Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PathoPhys > Lecture 11 - GIT Disorders > Flashcards

Lecture 11 - GIT Disorders Flashcards

1
Q

What does a structural/neural abnormality of GIT involve?

A

Altered Chyme movement: Slowing, obstructing, acceletration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does inflammatory/ulcerative conditions of GIT involve?

A

Changes in secretion, motility and absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Anorexia associated with?

A

Nausea, abdo pain, diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Anorexia definition

A

Lack of desire to eat in presence of physiologiical stimuli, normally eliciting hunger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Vomiting reflex initiated by

A
  • Duodenal presence of ipecac
  • Severe pain
  • Distension of stomach or duodenum
  • Torsion or trauma of testes, ovaries, uterus, bladder or kidneys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where is the ‘vomiting centre ‘?

A

‘Chemoreceptor trigger zone’ in postrema of medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which neurotransmitters activate ‘chemoreceptor trigger zone’ of vomiting?

A

5-HT (Serotonin) - from intestinal enteroendocrine cells. (Also dopamine, acetylcholine, histamine and Substance P)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which drugs are used as anti-emetics? (Antinausea)

A

Dopamine and serotonin receptor antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Vomiting is preceded by?

A

Nausea and retching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is retching?

A

Reverse peristalsis against closed upper oesophageal sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are sympathetic actions associated with vomiting?

A

tachycardia, tachypnoea, sweating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are parasympathetic actions associated with vomiting?

A

Hypersalivation, Increased gastric motility, Relaxation of upper and lower oesophageal sphincters.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mechanism of vomiting (Steps):

A
  • Reverse peristalsis duodenum and pyloric antrum
  • Oesophagus and gastric body reflex
  • Contraction abdo muscles = force diaphragm up
  • Stomach relax -> upper oesophagus contracts -> remaining chyme drops back into stomach
  • repeat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Metabolic consequences of vomiting?

A

Disturbance of fluid, electrolyte and acid-base balance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Definition of constipation?

A

Decrease or infrequent defaecation (decrease in weekly bowel movements)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes constipation?

A

Personal habits, drugs, various disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Clinical manifestations of constipation?

A

Difficulties/change in bowel evacuation patterns. Smaller stool volume. Feeling of bowel fullness and discomfort.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Neurogenic constipation pathophysiology:

A

Defective neural pathways and altered mechanisms.

Slow transit time (Abdo muscles weakness and pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Personal Habit constipation pathophysiology:

A

Low residue diet -> Decreased volume and stools.
Sedentary lifestyle and lacking regular exercise.
Lack of access to toilet facilities and consistent suppression of urge to defaecate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Systemic disease pathophysiology of constripation:

A

Hypothyroidism -> decreased bowel motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pathophy of drug caused constipation

A

Antacid use
Opiates inhibit bowel motility
Antidepressants (Anticholinergic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Diagnosis of Constipation involves?

A

History: How long? sudden onset may indicate organic lesions.
Physical exam: palpation (colon distention, masses, tenderness).
Digital rectal exam (Sphincter tone and anal lesions)
Stool transit time
proctosigmoidoscopy
Barium Enema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Constipations treatment:

A 
Bowel retraining
Exercise
More fluids
Increased fibre intake
Bilk supplements
Stool softeners
Laxative
Infrequent enemas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diarrhoea Definition

A

Increased frequency, fluidity, volume and weight of faeces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What influences stool volume and consistency?

A 
Colonic H2O Content
Presence of unabsorbed food
Presence of unabsorbable material 
Intestinal secretions
Adult stool volumes <200g a day
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How much water is lost in stool per day?

A

150mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Two forms of diarrhoea:

A

Large vol. Diarrhoea: (Increased volume of faeces due to:
Increased amounts H20, secretions or both.)
Small volume diarrhoea: Depending from intestinal motility (vol. not increased)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Mechanisms of osmotic diarrhoea?

A

Nonabsorbable substances draw H20 into lumen (Increased weight and vol. of stool).

  • Mg, Sulphate, Phosphate (poorly absorbed)
  • Deficiency (lactase, panreatic enzymes)
  • ingestion synthetic, non-absorbable sugars
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Mechanism of secretory diarrhoea?

