General Surgery - Upper GI Flashcards

1
Q

Causes of ACUTE upper GI bleeding?

A
  • Peptic ulcer (duodenal and gastric).
  • Mallory Weiss tear.
  • Chronic liver disease (oesophageal varices).
  • Gastric carcinoma.
  • Following PCI (anti-thrombotics e.g.heparin, fondaparinux) in those who are also on anti-platelets (e.g. clopidogrel, ticagrelor).
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2
Q

Signs of acute upper GI bleeding?

A
  • Haematemesis.
  • Malaena.
  • Shock (tachycardia, pallor, cold peripheries, low BP).
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3
Q

Causes of vomiting?

A
  • Any GI disease.
  • Infection (flu, norovirus, pertussis, UTI).
  • CNS disease (raised ICP, vestibular disturbance e.g. motion sickness, migraine).
  • Metabolic (uraemia, hypercalcaemia).
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4
Q

Conditions associated with early morning nausea and vomiting?

A
  • Pregnancy.
  • Alcohol dependence.
  • Metabolic disorders e.g. uraemia.
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5
Q

Vomiting is regulated by?

A
  • Central neural control centres located in the lateral reticular formation of the medulla.
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6
Q

Central neural control centres which regulate vomiting are stimulated by?

A
  • Chemoreceptor trigger zones in the floor of the fourth ventricle.
  • Vagal afferents from gut.
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7
Q

What can directly stimulate central trigger zones responsible for stimulating the central neural control centres which regulate vomiting?

A
  • Luminal toxins.
  • Inflammation.
  • Mechanical obstruction.
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8
Q

Proctalgia fugax is?

A

Severe, deep rectal pain of sudden onset but short duration.

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9
Q

Causes of mouth ulcers?

A
  • Idiopathic aphthous ulceration (most common),
  • GI disease (e.g. IBD, coeliac).
    Infection (e.g. HSV, HIV, Coxsackie, candidiasis, syphilis, TB).
  • Systemic disease (e.g. reactive arthritis, Behcet syndrome, SLE).
  • Trauma (e.g. dentures).
  • Neoplasia (e.g. SCC).
  • Drugs (e.g. erythema multiforme major, toxic epidermal necrolysis, chemotherapy, antimalarials).
  • Skin disease (e.g. pemphigoid, pemphigus, lichen planus).
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10
Q

Causes of dry mouth?

A
  • Sjogren’s.
  • Drugs (e.g. anti-muscarinics, anti-parkinsonian, lithium, tricyclics, MAOIs).
  • Radiotherapy.
  • Psychogenic.
  • Dehydration.
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11
Q

Causes of sialadenitis (salivary gland infection)?

A
  • Viral e.g. mumps.

- Bacterial e.g. staphylococcus, streptococcus.

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12
Q

What kind of neoplasms affect the salivary glands?

A
  • Pleomorphic adenoma.

(15% become malignant and can cause CN VII lower motor neurone signs).

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13
Q

HIV is associated with oral manifestations of which diseases?

A
  • Candidiasis (with erythema &/or white exudates).
  • Oral hairy leucoplakia.
  • Kaposi’s sarcoma.
  • Non-Hodgkin’s lymphoma.
  • Necrotising ulcerative gingivitis.
  • Necrotising ulcerative periodontitis.
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14
Q

With regards to oesophageal mucosal defence mechanisms, the mucus and unstirred water layer trap what & why?

A
  • Bicarbonate.

- Weak buffering mechanism.

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15
Q

What is the role of epithelium in oesophageal mucosal defence?

A
  • Limit diffusion of H+ into cells.

(Apical cell membranes and junctional complexes between cells limit H+ diffusion into cells). In oesophagitis, junctional complexes are damaged > increased H+ diffusion > cellular damage).

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16
Q

When will stitches normally be removed following a laparoscopic cholecystectomy and by whom?

A

If required, 5-7 days post op by patient’s practice nurse.

17
Q

When can a patient return to work following a laparoscopic cholecystectomy?

A

Some time off is required - 2 weeks sick note will be provided upon discharge. Further time off can be requested from GP.

18
Q

When can a patient drive following a laparoscopic cholecystectomy?

A

Not until after at least 24 hours and must be able to safely perform an emergency stop.

19
Q

When should a patient seek medical attention following discharge after a laparoscopic cholecystectomy?

A
  • Severe pain uncontrolled by medication.
  • Pain complicated by symptoms such as vomiting.
  • Pain from a site other than operation sites, ribs or shoulders.
  • Large amounts of blood stained fluid discharge from wounds.
  • Fever or chills.
20
Q

Gastric acid is stimulated by?

A
  • Acetylcholine.
  • Gastrin.
  • Histamine.
21
Q

Gastric acid is inhibited by?

A
  • Somatostatin.
  • Secretin.
  • Cholecystokinin.
22
Q

Gastric acid is composed of?

A
  • Hydrochloric acid.
  • Potassium chloride.
  • Sodium chloride.
23
Q

Describe the cephalic phase of gastric acid secretion.

A

Gastric acid produced before food enters the stomach - triggered by sight, smell, thought, tasted of food acting via vagus nerve.

24
Q

Describe the gastric phase of gastric acid secretion.

A

Initiated by food in stomach (particularly protein-rich food). Due to G cell stimulation > gastrin release.

25
Q

Describe the intestinal phase of gastric acid secretion.

A

Luminal distension + presence of amino acids + food in duodenum > stimulates acid production.

26
Q

Describe Zollinger-Ellison syndrome.

A

Gastrinoma(s) form in pancreas or dudodenum. These are neuroendocrine tumours which secrete gastrin.

27
Q

Signs of Zollinger-Ellison syndrome.

A
  • Excess gastrin production can lead to increased gastric acid production.
  • Multiple, severe gastric ulcers.
28
Q

Very elevated ALP in the presence of jaundice indicates?

A

Extrahepatic obstruction - typically due to common bile duct stone or carcinoma of the head of the pancreas.

29
Q

High levels of AST suggest?

A

Intra-hepatic disease.

- AST is a marker of liver cell damage.

30
Q

Common causes of intra-hepatic cholestasis?

A

Drugs, alcohol, infective hepatitis, liver lesions.

31
Q

High AST + jaundice indicates?

A

Intrahepatic cholestasis.