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JMP Semester 2 > Week 18 > Flashcards

Week 18 Flashcards

1
Q

What is epidemiology?

A

the branch of medicine which deals with the incidence, distribution, and possible control of diseases and other factors relating to health.

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2
Q

How common is abdominal pain?

A

Common - 25% of the adult population has some form of abdominal pain at any one time.

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3
Q

What are the common causes of upper abdominal pain?

A
  1. Gas
    1. Indigestion
    2. Gastritis
    3. Stomach virus
    4. Muscle pain
    5. Appendicitis
    6. Gallstones
    7. Liver issue
    8. pancreatic issues
      Etc
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4
Q

What is functional abdominal pain?

A

Ongoing abdominal pain for which there is no known medical explanation .

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5
Q

What is gastritis vs gastropathy?

A
  1. Gastritis refers to inflammation of the gastric mucosa, whereas
  2. Gastropathy is a nonspecific microscopic injury pattern with little or no inflammatory cell infiltration.
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6
Q

Risk factors for peptic ulcers?

A
  1. Chronic use of NSAID
    1. Helicobacter pylori
    2. Smoking
    3. Alcohol
    4. Stress
      1. Spicy food
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7
Q

What is the typical pathophysiology of gastritis and how does it present in the clinic?

A
  1. Gastritis- inflammation of the stomach lining. Commonly by infection
  2. Presents as Nausea or recurrent upset stomach. Abdominal bloating. Abdominal pain. Vomiting. Indigestion.
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8
Q

What is the typical pathophysiology of Reflux oesophagitis and how does it present in the clinic?

A
  1. When acid reflux from the stomach is frequent and persistent, the result is damage to the lining of the oesophagus.
    1. Can present as eroded teeth, vomiting etc (white gastric acid)
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9
Q

What is the typical pathophysiology of duodenal ulcer and how does it present in the clinic?

A
  1. Ulcer in duodenum

2. Can present as pain a few hours after eating

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10
Q

Most common causes of GI haemorrhage?

A 
Upper:
	1. Peptic ulcer
	2. Mallory-Weiss tears (oesophageal tears)
	3. Esophageal varices (enlarged veins)
	4. Esophagitis 
Lower:
	1. Diverticulosis (small budging pouches in the GI tract)
	2. IBD
	3. Tumours 
	4. Colon polyps
	5. Hemorrhoids (swollen veins in anus)
	6. Anal fissures (anal tears)
Proctitis (rectum inflammation)
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11
Q

What are some symptoms for GI haemorrhage?

A
  1. Hypovolemic shock (low bp)
    1. Vomiting blood
    2. Bloody stool
    3. Abdominal pain
    4. Chest pain
    5. Difficulty breathing
    6. Lightheaded
    7. Fainting
    8. Tachycardia
  2. Oliguria (decreased urine output)
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12
Q

What are types of vomitus and their clinical implications (7 colours)

A
  1. Clear- Gastroenteritis, gastric outlet obstruction.
    1. White or foamy- acid reflux, gastritis,
    2. Green or yellow- Bile reflux, Gastroenteritis
    3. Orange- Gastroenteritis
    4. Pink or red- Peptic ulcer, cancer
    5. Brown- stomach cancer, peptic ulcer, injury, severe constipation.
  2. Black- injury, peptic ulcer, infection (fungal), cancer, severe constipation
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13
Q

What is the scale for stool classification known as?

A

Bristol stool scale

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14
Q

What are the different types in the bristol stool scale. (7 types)

A

Type 1- separate hard lumps, like nuts (hard to pass)
Type 2- sausage shaped but lumpy
Type 3- Sausage but with cracks on the surface
Type 4- sausage but smooth and soft
Type 5- soft blobs with clear cut edges
Type 6- fluffy pieces- a mushy stool
Type 7- entirely liquid

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15
Q

What do some of the types of stool indicate?

A
  1. Type 1-2 indicate constipation
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16
Q

What do colours of stool indicate? (6 different colours but 2 are black)

A
  1. Black stools not sticky- can be medication or GI bleeding
    1. Black stool and sticky- usually GI bleeding
    2. Red stools- haemmorhoids, anal fissure
    3. Gray stool- lack of bile in the stool (liver disease)
    4. Yellow stool- malabsorption, lipids, pancreatic issues
      Green stool- fast tract through GI, Diarrhoea
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17
Q

What is the purpose of an endoscope?