A

Altered mucosal secretion and fluid electrolyes

  • Bacterial enterotoxins, neoplasms. (Large vol. Diarrhoea)
  • Inflammatory diseases such as Crohns and ulcerative colitis. Faecal impaction stimulates secretions to lubricate and move faeces. (Small vol. diarrhoea)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Mechanism of motility diarrhoea?

A

Inadequate food mixing and impaired digestion. Causes:

  • Resection small intestine
  • Surgical Bypass
  • Fistula formation between loops intestine
  • Hampered motility due to diabetic neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Clinical manifestations of chronic diarrhoea?

A
  • Dehydration
  • Electrolyte imbalance
  • Acidosis
  • Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Clinical manifestations of acute diarrhoea?

A

Fever with or without cramping pain with presence of diahhroea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Diagnosis of diarrhoea:

A

History: Onset and frq, travel? previous surgery? Iatrogenic?
Physical exam to identify systemic disease.
Abdominal X-ray, biopsies, stool culture, stool blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

3 Types of abdo pain causes?

A

Mechanical, inflammatory, ischaemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe mechanical cause for abdo pain

A

Abdo organs sensitive to:
- Rapid stretch and distension
- traction on peritoneum
- Common bile duct distension
- Forceful peristalsis from intestinal obstruction.
Encapsulated organs:
- Contain pain afferent for stretch (gall bladder and liver)

36
Q

Describe inflammatory causes of abdo pain?

A

Biochemical mediators: Histamine, bradykinin, serotonin stimulate visceral nerve endings
Oedema, vascular congestion -> Stretching: Seen with chemical, bacterial and viral inflammation

37
Q

Describe ischaemic cause of abdo pain

A

Obstruction of blood flow from distension through bowel obstruction.
Mesenteric vessels thrombosis.
Increases tissue metabolites stimulates pain receptors.

38
Q

Describe parietal abdo pain?

A

Parietal Peritoneum:

  • Localised, intense
  • Lateralised (innervated at any particular point, from only one side of nervous system)
39
Q

Describe Visceral abdo pain?

A

Abdominal Organ:

  • poorly localised, dull, diffuse, vague with radiating patten,
  • nerve endings sparse (e.g. stomach pain manifests as sensation of fullness, cramping, gnawing at mid-epigastric
40
Q

Describe refereed abdo pain?

A

Felt at distance from affected organ:

  • Well-localised, felt in skin or deeper tissues that:
  • -‘Share a general afferent pathway with organ’
  • -e.g. gall-bladder pain starts as vague right epigastric pain, then referred to shoulder blades as sharp and localised.
41
Q

Upper GIT Bleeding locations:

A

Oesophagus, stomach, duodenum

42
Q

Causes of upper GIT bleeding?

A
  • Oesophageal or gastric varices
  • Peptic ulcers
  • Mallory weiss tear at oesophageal-gastric junction from severe retching
43
Q

Location of lower GIT bleeding?

A

jejunum, ileum, colon, rectum

44
Q

Causes of lower GIT bleeding:

A
  • polyps,
  • inflammatory disease
  • cancer
  • haemorrhoids
45
Q

Signs of gastrointestinal bleeding

A
  • changes in blood pressure
  • postural hypotension, lightheadedness, loss of vision,
  • increased HR
  • Blood in stool
46
Q

Physiological response to GIT bleeding:

A
  • Increased TPR to shunt blood to core.
47
Q

Prolonged GIT bleeding leads to :

A 
Hypovolaemic shock ->
Decreased renal output ->
Decreased urine output ->
Tubular necrosis ->
Renal failure ->
Decreased cerebral and coronary blood flow ->
Anoxia and death
48
Q

Presentations of acute GIT Bleeding

A

Haematemesis
Melena
Haematochezia
Occult Bleeding

49
Q

What is haematemesis?

A

Sign of acute GIT bleeding: Black vomitus: either fresh bright red or dark grainy digested blood

50
Q

What is melena?

A

Sign of acute GIT bleeding: Black, sticky, tarry foul smelling stools caused y digestion of blood in GIT

51
Q

What is Haematochezia?

