pt19 Flashcards

(50 cards)

1
Q

What prognostic factor most influences prostate cancer outcome?

A

Stage at diagnosis

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2
Q

How many layers does the GI tract wall have, and what are they?

A

Four layers—mucosa, submucosa, muscularis (inner circular & outer longitudinal), and serosa

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3
Q

What epithelium lines the oesophagus?

A

Non-keratinised stratified squamous epithelium

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4
Q

What is the “functional” lower oesophageal sphincter (LES)?

A

An acute musculomucosal angle plus mucosal folds at the gastro-oesophageal junction that prevent reflux

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5
Q

By what mechanism is a food bolus propelled down the oesophagus?

A

Coordinated peristalsis under control of the oesophageal (enteric) plexus

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6
Q

What is dysphagia and what are its main causes?

A

Difficulty swallowing; caused by obstructive rings/strictures (scar tissue), carcinoma (late stage), stroke, or neurological disease

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7
Q

Define oesophagitis and list its key causes.

A

Inflammation of oesophageal mucosa; from GORD (reflux HCl), CNS depressants, pregnancy, alcohol relaxing LES

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8
Q

What histological changes occur in acute reflux oesophagitis?

A

Neutrophil infiltration into squamous epithelium and mucosal hyperaemia

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9
Q

What is Barrett’s oesophagus and why is it important?

A

Replacement of squamous mucosa by metaplastic columnar epithelium in chronic GORD (10% cases), a precursor to carcinoma

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10
Q

How is oesophageal inflammation visualized endoscopically?

A

Gastroscopy shows erythematous, friable mucosal patches at the LES

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11
Q

What are the three main secretagogues for gastric acid?

A

Gastrin (endocrine), histamine (paracrine), and acetylcholine (neural)

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12
Q

What volume changes can the stomach undergo?

A

From an empty ~75 mL to a post-prandial capacity of ~2 L

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13
Q

Name the protective factors that guard the gastric mucosa.

A

Mucus layer, bicarbonate secretion, rich blood flow

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14
Q

Define gastritis and differentiate acute vs. chronic.

A

Gastric mucosal inflammation; acute shows neutrophils, chronic shows lymphocytes, atrophy, metaplasia

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15
Q

List the four principal aetiologies of gastritis.

A

NSAIDs (↓ mucus/HCO₃⁻), H. pylori infection, alcohol/tobacco (↑ acid, ↓ blood flow), autoimmune parietal-cell loss

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16
Q

How is H. pylori gastritis diagnosed?

A

Urea-breath test, stool antigen, or biopsy with rapid urease assay

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17
Q

What complications arise from untreated gastritis?

A

Mucosal erosion → ulceration/perforation (peritonitis), bleeding, strictures, cancer risk

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18
Q

Outline first-line pharmacological treatments for gastritis.

A

Antacids (Al/Mg hydroxide), H₂-blockers, proton-pump inhibitors; add antibiotics for H. pylori

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19
Q

What endoscopic finding confirms gastric perforation?

A

Visible hole in gastric wall with free air/fluid on CT or serosal inspection

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20
Q

What are the three main categories of malabsorption syndromes in the small intestine?

A

Defective intraluminal digestion, mucosal (absorptive) defects, and disorders reducing small-intestinal surface area

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21
Q

Give three causes of defective intraluminal digestion.

A

Pancreatic insufficiency (e.g., pancreatitis, cystic fibrosis), biliary insufficiency (no bile for fat emulsification), Small Intestinal Bacterial Overgrowth (SIBO)

22
Q

What is Small Intestinal Bacterial Overgrowth (SIBO)?

A

Excessive colonic-type bacteria in the small intestine due to impaired peristalsis, loss of gastric acidity, ileocaecal valve failure, or immunodeficiency

23
Q

Name four causes of mechanical small-intestinal obstruction.

A

Herniation (gut wall defect), surgical adhesions (post-peritonitis scars), intussusception (telescoping), volvulus (twisting from malrotation)

24
Q

Which hernia type commonly causes small-bowel obstruction?

A

Loop of intestine protrudes through abdominal wall weakness, strangulates, and blocks lumen & blood supply

25
How do surgical adhesions lead to obstruction?
Fibrous bridges form after surgery or peritonitis, strangling bowel segments and blocking passage
26
What is intussusception and its effect?
A proximal segment of bowel telescopes into a distal one during peristalsis, causing lumen blockage
27
What is volvulus and when does it occur?
A congenital malrotation causing bowel to twist on its mesentery, leading to obstruction and ischaemia
28
What clinical features suggest small-bowel obstruction?
Colicky abdominal pain, distension, vomiting, constipation, and trapped gas
29
What is the small-intestinal “string sign” on barium study?
A thin stream of contrast through a narrowed, inflamed segment as seen in Crohn’s disease
30
How long and wide is the small intestine?
~6–7 m long; “small” refers to its narrow luminal diameter
31
How does the small intestine maximize absorptive surface area?
Mucosal folds, villi, and microvilli increase surface area ~600-fold
32
What separates small and large intestine to prevent SIBO?
The ileocaecal valve, peristalsis, gastric acidity, and mucosal immunity
33
What are the features of lactase deficiency?
↓ brush-border lactase; high at birth, declines in childhood; undigested lactose causes osmotic diarrhoea and bacterial fermentation (gas, cramp), reversible, no mucosal damage
34
What population prevalences exist for lactase deficiency?
≈15% of Caucasians; 70–90% of other ethnic groups
35
How is lactase deficiency managed?
Remove lactose from diet
36
What are general clinical features of maldigestion/malabsorption?
Chronic diarrhoea, steatorrhea (pale, fatty floating stools), weight loss/failure to thrive, anorexia, abdominal distension, borborygmi, and muscle wasting
37
What are three causes of fat malabsorption?
Bile insufficiency (no emulsification), pancreatic lipase deficiency, mucosal chylomicron assembly defects (e.g., abetalipoproteinaemia)
38
How is pancreatic lipase deficiency diagnosed?
Faecal elastase-1 (FE-1) assay
39
What genetic phenotype is linked to coeliac disease?
HLA-DQ2 or DQ8
40
What skin manifestation is pathognomonic for coeliac disease?
Dermatitis herpetiformis—pruritic, subepidermal blisters in 15–25% of patients
41
How is coeliac disease definitively diagnosed?
Small-intestinal biopsy showing villous atrophy, crypt hyperplasia, and intraepithelial lymphocytes; reversible on gluten-free diet
42
What serological tests support coeliac disease diagnosis?
Anti-gliadin IgA and anti-tissue transglutaminase (tTG) antibodies (95% sensitivity)
43
Which foods must be excluded in coeliac disease?
Gluten sources: wheat (gliadin), barley, rye (oats often contaminated)
44
What complications arise if coeliac disease is untreated?
Persistent malabsorption, nutritional deficiencies, and increased risk of intestinal lymphoma
45
What are the four most common urinary tract diseases?
Benign prostatic hyperplasia (men), urinary tract infection (women), bladder cancer, and urinary incontinence.
46
What two functions does the bladder perform?
Stores urine and voids it under voluntary control.
47
What four symptoms suggest a urinary tract problem?
Frequency, dysuria (pain on urination), haematuria, and urinary retention.
48
How common is UTI in primary care?
UTIs account for about 1–2% of GP consultations.
49
What is the annual incidence of UTIs?
Approximately 50,000 cases per million people per year.
50
Which form of UTI primarily affects the bladder?
Cystitis (bladder inflammation).