A

Visualize and biopsy.

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18
Q

Effect of acid suppression on nutrition?

A
  1. Food breakdown reduced
    1. Protein breakdown reduced
      Hence malabsorption.
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19
Q

What is the difference between norovirus and rotavirus?

A

Noravirus can affect anyone, hard to get immunity, no vaccine
Rotavirus affects people under 5, easy to get immune, vaccine available.

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20
Q

What are brush border enzymes?

A

Enzymes of the microvilli, allow for nutrient absorption

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21
Q

What is ghrelin?

A

Ghrelin is a hormone that is produced and released mainly by the stomach with small amounts also released by the small intestine, pancreas and brain. Ghrelin has numerous functions. It is termed the ‘hunger hormone’ because it stimulates appetite, increases food intake and promotes fat storage.

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22
Q

What are the major structures of the oral cavity?

A
  1. Teeth
    1. Tongue
    2. Lips
    3. Salivary glands
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23
Q

What is the digestive purposes the oral cavity serves?

A
  1. Receives food
    1. Mechanical digestion (mastication with teeth and tongue)
    2. Mixing food with saliva (enzymes in saliva, lubricates and helps form bolus to allow transfer to the oesophagus)
    3. Gustation (tongue has taste receptors)
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24
Q

What cranial nerves do taste buds use to send signals to the gustatory centers of the brain?

A
  1. Cranial nerves (7) VII
    1. (9) IX
    2. (10) X.
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25
Q

What are the three major salivary glands in the oral cavity?

A
  1. Parotid (upper molars) (20% of saliva)
    1. Sublingual (under the tongue) (70% of saliva)
    2. Submandibular gland (10% of saliva)
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26
Q

What are the main components of saliva?

A
  1. Water (99.5%)
    1. Enzymes
      - Amylase- starch to sugars (glucose and maltose)
      - Lipase- lipid digestion (triglycerides to diglycerides and free fatty acids)
    2. Mucous
      - Lubricates food
      - Protects mouth lining (like from acid when vomiting)
      - Antimicrobial activity (Leukocytes, lysozyme, IgA)
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27
Q

What is the impact of sympathetic and parasympathetic input on salivary glands?

A
  1. Sympathetic- more viscous saliva to facilitate respiration- sticks to surfaces and prevents desiccation.
    1. Parasympathetic- input creates watery saliva (to facilitate digestion)
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28
Q

What is the three main phases of the swallowing reflex?

A 
Oral phase (voluntary)
Pharyngeal phase (involuntary)
Oesophageal phase (involuntary)
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29
Q

What are the two steps in the oral phase of swallowing?

A
  1. Moistening of the food with saliva/mastication
    • Lubricates
    • mechanical mastication
    • lingual nerve senses the state of the bolus (if too dry swallowing will not continue)
      2. Trough formation and posterior bolus movement.
    • Trough in back of tongue
    • Bolus forced back
    • Lips contract to seal the oral cavity
    • Bolus moved to palatoglossal arch
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30
Q

What are the four main steps in the pharyngeal phase of swallowing?

A
  1. Soft palate is elevated- prevent bolus from entering nasal cavity.
    1. Initiation of pharyngeal peristalsis- bolus moved to the oesophageal sphincter
    2. Elevation and closure of the larynx- by the epiglottis
    3. Relaxation of upper oesophageal sphincter.
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31
Q

What are the 5 main steps in the oesophageal phase in swallowing?

A
  1. Bolus enters oesophagus- peristaltic wave pushes towards stomach
    1. Peristaltic wave from alternating relaxation (ahead of bolus) and contraction (behind)
    2. Lower oesophageal sphincter relaxes and allows bolus to enter stomach
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32
Q

What is the relative speed of the bolus in the pharyngeal phase vs the oesophageal phase?

A

Pharyngeal- fast (40cm/sec)

Oesophageal- slow (5cm/sec)

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33
Q

What mechanisms allow food to propel down the oesophagus?

A

A peristaltic wave- contracting of circular muscle behind and relaxation in front of.

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34
Q

What is the normal function of the upper and lower oesophageal sphincters?

A
  1. Upper
    • prevent oesophageal air during inspiration
    • prevent esophagopharyngeal/laryngeal reflux during oesophageal peristalsis.
      2. Lower
    • Prevent retrograde movement of stomach acid.
    • ??????
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35
Q

What are the four main parts of the stomach?