A

Sign of acute GIT bleeding: Fresh bright red blood passed from rectum

52
Q

What is occult bleeding

A

Trace amounts of blood in normal appearing stools or gastric secretions: Detectable only with a Guaiac Test

53
Q

What does GERD stand for?

A

Gastrooesophageal reflex disease

54
Q

What is GERD?

A

Regurgitation of stomach chyme through lower oesophageal sphincter into oesophagus.

55
Q

What are complications of GERD?

A

Reflux Oesophagitis
Oesophageal ulcers,
Oesophageal scarring (Dysphagia)

56
Q

What are the consequences of ssnk mucosa of oesophagus exposure to refluxed acid?

A
  • Cell injury
  • Accelerated desquamation
  • Compensatory basal cell hyperplasia = Increased immature epithelium cells, elongated C.T papillae, low grade inflammatory response
57
Q

Consequences of severe reflux

A
  • Cell proliferation fails to keep pace with desquamation -> ulceration-> haemmorhage or perforation
  • Haling occurs through fibrosis and epithelial regeneration
  • Shrinkage of fibrous tissue = Stricture of oesophagus (narrowing of opening)
58
Q

What occurs if epithelium of oesophages regenerates as columnar epithelium after reflux damage?

A

Barretts Oesophagus Disease

59
Q

Causes of Reflux Oesophagitis?

A
  • Inadequate resting tone of lower oesoph sphincter
  • Increased intra-abdo pressure (vomiting, coughing, lifting, bending)
  • Weak oesophageal peristalsis
  • Delayed gastric emptying: (Increased chyme acidity, increased time-span for reflux) caused by gastric duodenal ulcers, pyloric strictures, hiatal hernia.
  • gastric surgery.
60
Q

What does the severity of oesophagitis depend on?

A

Composition of of gastric contents, duration of exposure to mucosa.

61
Q

Clinical manifestations of reflux oesophagitis 1 hr after meal?

A

Within 1hr of meal:

  • Heartburn
  • Acid regurgitation
  • Dysphagia
  • chronic cough
  • athsma
  • upper abdo pain
62
Q

How is reflux oesophagitis diagnosed?

A
  • Manifestations
  • Endoscopy (looking for erosions, oedema, dysplasia (Barrett’s), carcinoma
  • pH monitoring
    Baa++ swallow, associated with hiatal hernia, gastric ulcers
63
Q

Aetiology of Barrett’s Oesophagus?

A 
Epithelial substitution (Migration of cells from distal 2cm or from ducts of submucosal glands)
Metaplasia (Differentiation from common stem cell - response to injury)
64
Q

Clinical significance of Barrett’s Oesophagus?

A
  • Premalignant condition
  • Risk of cancer is 100x higher in these patients vs normal pop.
  • After diagnosis, regular colonoscopies check for dysplasia
65
Q

Barrett’s Oesophagus:

3 types of columnar mucosa and their function.

A
  • Junctional type: normal gastric cardia
  • Atrophic fundal type: scanty specialised secretory cells
  • ‘Specialised mucosa’: epithelium undergoing further metaplastic changes towards intestinal type with acquired goblet cells.
66
Q

What is peptic ulcer disease?

A

Ulceration of mucosal lining of (oesophagus, stomach, duodenum)

67
Q

Difference between an erosion and a true ulcer in peptic ulcer disease?

A

Erosions: superficial, do not penetrate muscularis mucosae.

True Ulers: Penetrate muscularis mucosae and blood vessel damage

68
Q

Peptic ulcer risk factors:

A

smoking, advanced age, habitual NSAID use, EtOH, chronic diseases (emphysema, Rheumatoid arthritis, cirrhosis, diabetes). Helicobacter pylori infection of gastric duodenal mucosa., stress

69
Q

Duodenal ulcers occur most in (population)..

A

Men, younger people, type O blood.

