NK cells

Tissue mast cells

Eosinophils

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14
Q

What is the role of eosinophils in the gut and their clinical importance?

A

Act against worms

Eosinophilia may indicate parasiste infection

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15
Q

What conditions may also produce eosinophilia?

A

Asthma and Hayfever

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16
Q

What is the clinical relevance of mast cells in the GI tract?

A

Gut infections may activate complement, recruiting Mast cells

Mast cells degranulate and release histamine, increasing capillary permeability

This can lead to massive fluid loss

In the case of cholera, up to 1L/hour

60% mortality untreated

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17
Q

What are two clinical signs of cholera?

A

Washerwomans hands:

Severe dehydration

Ricewater stool:

Rapid fluid loss

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18
Q

What is the definition of a ‘portal system’?

Give an example

A

Definition:

Two capillary systems in series

Example:

Hepatic portal system

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19
Q

What are the two capillary systems linked in the hepatic portal system?

A

Villus capillaries along the gut wall

System of capillaries suppliying the hepatic lobules

Blood flow is from villus to lobule via the portal vein and other intermediate veins

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20
Q

List some examples of causes of liver failure

A

Viral Hepatitis

Alcohol

Drugs (Paracetamol, halothane)

Industrial solvents

Mushroom poisoning

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21
Q

Describe the effects of liver failure on the GI tract

A

Infection:

Increased susceptiblity to infection

Toxins, drugs, hormones:

Increased susceptibility

Ammonia:

Ammonia produced by colonic bacteria may not be cleared due to failure of the urea cycle

Hepatic encephalopathy may result

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22
Q

Describe the effects of cirrhosis

A

Hepatic fibrosis:

Leads to reductions in liver function (liver failure)

Also portal hypertension (>20mmHg)

Porto-systemic shunting:

Portal hypertension leads to shunting of blood into systemic circulation (therefore toxins are also shunted)

Can cause:

    • Oesophageal varices*
    • Haemorrhoids*
    • Caput medusae*
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23
Q

Describe fully the symptoms of Porto-systemic shunting in liver cirrhosis

A

Haemorrhoids:

Highly vascular ‘cushions’ in the anal canal become swollen due to increased venous pressure

Oesophageal varices:

Venous dilation in the lower third of the oesophagus due to increased venous pressure

Caput medusae:

Engorged para-umbilical veins visible on the peri- umbilical skin due to increased venous pressure

Ascites:

Portal anstomoses with retroperitoneal veins cused capillary leakage into peritoneum

Splenomegaly:

Congestion due to portal hypertension

Spider naevi:

Small spiderwebs of swollen veins on the skin surface, found in the areas drained by the SVC only

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24
Q

What are the cellular adaptive defenses releavant to the GI tract?

A

B lymphocytes:

Production of antibodies (IgE, IgA) for defense against extracellular microbes

T Lymphocytes:

Defense against intracellular organisms

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25
Q

Describe the distribution of lymphatic tissue in the GI tract

A

GALT:

Gut associated lymphoid tissue is diffusely distributed throughout the gut and surrounding tissues (E.g. Mesentery)

Also nodular in 3 locations:

    • Tonsils*
    • Peyer’s Patches*
    • Appendix*
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26
Q

Describe the drainage of the tonsils and the clincial relevance of this

A

Drainage:

Drain into cervical lymph nodes in the neck

Clincal:

Sore throats and cervical lymphadenopathy are a common presentation due to bacteria/viruses entering the body through the mouth

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27
Q

What are Peyer’s patches?

Major clincal relevance?

A

Peyer’s Patches:

Nodular GALT in the mucosa of the terminal ileum

Clinical:

Infection and subsequent inflammation of Peyer’s patches in typhoid fever can cause perforation of the terminal ileum, which can be rapidly fatal

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28
Q

What is mesenteric adenitis?

A

Inflammation of lymph nodes along the mesentery

Common cause of right iliac fossa pain in children, can be mistaken for appendicitis

Often caused by adenovirus/coxsackie virus

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29
Q

What is Appendicitis?

A

Appendix obstruction leads to fluid stasis within the lumen

Infection results and the appendix becomes inflammed

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30
Q

What are the common causes of appendicitis?