A
  1. Cardia
    1. Fundus
    2. Body
    3. Pylorus
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36
Q

How many muscle layers does the stomach have and what are their names?

A

There are 3 - Longitudinal, Circular, Oblique

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37
Q

How does the stomach mainly achieve its role of food storage?

A

The interior mucosal layer folds (Rugae) allow for expansion of the stomach with assistance from smooth muscle.

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38
Q

What is the volume of an empty stomach vs a full stomach?

A

Empty 75ml

Full 1-5L-4L

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39
Q

How long does a typical meal take to empty from the stomach?

A

1 hour

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40
Q

What 3 things does the stomach secrete to aid digestion?

A
  1. HCL- denatures proteins and activates pepsinogen –> pepsin
    1. Pepsin- digests proteins
    2. Gastric lipase- hydrolyses lipids
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41
Q

How does the stomach achieve motility and what is the effect of this?

A
  1. When full peristaltic waves begin - contraction in all three muscle layers.
    1. Waves happen 3 times per minute
    2. Waves cause churning (mechanical digestion)
    3. Contractions move contents from pylorus –> antrum and back again.
    4. Contents become a watery acidic mixture (chyme)
    5. Pyloric sphincter opens with each wave.
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42
Q

What is the mucosal surface of the stomach covered with?

A

Gastric pits

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43
Q

What are the four cell types to gastric glands contain?

A
  1. Parietal cells
    1. Chief cells
    2. Goblet cells
    3. Enteroendocrine
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44
Q

Where are parietal cells found and what do they do?

A
  1. They are found in the fundus, corpus and antrum

2. Secrete HCL by secreting H+ and Cl separately.

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45
Q

Where are chief cells found and what do they do?

A
  1. Found predominately in the corpus
    1. Secrete pepsin precursor (pepsinogen)
    2. When pepsinogen is exposed to acid it is activated
    3. Pepsin then hydrolyses protein residues in the chyme
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46
Q

Where are Goblet cells found and what do they do?

A
  1. Found in the gastric pits
    1. Secrete alkaline mucous
    2. Mucous protects the epithelium
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47
Q

What do the enteroendocrine cells do in the stomach?

A
  1. Secrete hormones
    • G cells - secrete gastrin (stimulates acid secretion)
    • D cells - secrete somatostatin (inhibits acid secretion)
48
Q

What do enterochromaffin-like cells (ECL) secrete?

A

Histamine

49
Q

What are the three phases in the regulation of acid secretion?

A
  1. Cephalic
    1. Gastric
    2. Intestinal
50
Q

What are the factors in the cephalic phase regulation of acid secretion?

A
  1. Sight, smells, tastes of food - activate parasympathetic enteric neurons
    1. Acetylcholine acts directly of parietal cells to increase acid secretion
    2. G cells and ECL’s also excited and increase acid secretion
51
Q

What are the factors in the Gastric phase regulation of acid secretion?

A
  1. Food stretch - neural reflexes to release acetylcholine from enteric neurons (increases acid secretion)
    1. Food peptides - stimulate G cells to release Gastrin (increases acid secretion)
    2. Food related pH change - raised alkalinity - prevents somatostatin release by D- cells - increases acid secretions.
52
Q

What are the factors in the intestinal phase regulation of acid secretion?

A
  1. Chyme in duodenum - negative feedback to slow acid production
    1. Neural reflexes prevent acetylcholine release - reduces acid secretion
      Enterogastrones (hormones) - inhibit the ECL’s and G-cells - decrease acid secretion
53
Q

What is autocrine?

A

Cell secretes molecules that act on itself.

54
Q

What is paracrine?

A

Cells secrete molecules that act on nearby cells.

55
Q

What is Endocrine?

A

Cells secrete molecules that act on distant cells.

56
Q

What is the effect type of histamine, gastrin and somatostatin?

A

Histamine- paracrine
Gastrin- endocrine/paracrine
Somatostatin- endocrine/paracrine

57
Q

What are the defences that the stomach uses against acid?

A
  1. Alkaline mucous- neutralises low pH in a gradient over the epithelial cells
    1. High cellular turnover- epithelial cells are short lived and replaced often
    2. Secretion of inactive precursors- HCL is secreted as ions, pepsin as pepsinogen to prevent damage to the epithelial cells.
58
Q

What is the primary defences against microbial growth in the stomach?