70
Q

Pathophysiology of Duodenal ulcers:

A

i. NSAIDS inhibit prostaglandins = Decreased HCO-3 and mucus production
ii. H.pylori urease -> formation of cytotoxic ammonia.
iii. H.pylori phospholipases and other enzymes from micoorg -> damage to mucosa
iv. H.pylori -> Increased gastrin production -> HCl secretion -> ulcer formation
v. rapid gastric emptying exceeds buffer capacity of HCO-3 righ panc. juice
vi. Increase secretion form parietal cells
vii. Smoking
Viii. Decreased mucosal HCO3 secretion

71
Q

Clinical manifestations of duodenal ulcers:

A
  • Epigastric pain (chronic intermittent) :2-3 hours post-grandial, relieved by food consumption or antacids
  • haemorrhage: with history of asprin or anticoag use, most common in elderly
  • perforation: if all wall layers destroyed, sudden severe epigastric pain
  • obstruction of duodenum: oedema from inflammation or scarring.
  • haematemesis or melena
72
Q

Diagnosis of duodenal ulcers:

A
  • X-ray with barium contrast meal
  • flexible endoscope
  • radioimmune assays of gastrin levels
  • detection of helicobacter pylori
73
Q

Prevention of duodenal ulcers

A

high vit A and fibre diet

74
Q

Gastric ulcers epidemiology

A

Equal in males and females
55-65 yrs
25% less common than duodenal ulcers

75
Q

Clinical manifestations of gastric ulcers:

A

similar to duodenal

  • pain-food relief
  • pain may occur post-prandial
  • tends to be chronic
  • anorexia, vomiting, weight loss
76
Q

Gastric ulcer pathophys:

A
  • Increased mucosa permeability to H+ ions
  • Gastric secretions decreased (chronic gastritis)
  • Chronic gastritis -> ulcer,
  • duodenal reflux
  • ulcerogenic drugs
  • Increased bile salt = electrical potential disruption -> H+ diffuse back into mucosa.
  • Histamine from damaged mucosa -> increased blood flow pepsinogen and acid production and capillary permeability
77
Q

What is ulcerative colitis?

A

Chronic inflammation of rectum an sigmoid colon

78
Q

UC most common in… (population)

A
  • Genetically susceptible (20-40yrs), Jewish descent, white
79
Q

Causes of UC?

A
  • infection
  • genetics
  • immunological: humoral factors (anticolon antibodies in sera), activated macrophages, cytotoxic T cells attack colonocytes, often accompanied by other immune disorders
80
Q

Pathophysiology of UC?

A

Primary lesion at base of colonic crypts. Hyperaemic mucosa. SMall erosions merge into ulcers.

  • Abscess formation (necrosis, ragged mucosal ulceration)
  • Oedema and thickening of m.mucosa > narrow lumen
  • mucosal destruction
  • Bleeding, cramping pain, urge to defaecate, purulent mucus = decreasing colonic transit time = large volumes of watery diarrhoea
81
Q

Clinical manifestations of mild UC?

A

Intermittent periods of remission and exacerbation. (less mucosa)
- increased frequency of BMs, bleeding, pain.

82
Q

Clinical manifestations of severe UC?

A

(entire colon)

  • fever, increased pulse rate
  • frequent diarrhoea (10-20/day)= dehydration
  • urgency
  • bloody stool
  • continuous bloody stools = anaemia
  • continuous crampy pain
  • weight loss
  • increased colon cancer risk
83
Q

Diagnosis of UC?

A

Medical history and clinical manifestations.
Differential diagnosis with Crohn’s disease
- Sigmoidoscopy
- X-rays with barium enema
- Stool culture rules out infection

84
Q

Where does crohns occur?

A

Large and small intestine but seldom rectum.

85
Q

Crohns disease immune system effects:

A 
Decreased suppressor T cells
IgA production
Macrophage activation
luminal flora
antigens
86
Q

Pathophysiology of Crohns:

A

Begins in intstinal submucosa

  • tissue injury from activated neutrophils and macrophages
  • ascending and transverse colon and small intestine (skip lesions)
  • may be unilateral
  • fissures that penetrate lymphoid tissue
  • granuloma is typical lesion
  • fistulae between intestinal loops in perineal area or into bladder
87
Q

Crohns vs UC

A

Crohns: Focal or patchy mucosal involvement. Fissure ulcers. Aggregated transmural chronic inflammatory cell infiltrate.
UC: Horizontal undermining ulcers. Diffuse mucosal Inflammation

PathoPhys (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions