Disorders aorta, oesophagus, stomach, small intestine and liver, gall bladder and pancreas Flashcards

1
Q
Abdominal Aortic Aneurysm
aeitiology?
clinical features?
complications?
management?
A

Aetiology-any factor that disrupts the collagen and elastin fibres in arterial wall predisposes it to dilation e.g. HTN, atherosclerosis

Features: pressure on surrounding structures e.g. dysphagia, dyspnoea
rupture-acute abdominal pain, features of hypovolaemic shock

Complications: dilation and rupture, stagnant blood flow can undergo thrombosis, thromboembolism can obstruct peripheral flow

Management: surgery/prosthtic graft for rupture, anti-hypertensive drugs and smoking cessation for early diagnosis

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2
Q

Define Barrett’s Mucosa
what condition can lead to Barrett’s Mucosa?
what implication does Barrett’s Mucosa have for oesophageal pathology?

A

A change in the lining of the lower Oesophagus from stratified squamous to simple columnar epithelium.

Hiatal Hernia may cause BM

BM can cause metaplasia, which is a pre-malignant process

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3
Q

state the clinical triad for oesophageal cancer

A

dysphagia, odynophagia, weight loss

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4
Q

list 2 types of hiatal hernia

A

sliding

rolling

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5
Q

how can the risk factors for GORD be classified?

A
  1. decreased tone of Lower Oesophageal Sphincter
  2. impaired mucosal defences
  3. increased IAP
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6
Q

3 common presentations of GORD

3 medications for GORD and mechanism of action

A

heartburn, dyspepsia, dysphagia, odynophagia

histamine H2 receptor antagonists-inhibit action of Histamine at H2-receptors on gastric parietal cell

  1. Proton Pump Inhibitor- inhibits H+ K+ ATPase pump
  2. Antacids-neutralises HCL in oesophageal lumen
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7
Q

common sites for peptic ulcers

A

Duodenal ulcers are more common than gastric ulcers.
duodenal ulcers-D1
gastric ulcers- lesser curvature

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8
Q

Define Coeliac Disease
Which region of the bowel is most affected by Coeliac Disease?
Summarise pathological changes that occur in Coeliac Disease

A

Genetically determined, abnormal hypersensitivity reaction to gluten or it’s peptide derivative gliadin

proximal bowel, especially the duodenal jejunal flexure

type 4 (cell mediated) hypersensitivity reaction
immune cells infiltrate lamina propria
T Lymphocytes release inflammatory cytokines
plasma cells produce IgA antibodies
damage to mucosa and atrophy of villi
impaired intracellular metabolism

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9
Q

Describe the role H. Pylori plays in peptic ulceration by listing its 4 pathogenic properties

A
  1. produce urease (allows survival in low pH)
  2. helical structure and flagella (burrowing capacity)
  3. release bacterial toxins and Reactive Oxidative Species (damages mucosa)
  4. recruitment of inflammatory cytokines e.g. neutrophils, mast cells and macrophages (further damage)
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10
Q

list the 4 mechanisms by which antibiotics work

A
  1. inhibit cell wall synthesis
  2. disrupts cell wall membrane
  3. inhibits protein synthesis
  4. interference of metabolic processes
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11
Q

what are the preferred antibiotics for H. Pylori eradication?

A

Clarithromycin (inhibits protein synthesis)
Amoxycilin (inhibits cell wall synthesis)
Metronidazole (prevents DNA replication)

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12
Q

explain how prolonged use of NSAIDS may predispose a patient to peptic ulceration

A

reduces prostaglandin content of mucosal cells, therefore reduces mucous secretion
aspirin can directly damage cell membranes

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13
Q

Define jaundice and identify 3 types of Jaundice

A

Jaundice is the yellow discolouration of the skin, sclerae and mucous membranes due to excess biliruben; a sign of liver disease.

  1. Haemolytic jaundice- excessive RBC destruction
  2. Hepatic Jaundice- imparied hepatocyte function (e.g. neonatal)
  3. Cholestatic Jaundice- obstruction of intrahepatic or extrahepatic bile ducts
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14
Q

how does chronic alcohol abuse cause liver damage?

list the stages of alcoholic liver disease

A

in the liver, alcohol causes the induction of oxidases, which damage hepatocytes with chronic exposure

stage 1 fatty liver
stage 2 alcoholic hepatitis
stage 3 cirrhosis

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15
Q

other than alcohol, what can cause cirrhosis?

A

non-alcoholic liver disease (risk factors are obesity, hyperlipidaemia, insulin resistance)
viral & autoimmune hepatitis
cholestasis
metabolic disorders e.g. haemochromatosis

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16
Q

risk factors associated with gall stones

A

women
over 40 years old
diabetes

17
Q

what is the most common type of gall stone in Western cultures

A

cholesterol variety

18
Q

list complications of gall stones

A
acute cholecystitis
chronic cholecystitis
mucocele development
infection
increased risk for carcinoma
choledocolithiasis
acute pancreatitis
19
Q

which hepatic viruses are vaccine preventable?

how are the three hepatic viruses transmitted?

A

HAV and HBV are vaccine preventable
HAV-faecal-oral route
HBV/HCV-parenteral, perinatal and sexual

20
Q

list the 4 stages of acute hepatitis

A
  1. preclinical
  2. prodromal/pre-icteric
  3. icteric *jaundice
  4. convalescent
21
Q

list 3 potential complications for both portal HTN and hepatocellular failure

A

PORTAL HTN:
ascites
splenomegaly (passive congestion)
varicose veins

HEPATOCELLULAR FAILURE:
hepatic encephalopathy (fail remove neurotoxic nitrogenous wastes)
coagulation defects (no coagulation factors)
endocrine changes (fail deactivate hormones)
peripheral odema (no albumin)
22
Q

what is the most common form of primary liver tumour?

A

hepatocellular carcinoma; arises from liver epithelial cells

23
Q

list 4 complications of gall stones

A
  1. acute cholecystitis (impacts cystic duct)
  2. chronic cholecystitis (GB wall fibrotic, shrunken)
  3. choledocolithiasis (impact bile duct)
  4. acute pancreatitis (hepatopancreatic ampulla afected)
24
Q

which gene is responsible for cystic fibrosis?

list 4 types of features associated with cystic fibrosis

A

CTFR gene which is found on chromosome 7 and codes for a membrane-bound chloride channel

  1. pulmonary features
  2. pancreatic features
  3. biliary features
  4. reproductive features