A

Obstruction:

Faecoliths

Lymphoid hyperplasia

Lymphoid infection/inflammation

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31
Q

What are some of the complications of appendicitis?

A

Strangulation leading to ischaemia and necrosis

Rupture of the appendix can lead to peritonitis and septicaemia

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32
Q

Why is hepatic/intestinal ischaemia so harmful?

A

GI tract relies on intact blood supply for successful defense

Ischaemia commonly leads to overwhelming sepsis and death within hours

33
Q

What are the functions of the liver?

A

Bile production

Carbohydrate, protein and lipid metabolism

Protein synthesis

Vit D snythesis

Detoxification

Vitamin and mineral storage

Phagocytosis

34
Q

What are the common liver function tests?

Wat are they testing for?

A

Tests for hepatocellular damage:

Serum ALT/AST (aminotransferases)

Serum g-GT (gamma-glutamyl transpeptidase)

Tests for cholestasis (bile duct obstruction):

Serum Bilirubin

Serum Alkaline phosphatase

Tests for Synthetic functions:

Serum albumin

Prothrombin time (clotting)

35
Q

Describe the presentation and classification of jaundice

A

Yellow pigmentation in eyes and skin

Classified as:

    • Prehepatic (Haemolytic)*
    • Hepatic (parenchymal)*
    • Post-hepatic (Cholestatic)*
36
Q

What is the cause of prehepatic jaundice?

How is this determined to be occuring clinically?

A

Cause:

Excessive haemolysis

Liver unable to cope with excess bilirubin

Testing:

Uconjugated hyperbilirubinaemia

Anaemia

37
Q

What are some of the causes of prehepatic jaundice?

A

Inherited:

Gilbert’s syndrome

Acquired:

Autoimmune

Acquired membrane defects

Drugs

Burns

38
Q

What is hepatocellular junadice and how is jaundice determined to be hepatocellular in nature?

A

Cause:

Deranged hepatocyte function

Element of cholestasis

Testing:

Mixed conjugated and unconjugated hyperbilirubinaemia

Increased liver enzymes

Abnormal clotting (increased prothrombin time)

39
Q

What are some causes of hepatocellular jaundice?

A

Congenital:

Gilbert’s syndrome

Inflammation:

Viruses (Hep A, B, C, E + EBV)

Autoimmune hepatitis

Alcohol

Drugs:

E.g. Paracetamol

Cirrhosis:

Alcohol

Chronic hepatitis

Malignancy:

Hepatocellular carcinoma

Metastases

40
Q

What is post-hepatic jaundice and how might jaundice be determine to be post hepatic in nature?

A

Causes:

Obstruction of the billary system

Intra/Extrahepatic

Passage of conjugated bilirubin therefore blocked

Tests:

Conjugated hyperbilirubinaemia

Bilirubin in urine

Increased serum liver enzymes

41
Q

What are the common causes of post-hepatic jaundice?

A

Intrahepatic:

Heapatitis

Drufs

Cirrhosis

Extrahepatic:

Gallstones

Billary stricture

Carcinoma (E.g. in head of pancreas or Ampulla of vater)

Pancreatitis

42
Q

What is Courvoisier’s law?

Explain the rationale

A

In the presence of a non-tender, palpable gallbladder, painless juandice is unlikelt to be caused by gallstones

Explanation:

Gallstones formed over a long period of time result in a shrunken, fibrotic gallbladder (not palpable)

Palpable enlarged gallbladder normally caused by more rapid billary obstruction (E.g. Malignancy)

Acute cholecystisitis often causes a tender and distended gallbladder (Distended with mucocele or empyema

43
Q

What are the acute/chronic effects of hepatiti?

A

Acute:

AST/ALT release from hepatocytes

Jaundice

Chronic:

Snythetic failure

Reduced albumin and clotting factors

Increased prothrombin time

44
Q

List some causes of hepatitis

A

Viral:

Hep A, B, C

EBV

CMV

Autoiimune

Drugs:

Methyldopa

Isoniazid (TB treatment)

Hereditary:

A1-antitrypsin deficiency

Wilson’s disease

Alcohol

45
Q

Describe the pathological prgoression in aloholic liver disease

What are some complications?