A
  1. Acidic environment
    1. Proteolytic environment
    2. Small effect from leukocytes present within the gastric mucosa
59
Q

What are some of the features of Helicobacter pylori that allow it to survive in the stomach?

A
  1. Flagella to burrow into epithelial cells (avoids acid)
  2. Secretes urease to convert urea to CO2 and ammonia (neutralises pH and creates a pH neutral bubble around the bacteria.
60
Q

What are the structural features of helicobacter pylori?

A
  1. Gram negative
    1. Spiral shaped (for cork screwing into gastric mucus)
    2. Multiple flagella
    3. Lives between the gastric epithelium and the mucous layer
61
Q

What is the most common way for someone to get a helicobacter pylori infection?

A

From mother to child in early childhood

62
Q

What are prostaglandins?

A

Lipid based compounds which have hormonal like effect.

63
Q

Where are prostaglandins synthesised?

A

In the mucosa from arachidonic acid through cyclooxygenase enzymes

64
Q

What are the effects of prostaglandins?

A
  1. Cytoprotective effect on the epithelial cells of the GIT.
    • Stimulate mucosal mucous/bicarbonate secretion
    • Stimulate mucosal blood flow
    • Supress diffusion of acid into the mucosa
65
Q

What is an NSAIDS?

A

Non-steroidal anti-inflammatory drugs

66
Q

What is the relationship between NSAIDS and prostaglandins?

A

NSAIDS can inhibit prostaglandin synthesis and hence their use are related to gastric erosions and ulcers.

67
Q

How is arachidonic acid formed?

A

From membrane phospholipids in the stomach (this is the rate limiting step) in particular by phospholipase A2.

68
Q

What are eicosanoids?

A

Metabolites of arachidonic acid

69
Q

What are some examples of eicosanoids?

A
  1. Prostaglandins (PG)
    1. Prostacyclin
    2. Thromboxane A2
    3. Leukotrienes
70
Q

Are eicosanoids stored?

A

No, they are produced when needed.

71
Q

What are some of the general functions of eicosanoids?

A
  1. Inflammation
    1. Smooth muscle tone
    2. Haemostasis
    3. Thrombosis
    4. Parturtion
    5. Gastrointestinal secretion
72
Q

What is the general pathway from phospholipid to prostacyclin, prostaglandins and thromboxane?

A
  1. Phospholipid –> processed by Phospholipase A2
    1. Arachidonic acid produced
    2. Arachidonic acid processed by cyclo-oxygenase (cox1/cox2)
    3. Processed to endoperoxides
    4. Endoperoxides –> prostacyclin, thromboxane and prostaglandins
73
Q

What is the general pathway from phospholipid to leukotrienes?

A
  1. Phospholipid –> phospholipase A2 –> Arachidonic acid
    1. Arachidonic acid–> 5- lipoxygenase –> HPETE
    2. HPETE –> LTA4 –> range of Leukotrienes (LTB, LTC, LTD, LTE)
74
Q

What is the two forms of cyclooxygenase?

A

COX1 and COX2

75
Q

How is COX-1 expressed in the body?

A

Constitutively - constantly in most cells.

76
Q

What type of enzyme is COX-2?

A

Inducible enzyme - it can be upregulated (not constitutively like COX1)

77
Q

What is the principle purpose of the Cyclooxygenase?

A

Enzyme involved in prostaglandin and thromboxane formation in inflammation and cancer.

78
Q

What are some triggers for COX2 upregulation?

A
  1. Cytokines
  2. Shear stress
  3. Growth factors
79
Q

What are two types of NSAIDS?

A
  1. Non selective COX inhibitors (block COX1 and COX2) - eg ibuprofen, aspirin
    1. Selective COX2 inhibitors (coxibs)
80
Q

What is the general mechanism for NSAID effect?

A
  1. Blocks cyclooxygenase activity

Less prostaglandins and thromboxane formation

81
Q

What are some of the effects of NSAIDs on gastric mucous?

A

The loss of prostaglandins- in particular PGE2:
1. Prostaglandin PGE2- activates EP3 receptors: (which protects gastric mucosa)
- Inhibits gastric acid secretion
- Increases gastric mucous secretion
- Cell repair
- Local blood flow
Epithelial cell bicarbonate secretion.

82
Q

What are substances that increase secretion of gastric acid from parietal cells?

A
  1. Histamine
    1. Gastrin
    2. Acetylcholine
83
Q

What are some mechanisms which drugs utilise to decrease acid secretion?

A
  1. Histamine (H2) receptor antagonist

2. Proton pump inhibitors

84
Q

How do Histamine (H2) receptor antagonists suppress gastric acid secretion?

A
  1. Competitively and reversibly blocking histamine binding to H2 receptors.
    1. Antagonistic binding to these receptors decreases gastrin and acetylcholine induced gastric acid secretion
    2. Drug examples - ranitidine (Zantac)
85
Q

Exact mechanism for H2 receptor antagonist in gastric acid secretion?

A
  1. Receptor
    1. PKA
    2. Tubulovesicle (contains H+/K+ ATPase)
    3. Hence blocking of this, blocks H+ secretion.
86
Q

How do proton pump inhibitors (PPIs) suppress gastric acid secretion?

A
  1. They inhibit the H+/K+-ATPase.
    1. They are irreversible blockers- half life small but affects the cell until they are replaced.
    2. They are all “pro-drugs” requiring to be activated in the acidic environment.
    3. Drug examples- omeprazole
87
Q

What are some drugs that prevent acid damage to mucosal surfaces?

A
  1. Antacids- eg aluminum hydroxide and magnesium hydroxide
    1. Coating agents
    2. Prostaglandin (PG) analogue
88
Q

How do antacids protect mucosal surfaces?

A
  1. Hydroxide ions react with H+ ions to form water
    1. The aluminium/magnesium react with bicarbonate and phosphates to form salts
    2. Mechanism to NEUTRALISE ACID.
89
Q

How do coating agents prevent mucosal damage from acid?

A
  1. Sucralfate- salt of sucrose sulfate AND aluminium hydroxide
    • in acidic environments forms a viscous gel
    • Gel binds to positive changed proteins
    • Adheres to epithelial cells
      2. Colloidal bismuth
    • Bismuth salts bind to mucus glycoproteins
    • Makes barrier to protect gastric mucosa
    • May stimulate bicarbonate and PGE2 secretion
    • Can slow growth of H. pylori
      3. MECHANISM IS PROTECT STOMACH LUMINAL SURFACE FROM ACID AND PEPSIN
90
Q

How do PG analogues prevent mucosal surface acid damage?

A
  1. Misoprostol (PGE2 analogue)
    • The prostaglandin analogue
    • reduces gastric acid secretion
    • enhances bicarbonate secretion
    • Increases mucus production
    • Increases blood flow.
  2. MECHANISM - COMMONLY USED TO PREVENT NSAID-induced peptic ulcers.
91
Q

What is the potential effects of pH on drug availability and absorption?

A
  1. pH affects what form a drug will be in (non-ionised or ionised (charged))
    • Non-ionised molecules- more lipid soluble–> diffuse well across cell membrane
    • Ionised molecules- low lipid solubility–> less able to penetrate cell walls.
      2. Acid can destroy or activate a drug (so altered stomach pH can change drugs absorption)
92
Q

Where are weakly acidic vs weakly basic drugs soluble?

A
  1. Weakly acidic- lipid soluble at a low pH - in the stomach

2. Weakly basic drugs- lipid soluble at high pH - in the duodenum

93
Q

What is the effects of GIT motility on drug absorption?

A
  1. Increase Gastric emptying –> faster drug absorption in small intestines –> eg dopamine receptor antagonists
    1. Decrease Gastric emptying –> slower drug absorption in small intestines –> eg muscarinic receptor antagonists.
    2. Increase time in GIT can increase the chance for absorption (but at a slower rate)
94
Q

What are the effects of food on drug availability and absorption?

A
  1. The composition of food can alter gastric emptying
    • High fat - delay gastric emptying - delay absorption in small intestine
      2. Some drugs bind to protein- digoxin may bind to fibre - increased drug excretion
      3. Empty stomach- less acidic- good for acid labile drugs - PPIs etc
      4. Full stomach - more acidic- good for drugs needing acid activation - eg some antifungals.
95
Q

What is the drug interaction between clopidogrel and PPIs?

A
  1. Clopidogrel –>inhibits platelet activation –> inhibits blood clotting
    • Administered as a pro-drug- metabolised in the liver by CYP2C19 enzyme
      2. PPIs inhibit this enzyme so can reduce plasma levels and effectiveness of clopidogrel
  2. Recommended to take these drugs at different times of day.
96
Q

What are common causes of inflammation of the oesophagus?

A
  1. Gastro-oesophageal reflux disease (GORD)
    1. Hiatus hernia
    2. Medications - NSAIDS, Antibiotics, steroidal treatments etc
    3. Alcohol
    4. Vitamin and mineral supplements - Vitamin C, potassium, iron supplements
    5. Infections - patients with decreased immunity - HIV, diabetes
    6. Bonus -Radiation therapy, Scleroderma, Allergies
97
Q

What is the definition of GORD?

A

Normal- The transient involuntary reflux of gastric juices into the oesophagus is considered a normal occurrence in healthy humans across the lifespan
Dysfunction- If the symptoms of reflux (heartburn and regurgitation) impair quality of life or put patients at risk of complications, it is regarded as a dysfunction.

98
Q

What are some complication of GORD?

A
  1. Oesophagitis with ulceration and scarring
    1. Barret’s oesophagus- precancerous
    2. Oesophageal cancer
    3. Strictures of the oesophagus - narrowing
99
Q

Common causes of inflammation of the stomach?

A
  1. Long term use of medications- aspirin, ibuprofen
    1. Alcohol (excessive)
    2. Presence of H.pylori bacteria
    3. Illness - diabetes, kidney failure
    4. Immunocompromised
    5. Stress (can affect immune system)
    6. Bile flowing into the stomach- or bile reflux
100
Q

What are some causes of inflammation of the duodenum?

A
  1. H.Pylori
    1. Long term use of NSAID
    2. Substance abuse- alcohol, cocaine
    3. Tobacco/smoking
    4. Debilitation illness
    5. Stress
    6. Other medications like corticosteroids
    7. Crohn’s disease (IBD)
    8. Others- radiation, autoimmune, other infections
101
Q

What is an ulcer?

A

an open sore on an external or internal surface of the body, caused by a break in the skin or mucous membrane which fails to heal.

102
Q

What is peptic ulcer disease?

A
  1. A group of stomach (gastric) and duodenal ulcers together.
    1. Peptic ulcers characterised -mucosal erosive injury about 5 mm or more in depth.
    2. The damage exposes the underlying smooth muscle, blood vessels and sensory nerves to the gastrointestinal contents in the lumen.
103
Q

Generally why do ulcers form in the GIT?

A
  1. Aggressive action of the gastric juices on the mucosa (acidic and proteolytic)
    1. Weakened mucosal protection
104
Q

What are the two factors strongly linked to peptic ulcer disease (PUD)?

A
  1. Chronic use of NSAID

2. Helicobacter pylori

105
Q

Define crohn’s disease.

A
  1. Inflammatory condition
    1. may occur in any part of the GIT - most common in ileum
    2. Inflammation occurs in all four layers of intestinal wall.
106
Q

What is the effect of chronic acid exposure on the oral cavity?

A
  1. Teeth enamel erosion (enamel is soluble in acid)
107
Q

What is the effect of chronic acid exposure on the oesophagus?

A
  1. GORD
    1. Oesophagitis
    2. Barret’s oesophagus
    3. Oesophageal cancer
108
Q

What are the effects of chronic acid secretion on the stomach?

A
  1. Peptic ulcers

2. Gastric tumours

109
Q

How common is H.pylori?

A

50% of people have it. - for about the last 100,000 years

110
Q

What are the common cancer types in the oesophagus?

A
  1. Squamous cell carcinomas (most common)

2. Adenocarcinomas

111
Q

What are the common cancer types of the stomach?

A
  1. Adenocarcinomas - (85%)

2. (Lymphomas, gastro intestinal stromal tumours, leiomyosarcomas) (15%)

112
Q

What is the Hampton line?

A
  1. Indicating that an ulcer is benign.
    1. Caused by a thin line of mucosa overhanging the ulcer’s crater.
    2. Seen at the neck of agastric ulcerin barium studies as a radiolucent line (clear)
113
Q

What is the Carmen meniscus sign?

A
  1. Indicates malignancy
    1. Is a shallow gastric ulcerating malignancy
    2. It is always convex inwards to the lumen
      Does not project beyond the wall
114
Q

What is the use of RCTs?

A

Gold standard to know if a drug actually works. Case controls could be bias through unconscious manipulation of groups.

115
Q

What are the design features of a randomized control trial?

A

Double blinding techniques-
Therapy choice is random- patient nor doctors can choose who gets what treatment. Helps to rule out confounding factors both known and unknown.

JMP Semester 2 (8 decks)

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