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ESA 3 Callum's Cards > GI S7 (Done) > Flashcards

GI S7 (Done) Flashcards

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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
Describe the distribution of lymphatic tissue in the GI tract
**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*
26
Describe the drainage of the tonsils and the clincial relevance of this
**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
27
What are Peyer's patches? Major clincal relevance?
**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
28
What is mesenteric adenitis?
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
29
What is Appendicitis?
Appendix obstruction leads to fluid stasis within the lumen Infection results and the appendix becomes inflammed
30
What are the common causes of appendicitis?
**Obstruction:** Faecoliths Lymphoid hyperplasia Lymphoid infection/inflammation
31
What are some of the complications of appendicitis?
Strangulation leading to ischaemia and necrosis Rupture of the appendix can lead to peritonitis and septicaemia
32
Why is hepatic/intestinal ischaemia so harmful?
GI tract relies on intact blood supply for successful defense Ischaemia commonly leads to overwhelming sepsis and death within hours
33
What are the functions of the liver?
Bile production Carbohydrate, protein and lipid metabolism Protein synthesis Vit D snythesis Detoxification Vitamin and mineral storage Phagocytosis
34
What are the common liver function tests? Wat are they testing for?
**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
Describe the presentation and classification of jaundice
Yellow pigmentation in eyes and skin Classified as: * - Prehepatic (Haemolytic)* * - Hepatic (parenchymal)* * - Post-hepatic (Cholestatic)*
36
What is the cause of prehepatic jaundice? How is this determined to be occuring clinically?
**Cause:** Excessive haemolysis Liver unable to cope with excess bilirubin **Testing:** Uconjugated hyperbilirubinaemia Anaemia
37
What are some of the causes of prehepatic jaundice?
**Inherited:** Gilbert's syndrome **Acquired:** Autoimmune Acquired membrane defects Drugs Burns
38
What is hepatocellular junadice and how is jaundice determined to be hepatocellular in nature?
**Cause:** Deranged hepatocyte function Element of cholestasis **Testing:** Mixed conjugated and unconjugated hyperbilirubinaemia Increased liver enzymes Abnormal clotting (increased prothrombin time)
39
What are some causes of hepatocellular jaundice?
**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
What is post-hepatic jaundice and how might jaundice be determine to be post hepatic in nature?
**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
What are the common causes of post-hepatic jaundice?
**Intrahepatic:** Heapatitis Drufs Cirrhosis **Extrahepatic:** Gallstones Billary stricture Carcinoma (E.g. in head of pancreas or Ampulla of vater) Pancreatitis
42
What is Courvoisier's law? Explain the rationale
**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
What are the acute/chronic effects of hepatiti?
**Acute:** AST/ALT release from hepatocytes Jaundice **Chronic:** Snythetic failure Reduced albumin and clotting factors Increased prothrombin time
44
List some causes of hepatitis
**Viral:** Hep A, B, C EBV CMV **Autoiimune** **Drugs:** Methyldopa Isoniazid (TB treatment) **Hereditary:** A1-antitrypsin deficiency Wilson's disease **Alcohol**
45
Describe the pathological prgoression in aloholic liver disease What are some complications?
**Progression:** Steatosis (fatty change) Aloholic hepatitis Cirrhosis **Complications:** Hepatocaellular carcinoma Liver failure Wernicke-Korsakoff syndrome Encephalopathy Dementia Epilepsy
46
Briefly describe liver cirrhosis
Liver cell necrosis followed by nodular regeneration and fibrosis Results in increased resistance to blood flow and deranged liver function
47
What are the common causes of cirrhosis?
ALCOHOL Hep B or C Autoimmune hepatitis Wilson's disease Haemochromotosis
48
What are the clinical features of cirrhosis?
**Liver:** Jaundice Anaemia Bruising Palmar erythrema Dupuytren's contracture (fixed flexion deformity of the fingers) **Portal hypertension** **Spontaneous bacteria peritonitis**
49
What are the haematological signs of cirrhosis?
Raised ALT/AST Raised Alkaline phosphatase Raised bilirubin Reduced Albumin Increased prothrombin time Decreased Na+
50
What are the management methods for cirrhosis?
Stop drinking Treatment of complications Transplantation
51
Describe the cause, clinical signs and treatment of primary billary cirrhosis
**Cause:** Chronic destruction of bile ducts **Clincal signs:** Jaundice Pruritis Xanthelasma Hepatosplenomegaly **Treatment:** Supportive treatment and transplantation
52
What is hereditary haemochromotosis? What diseases may occur as a result?
**Autosomal dominant disease:** Abnormal iron transport and deposition **Can cause:** Cardiomyopathy Diabetes Hypergonadism Hepatitis/cirrhosis
53
What is Wilson's disease? What can result? How is it treated?
**Autosomal recessive:** Disordered copper transport and deposition **Can cause:** Heaptitis/Cirrhosis Tremore, dementia Kidney tubular degneration **Treatment:** Penecillamine (chelation therapy)
54
What is A1-antitrypsin deficiency? What can it cause? How is it treated?
**Autosomal recessive:** Deficient A1-antitrypsin **Can cause:** Liver cirrhosis Emphysema **Treatment:** Transplant
55
What are the causes of portal hypertension?
**Obstruction of portal vein:** Congenital Thrombosis Extrinsic compression **Obstruction of flow within the liver:** Cirrhosis Hepatoportal sclerosis Schistosomiasis
56
Where does the hepatic portal system anastomose with the systemic circulation? Link this to the symptoms of portal hypertension
**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
What can be the complications of Oesophageal varices?
Rupture of the swollen vessels or ulceration Haemorrhage can potentially be significant
58
What is fulminant hepatic failure?
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
What are the causes of fulminant hepatic failure?
Hep A, D, E Drugs: * Paracetamol* * Isoniazid* Wilson's disease Pregnancy Alcohol
60
What are the clinical featuers of fulminant hepatic encephalopathy? How is it managed?
**Symptoms:** Jaundice Encephalopathy Loss of consiousness Hypoglycaemia Decreased K+/Ca2+ Haemorrhage **Management:** Supportive therapy and transplant
61
What is hepatic encephalopathy and what might precipitate it?
**HE:** Reversible neuropsychiatric deficit Inability to remove toxins from blood (Ammonia) **Precipitating factors:** Sepsis/Infection Constipation Diuretics GI bleed Alcohol withdrawal
62
What are the clinical features of hepatic encephalopathy?
Flapping tremor Loss of conciousness Personality changes Intellectual deterioration (Constructional apraxia, slow, slurred speech)
63
Give examples of benign and malignant liver tumours
**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
What are the pathological processes which can affect the billary tree?
Obstruction Infection Inflammation Neoplasia
65
How common are gallstones and what are the risk factors?
**10 - 20% of population** **Risk factors:** Female Increasing age Obesity Diet Developed country Ilial disease/resection Haemolytic disease
66
What are the different types of stones that cause cholelithiasis?
**Mixed:** 80% Cholesterol with Ca2+ and bile pigment **Pure cholesterol:** 10% Usually solitary **Pigment stones:** 10% Calcium bilirubinate Multiple small stones
67
What are the common clincal consequences of gallstone formation?
**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
What are the possible complications of cholelithiasis?
**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
What are the functions of the pancreas?
**Endocrine:** Insulin, glucagon, somatosatin secretion **Exocrine:** Fluid (HCO3-) Enzymes (proteolytic, amylase, lipolytic)
70
What is pancreatitis? What are the acute and chronic effects?
**Pancreatitis:** Inflammatory process caused by the effects of enzymes released from pancreatic acini **Acute effects:** Oedema Haemorrhage Necrosis **Chronic effects:** Fibrosis Calcification
71
What are the causes of acute pancreatitis?
**GET SMASHED:** **G**allstones **E**thanol **T**rauma **S**teroids **M**umps **A**utoimmune **S**corpion bite **H**yperlipidaemia **E**RCP/Iatrogenic **D**rugs
72
Describe the pathogenesis of acute pancreatitis
**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
What are the biochemical markers of pancreatitis?
**Markers:** Serum amylase Decreased Ca2+ Hyperglycaemia Increased ALP/Bilirubin
74
What are the symptoms of acute pancreatitis?
Severe pain Vomiting Dehydration Shock/SIRS Ileus (Paralytic)
75
How is pancreatitis treated?
Supportive treatments only
76
Describe chronic pancreatitis Include causes and symptoms
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
What is the most common form of pancreatic cancer and what are the risk factors?
90% ductal carcinoma **Risk factors:** Smoking Familial pancreatitis Benzidine Beta napthylamine
78
What are the clinical features of pancreatic carcinoma?
Initially symptomless Obstructive jundice Pain Vomiting Carcinomatosis (dissemination/spread of cancer Malabsorption Diabetes
79
Describe the prognosis for pancreatic cancer
**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 Callum's Cards (55 decks)

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