A

Progression:

Steatosis (fatty change)

Aloholic hepatitis

Cirrhosis

Complications:

Hepatocaellular carcinoma

Liver failure

Wernicke-Korsakoff syndrome

Encephalopathy

Dementia

Epilepsy

46
Q

Briefly describe liver cirrhosis

A

Liver cell necrosis followed by nodular regeneration and fibrosis

Results in increased resistance to blood flow and deranged liver function

47
Q

What are the common causes of cirrhosis?

A

ALCOHOL

Hep B or C

Autoimmune hepatitis

Wilson’s disease

Haemochromotosis

48
Q

What are the clinical features of cirrhosis?

A

Liver:

Jaundice

Anaemia

Bruising

Palmar erythrema

Dupuytren’s contracture (fixed flexion deformity of the fingers)

Portal hypertension

Spontaneous bacteria peritonitis

49
Q

What are the haematological signs of cirrhosis?

A

Raised ALT/AST

Raised Alkaline phosphatase

Raised bilirubin

Reduced Albumin

Increased prothrombin time

Decreased Na+

50
Q

What are the management methods for cirrhosis?

A

Stop drinking

Treatment of complications

Transplantation

51
Q

Describe the cause, clinical signs and treatment of primary billary cirrhosis

A

Cause:

Chronic destruction of bile ducts

Clincal signs:

Jaundice

Pruritis

Xanthelasma

Hepatosplenomegaly

Treatment:

Supportive treatment and transplantation

52
Q

What is hereditary haemochromotosis?

What diseases may occur as a result?

A

Autosomal dominant disease:

Abnormal iron transport and deposition

Can cause:

Cardiomyopathy

Diabetes

Hypergonadism

Hepatitis/cirrhosis

53
Q

What is Wilson’s disease?

What can result?

How is it treated?

A

Autosomal recessive:

Disordered copper transport and deposition

Can cause:

Heaptitis/Cirrhosis

Tremore, dementia

Kidney tubular degneration

Treatment:

Penecillamine (chelation therapy)

54
Q

What is A1-antitrypsin deficiency?

What can it cause?

How is it treated?

A

Autosomal recessive:

Deficient A1-antitrypsin

Can cause:

Liver cirrhosis

Emphysema

Treatment:

Transplant

55
Q

What are the causes of portal hypertension?

A

Obstruction of portal vein:

Congenital

Thrombosis

Extrinsic compression

Obstruction of flow within the liver:

Cirrhosis

Hepatoportal sclerosis

Schistosomiasis

56
Q

Where does the hepatic portal system anastomose with the systemic circulation?

Link this to the symptoms of portal hypertension

A

Oesophageal varices:

Oesophageal branch of left gastric vein (portal) anastomose with the Oesophageal tributaries of azygous system (systemic)

Haemorrhoids:

Superior rectal branch of IMV (portal) anastomoses with the inferior rectal veins (systemic)

Caput medusae:

Portal veins in liver anastomose with ant. abd. wall veins

Ascites:

Portal tributaries of mesentery and retroperitoneal veins

57
Q

What can be the complications of Oesophageal varices?

A

Rupture of the swollen vessels or ulceration

Haemorrhage can potentially be significant

58
Q

What is fulminant hepatic failure?

A

Acute/Severe onset decompensation of liver function defined as:

Onset of hepatic encephalopathy within 2 months of diagnosis of liver disease which may be linked to brain oedema

Decompensation is due to increased metabolic demand

59
Q

What are the causes of fulminant hepatic failure?

A

Hep A, D, E

Drugs:

  • Paracetamol*
  • Isoniazid*

Wilson’s disease

Pregnancy

Alcohol

60
Q

What are the clinical featuers of fulminant hepatic encephalopathy?

How is it managed?

A

Symptoms:

Jaundice

Encephalopathy

Loss of consiousness

Hypoglycaemia

Decreased K+/Ca2+

Haemorrhage

Management:

Supportive therapy and transplant

61
Q

What is hepatic encephalopathy and what might precipitate it?

A

HE:

Reversible neuropsychiatric deficit

Inability to remove toxins from blood (Ammonia)

Precipitating factors:

Sepsis/Infection

Constipation

Diuretics

GI bleed

Alcohol withdrawal

62
Q

What are the clinical features of hepatic encephalopathy?

