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USMLE Step 1 > Gastrointestinal System > Flashcards

Gastrointestinal System Flashcards

1
Q

What are the features of glossitis?

A
  • Beefy red tongue
  • Smoothing of the tongue
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2
Q

What are the causes of glossitis?

A
  • Vitamin B2, B3, B6 and B12 deficiency
  • Iron deficiency
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3
Q

What is leukoplakia?

A

Areas of keratosis on the mucous membrane

>> Can be confused with oral candidiasis or oral hairy leukoplakia
>> More common in patients who smoke

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4
Q

What is oral hairy leukoplakia?

A

White patch on the side of the tongue

>> Caused by EBV
>> Typically in immunocompromised (e.g. HIV) patients

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5
Q

What are cold sores?

A

Oral HSV-1 (sometimes HSV-2) infection

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6
Q

What are the three salivary glands?

A
  • Parotid gland
  • Submandibular gland
  • Sublingual gland

>> Secretions has alpha-amylase, bicarbonates, mucin, antibacterial substances such as IgA and growth factors that promote epithelial renewal

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7
Q

Describe the innervation of the salivary glands.

A

Sympathetic stimulation

  • Very thick secretion
  • Superior cervical ganglion

Parasympathetic stimulation

  • Watery secretion
  • CNVII and CNIX
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8
Q

What structure does the facial nerve run through?

A

Parotid gland

>> Remember that even though the facial nerve runs through the parotid gland, the parotid gland itself is supplied by the glossopharyngeal nerve

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9
Q

What is xerostomia?

A

Severe drying of the mouth

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10
Q

What syndrome is associated with xerostomia?

A

Sjogren’s syndrome

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11
Q

What are the possible causes of xerostomia?

A
  • Sjogren’s syndrome
  • Antihistamines
  • Anticholinergic drugs
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12
Q

What is sialolithiasis?

A

Stone in the salivary gland duct >> blockage of the salivary gland duct

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13
Q

What are the presenting features of sialolithiasis?

A
  • Acute pain and swelling
    >> Submandibular gland
    >> Stensen’s duct of the parotid gland
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14
Q

What is the treatment of sialolithiasis?

A

Suck on candy/chew gum to increase salivary secretion

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15
Q

What is sialadenitis?

A

Inflammation of the salivary gland

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16
Q

What are the organisms that typically cause sialadenitis?

A
  • Staphylococcus aureus
  • Viridans streptococci
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17
Q

What is the most common salivary gland overall?

A

Pleomorphic adenoma

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18
Q

What is the most common benign salivary gland tumour?

A

Pleomorphic adenoma

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19
Q

What is the most common malignant salivary gland tumour?

A

Mucoepidermoid carcinoma

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20
Q

What is the second most common benign salivary gland tumour?

A

Warthin’s tumour

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21
Q

What makes up a pleomorphic adenoma?

A

Epithelial and mesenchymal cells
>> Chondromyxoid stroma and epithelium

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22
Q

What is a possible complication of pleomorphic adenoma?

A

Facial nerve injury

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23
Q

What is the underlying pathophysiology of cleft lip?

A

Failure of fusion of maxillary and medial nasal processes

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24
Q

What is the underlying pathophysiology of cleft palate?

A
  1. Failure of fusion of the 2 lateral palatine processes
    >> Formation of the primary palate
  2. Failure of fusion of the lateral palatine processes with the nasal septum and/or median palatine processes
    >> Formation of the secondary palate
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25
Q

What are the common causative organisms of the common cold/infectious rhinitis?

A
  • Coronavirus
  • Rhinovirus
  • Adenovirus
  • Echovirus
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26
Q

What is an important side effect of cocaine to the nose?

A
  • Cocaine is a potent vasoconstrictor >> ischemia
  • Can lead to perforation of the nasal mucosa with excessive use
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27
Q

What are the four paranasal sinuses?

A
  • Frontal sinus
  • Maxillary sinus
  • Ethmoid sinus
  • Sphenoid sinus

>> Infectious rhinitis for an extended period of time >> bacterial sinusitis

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28
Q

What are the presenting features of sinusitis?

A
  • Facial pain
  • Fever
  • Purulent nasal discharge

+ Nasal congestion

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29
Q

What is a common causative organism for tonsillitis?

A

Streptococcus pyogenes

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30
Q

Name two indications for tonsillectomy.

A
  • Recurrent tonsillitis
  • Obstructive sleep apnoea due to enlarged tonsils
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31
Q

What is the most common location of salivary gland tumours?

A

Parotid gland

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32
Q

What is congenital pyloric stenosis?

A

Hypertrophy of the pylorus, causing obstruction

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33
Q

What are the clinical features of congenital pyloric stenosis?

A
  • More often in firstborn males
  • Onset at ~2-6 weeks old
  • Palpable “olive” mass in epigastric region
  • Projectile vomiting
  • Visible peristalsis
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34
Q

What is extrahepatic biliary atresia?

A

Incomplete recanalization of the bile duct during the development of the bile duct

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35
Q

How does extrahepatic biliary atresia present?

A
  • Presents shortly after bith
  • Dark urine
  • Clay-coloured stools
  • Jaundice

>> Conjugated hyperbilirubinemia

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36
Q

What is the Meckel diverticulum?

A
  • Persistent remnant of the vitelline duct
  • Outpouching in the ileum
  • Can lead to ulcerations and bleeding
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37
Q

What is the rule of 2s for Meckel diverticulum?

A
  • 2% of the population
  • 2 inches long
  • 2 feet from the ileocecal valve
  • Presents in the first 2 years of life
  • May have 2 types of epithelia
    >> Gastric
    >> Pancreatic
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38
Q

What is malrotation of the midgut?

A
  • Usually in the 6th week of development, the midgut will herniate through the umbilicus and returns into the cavity in the 10th week of development to rotate around the superior mesenteric artery
  • In malrotation, the normal 270o rotation is not completed
  • Cecum and appendix lies in the upper abdomen
  • Associated with volvulus
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39
Q

What condition is malrotation of the midgut associated with?

A

Volvulus

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40
Q

What is intestinal stenosis?

A

Failure of the normal recanalization of the lumen

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41
Q

What is Hirschsprung disease?

A
  • Failure of the neural crest cells to migrate to the colon
  • No peristalsis
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42
Q

How does Hirschsprung disease present?

A
  • Usually presents in newborns
  • Constipation: failure to pass meconium
  • Abdominal distension
  • Bowel movement precipitated by digital rectal exam
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43
Q

What is anal agenesis?

A

Lack of anal opening

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44
Q

What is the pathogenesis of anal agensis?

A

Improper formation of the urorectal septum

  • Rectovesical fistula: anus to bladder
  • Rectovaginal fistula
  • Rectourethral fistula
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45
Q

What is the most common type of tracheoesophageal fistula?

A

Blind upper esophageal pouch witht e lower esophagus joined to the trachea

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46
Q

How does tracheoesophageal fistula present?

A
  • Drooling
  • Choking
  • Vomiting
    >>> Upon first feeding
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47
Q

How can TE fistula be diagnosed?

A

Failure to pass nasogastric tube into the stomach

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48
Q

What are the differences between an omphalocele and gastrochisis?

A
  • *Omphalocele**
  • Contents covered in a sac of peritoneum and amnion
  • Liver is often protruding
  • Other abnormalities common (in 50%)
  • *Gastrochisis**
  • Contents NOT covered with sac
  • Usually lateral to the umbilicus (R>L)
  • Liver is NEVER found protruding
  • Other abnormalities seen in 10-15%
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49
Q

What is the muscular composition of the esophagus?

A
  • Upper third: skeletal muscle
  • Middle third: skeletal and smooth muscle mixture
  • Lower third: smooth muscle
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50
Q

What is the pathophysiology of achalasia?

A

Failure of relaxation of LES due to the loss of Auerbach’s/myenteric plexus >>
UNCOORDINATED PERISTALSIS

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51
Q

How does achalasia present?

A

Dysphagia of BOTH solids and liquids

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52
Q

What is the characteristic sign for achalasia on barium swallow?

A

“Bird’s beak appearance”: dilated distal esophagus with an area of distal stenosis

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53
Q

What disease can achalasia be secondary to?

A

Chagas disease

(Infection by Trypanosoma cruzi)

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54
Q

What are the features of Chagas disease?

A
  • Cardiomegaly
  • Mega-esophagus
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55
Q

What is CREST syndrome?

A

CREST

  • Calcinosis
  • Raynaud’s phenomenon
  • Esophageal dysmotility: low pressure proximal to LES
  • Sclerodactyly
  • Telangiectasia
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56
Q

What are the presenting features of esophageal variceal bleeding?

A
  • Hematemesis
  • Associated with:
    >> Portal hypertension
    >> Caput medusa
    >> Ascites
    >> Alcoholic cirrhosis
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57
Q

What is Boerhaave syndrome?

A

Transmural rupture of the esophagus caused by severe retching >> SURGICAL EMERGENCY

Made lead to left pneumothorax

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58
Q

What is Mallory-Weiss syndrome?

A

Laceration of gastroesophageal junction caused by retching; less serious than Boerhaave syndrome

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59
Q

In what patient population is Mallory-Weiss syndrome more common?

A
  • Alcoholics
  • Bulimics
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60
Q

What are the presenting symptoms of GERD?

A
  • Heartburn
  • Regurgitation upon lying down
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61
Q

What are some associated symptoms with GERD?

A
  • Nocturnal cough and dyspnea
  • Adult-onset asthma
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62
Q

What is the treatment for GERD?

A
  • H2R blockers
  • Proton pump inhibitors
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63
Q

What condition is chronic GERD associated with?

A

Barrett esophagus

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64
Q

What is Barrett esophagus?

A

Metaplasia in the cells of the lower esophagus (squamous epithelium >> columnar epithelium and goblet cells)

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65
Q

What disease is Barrett esophagus associated wtih?

A

>> GERD
>> Esophageal adenocarcinoma

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66
Q

What is a hiatal hernia?

A

When the stomach herniates upward into the thorax through the esophageal hiatus of the diaphragm

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67
Q

What are the two types of hiatal hernias? Which one is more common?

A
  • Sliding hiatal hernia
    >> More common
    >> GE junction is displaced upwards into the thorax
    >> GEJ “slides” up to the thorax
    >> “Hour-glass” stomach
  • Paraesophageal/Rolling hiatal hernia
    >> GE junction remains at its original position
    >> Fundus is displaced upwards into the thorax
    >> Fundus ends up lying next to the GEJ
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68
Q

What are the presenting features of Plummer-Vinson syndrome?

A

Presentation triad

  1. Dysphagia due to esophageal webs
  2. Iron deficiency
  3. Glossitis
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69
Q

Name the esophageal pathology.

Specialized columnar epithelium seen in a biopsy from distal esophagus

A

Barrett’s esophagus

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70
Q

Name the esophageal pathology.

Biopsy of a patient with esophagitis reveals large pink intranucelar inclusions and host cell chromatin that is pushed to the edge of the nucleus

A

HSV esophagitis

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71
Q

Name the esophageal pathology.

Biopsy of a patient with esophagitis reveals enlarged cells, intranuclear and cytoplasmic inclusions and a clear perinuclear halo

A

CMV esophagitis

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72
Q

Name the esophageal lesion.

An esophageal biopsy reveals a lack of ganglion cells between the inner and outer muscular layers

A

Achalasia

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73
Q

Name the esophageal lesion.

Protrusion of the mucosa in the upper esophagus

A

Plummer-Vinson Syndrome (esophageal webs)

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74
Q

Name the esophageal pathology.

Outpouching of all layers of the esophagus found just above the LES

A

Epiphrenic diverticulum

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75
Q

Name the esophageal pathology.

Goblet cells seen in the distal esophagus

A

Barrett’s esophagus

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76
Q

Name the esophageal pathology.

A PAS stain on a biopsy obtained from a patient wtih esophagitis reveals hyphate organism

A

Candida esophagitis

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77
Q

Name the esophageal pathology.

Esophageal pouch found in the upper esophagus

A

Zenker diverticulum

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78
Q

What are the risk factors for esophageal adenocarcinoma?

A
  • GERD
  • Barrett esophagus
  • Smoking
  • Obesity
  • Nitrosamines
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79
Q

What is the most common esophageal cancer worldwide?

A

Esophageal squamous cell carcinoma

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80
Q

What is the most common esophageal cancer in the US?

A

Esophgeal adenocarcinoma

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81
Q

What are the risk factors for esophageal cancer?

A

AABCDEFFGH

  • Achalasia
  • Alcohol
  • Barrett’s esophagus
  • Cigarettes
  • Diverticula
  • Esophageal webs
  • Fat (Obesity)
  • Familial
  • GERD
  • Hot liquids
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82
Q

What structures does the celiac trunk supply?

A
  • Pharynx to the proximal duodenum
  • Liver
  • Gallbladder
  • Pancreas
  • Spleen (not derived from the foregut, a mesodermal structure)
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83
Q

What structures does the superior mesenteric artery supply?

A

Distal duodenum to the proximal 2/3rds of the transverse colon

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84
Q

What structures does the inferior mesenteric artery supply?

A

Distal 1/3rd of the transverse colon to the upper portion of the rectum

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85
Q

What are the main branches of the abdominal aorta in sequence from high to low?

A

>> Inferior phrenic artery
>> Suprarenal arteries
>> Median sacral artery

  1. Celiac trunk
  2. Superior mesenteric artery
  3. Left and right renal arteries
  4. Left and right gonadal arteries
  5. Inferior mesenteric artery
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86
Q

What are the three main branches of the celiac trunk?

A
  1. Common hepatic artery
  2. Splenic artery
  3. Left gastric artery
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87
Q

What are the three branches of the common hepatic artery?

A
  • Hepatic artery proper
  • Gastroduodenal artery
  • Right gastric artery
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88
Q

What are the branches of the gastroduodenal artery?

A
  • Right gastroepiloic artery/right gastro-omental artery
  • Anterior superior pancreaticoduodenal artery
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89
Q

What are the branches of the splenic artery?

A
  • Splenic artery continues to the spleen
  • Short gastric arteries
  • Left gastroepiploic artery/left gastro-omental artery
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90
Q

Name the four sites of important collateral circulatory arterial anastomoses in the gastrointestinal tract.

A
  1. Superior epigastric (internal thoracic artery) and inferior epigastric (external iliac)
  2. Superior pancreaticoduodenal (celiac trunk) and inferior pancreaticoduodenal (superior mesenteric artery)
  3. Middle colic (superior mesenteric artery) and left colic (inferior mesenteric artery)
  4. Superior rectal (inferior mesenteric artery) and inferior rectal (internal iliac)
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91
Q

What are the sites of anatomoses in the gastric circulation?

A
  1. Left gastroepiploic artery (splenic artery) and right gastroepiploic artery (gastroduodenal/common hepatic artery)
  2. Left gastric artery and right gastric artery (common hepatic artery)
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92
Q

What are the cells found in the stomach?

A
  • Parietal cells
    >> Hydrochloric acid
    >> Intrinsic factor
  • Chief cells
    >> Pepsinogen
  • Mucosal cells
    >> Mucin
    >> Bicarbonate
  • G cells
    >> Gastrin
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93
Q

What are the effects of gastrin?

A
  • Stimulates acid secretion
  • Stimulates growth of the gastric mucosa
  • Stimulates gastric motility
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94
Q

What stimulates gastrin secretion?

A
  1. Phenylalanine
  2. Tryptophan
  3. Calcium
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95
Q

How does gastrin promote acid secretion?

A
  1. Direct stimulation of the parietal cells
  2. Primary action: stimulates enterochromaffin-like cells (ECL cells), which then stimulates the parietal cells to secrete acid by releasing histamine
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96
Q

What stimulates gastric acid secretion?

A
  • Acetylcholine (M3R by vagus nerve)
  • Histamine (mainly by enterochromaffin-like cells/ECL cells)
  • Gastrin (by G-cells in the antrum)
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97
Q

What inhibits gastric acid secretion?

A
  • Somatostatin
  • GIP (gastric inhibitory polypeptide)
  • Secretin
  • Prostaglandins
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98
Q

What stimulates bicarbonate secretion?