A

Flapping tremor

Loss of conciousness

Personality changes

Intellectual deterioration (Constructional apraxia, slow, slurred speech)

63
Q

Give examples of benign and malignant liver tumours

A

Benign:

Haemangioma

Focal nodular hyperplasia

Liver cysts

Polycystic liver disease

Malignant:

Primary hepatocellular carcinoma

Secondary metastases (20x more common):

    • Colorectal (50%)*
    • Neuroendocrine*
    • Pancreas*
    • Lung*
64
Q

What are the pathological processes which can affect the billary tree?

A

Obstruction

Infection

Inflammation

Neoplasia

65
Q

How common are gallstones and what are the risk factors?

A

10 - 20% of population

Risk factors:

Female

Increasing age

Obesity

Diet

Developed country

Ilial disease/resection

Haemolytic disease

66
Q

What are the different types of stones that cause cholelithiasis?

A

Mixed:

80%

Cholesterol with Ca2+ and bile pigment

Pure cholesterol:

10%

Usually solitary

Pigment stones:

10%

Calcium bilirubinate

Multiple small stones

67
Q

What are the common clincal consequences of gallstone formation?

A

Biliary colic:

Impaction of stone

Gallbladder contraction (in attempt to clear)

Intermittent pain

Cholecystitis:

Stones lead to oedema in the mucosa and ulceration leading to fibropurulent exudate into the gallbladder

Pain, SIRS, Pyrexia, Sepsis

68
Q

What are the possible complications of cholelithiasis?

A

Mucocele:

Impaction of stone without infection but with mucus secretion leading to gallbladder distention

Empyema:

As in mucocele but with infection

Purulent exudate into gallbladder

Obstructive jaundice

Acute pancreatitis

Gallbladder perforation

Biliary-enteric fistula:

Fistula forms between gallbladder and ileum, large stones can obstruct ileum

69
Q

What are the functions of the pancreas?

A

Endocrine:

Insulin, glucagon, somatosatin secretion

Exocrine:

Fluid (HCO3-)

Enzymes (proteolytic, amylase, lipolytic)

70
Q

What is pancreatitis?

What are the acute and chronic effects?

A

Pancreatitis:

Inflammatory process caused by the effects of enzymes released from pancreatic acini

Acute effects:

Oedema

Haemorrhage

Necrosis

Chronic effects:

Fibrosis

Calcification

71
Q

What are the causes of acute pancreatitis?

A

GET SMASHED:

Gallstones

Ethanol

Trauma

Steroids

Mumps

Autoimmune

Scorpion bite

Hyperlipidaemia

ERCP/Iatrogenic

Drugs

72
Q

Describe the pathogenesis of acute pancreatitis

A

Duct obstruction:

Juice and bile reflex into pancreas

Acinar damage:

From reflux or drugs

Protease:

Tssue destruction

Lipase:

Fat necrosis

Elastase:

Blood vessel destruction

73
Q

What are the biochemical markers of pancreatitis?

A

Markers:

Serum amylase

Decreased Ca2+

Hyperglycaemia

Increased ALP/Bilirubin

74
Q

What are the symptoms of acute pancreatitis?

A

Severe pain

Vomiting

Dehydration

Shock/SIRS

Ileus (Paralytic)

75
Q

How is pancreatitis treated?

A

Supportive treatments only

76
Q

Describe chronic pancreatitis

Include causes and symptoms

A

Chronic inflammation

Parenchymal destruction, fibrosis, loss of acini, duct stenosis

Causes:

Chronic alcoholism

Cystic fibrosis

Biliary disease

Symptoms:

Pain

Malabsorption (Steatorrhoea, weight loss)

Diabetes mellitus

Jaundice

77
Q

What is the most common form of pancreatic cancer and what are the risk factors?

A

90% ductal carcinoma

Risk factors:

Smoking

Familial pancreatitis

Benzidine

Beta napthylamine

78
Q

What are the clinical features of pancreatic carcinoma?

A

Initially symptomless

Obstructive jundice

Pain

Vomiting

Carcinomatosis (dissemination/spread of cancer

Malabsorption

Diabetes

79
Q

Describe the prognosis for pancreatic cancer

A

5th cause of cancer death in UK

Resective surgery:

Best treatment, but only 5-15% suitable

5 yr survival is 15-35%

Overall:

1 yr survival is 12%

ESA 3 (54 decks)

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