A

Secretin

Prostaglandins
(Mainly induces mucin secretion, also increases bicarbonate secretion)

(Pancreatic and biliary secretion)

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99
Q

What cells in the body secretes HCO3-?

A
  • Mucosal cells in the stomach
  • Brunnner glands in the duodenum
  • Pancreatic ductal cells
  • Salivary glands
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100
Q

What is Zollinger-Ellison Syndrome?

A

Gastrin-secreting tumour (gastrinoma) in the duodenum or pancreas

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101
Q

How does Zollinger-Ellison Syndrome present?

A
  • Recurrent duodenal (and jejunal ulcers)
  • Due to acid hypersecretion
  • Abdominal pain
  • Diarrhea (malabsorption)

>> May be associated with MEN-1

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102
Q

What receptors found on gastric parietal cells regulate acid secretion?

A
  • M3 ACh receptors
  • H2 receptors
  • CCKB receptors (for gastrin)
  • Prostaglandin/misoprostal receptors
  • Somatostatin receptors
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103
Q

What is the treatment for Zollinger-Ellison Syndrome?

A
  • Proton pump inhibitors
  • Octreotide if octreotide receptors are present on the gastrinoma
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104
Q

What happens to serum pH at the time of gastric acid secretion?

A

Increases

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105
Q

What are the risks for malignancy in leukoplakia and erythroplakia?

A
  • Leukoplakia = 30% rate of progression to oral cancer
  • Erythroplakia = 60% rate of progression to oral cancer

>> Remember these lesions do NOT wipe off
>> Both are due to squamous hyperplasia of the epidermis

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106
Q

What are the possible causes of leuko/erythroplakia (i.e. what are the risk factors for oral cancer)?

A
  • Chronic irritation (e.g. dentures)
  • Smoking
  • Alcohol abuse
  • Human papillomavirus (HPV)
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107
Q

What is the histological appearance of Warthin’s tumour?

A

Cystic glandular structures with hetertrophic salivary tissue trapped within benign lymphoid tissue

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108
Q

What are the possible causes of dysphagia for solids AND liquids?

A
  • Oropharyngeal dysphagia: striated muscle dysmotility
    >> Dermatomyositis
    >> Myasthenia gravis
    >> Stroke
  • Lower esophageal dysphagia: smooth muscle dysmotility
    >> Systemic sclerosis
    >> CREST syndrome
    >> Achalasia
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109
Q

What is the VATER syndrome?

A
  • Vertebral abnormalities
  • Anal atresia
  • Tracheoesophageal fistula
  • Renal disease
  • Absent Radius
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110
Q

What are the conditions associated with hiatal hernia?

A
  • Sigmoid diverticulosis
  • Esophagitis
  • Duodenal ulcers
  • Gallstones
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111
Q

What are the risk factors for GERD?

A
  • Smoking
  • Alcohol
  • Caffeine, fatty foods, chocolate
  • Pregnancy
  • Obesity
  • Hiatal hernia
112
Q

What are the possible causes of infectious esophagitis?

A
  • CMV: basophilic intranuclear inclusions
  • HSV: multinucleated squamous cells with intranuclear inclusions
  • Candida: yeast and pseudohyphae

>> Usually a complication of AIDS

113
Q

What are some modes of treatment for esophageal varices?

A

Pharmacological

  • Isosorbide and beta-blockers
  • Octreotide drip IV for bleeding

Procedural

  • TIPS (transjugular intrahepatic portasystemic shunt)
  • Endoscopic ligation
  • Endoscopic sclerotherapy
  • Open surgery with stapling
114
Q

What is the treatment for achalasia?

A

Nonpharmacologic

  • Pneumatic dilation
  • Esophagomyotomy

Pharmacologic (short term)

  • Long-acting nitrates
  • Calcium-channel blockers
  • Botulinum toxin injection
115
Q

What is the most common benign tumour of esophagus?

116
Q

What is the difference between erosions and ulcers?

A
  • Erosion: breach in the epithelium of the mucosa
  • Ulcer: breach in the mucosa with the extension into the submucosa or deeper
117
Q

What are the possible causes of acute gastritis?

A

Oversecretion of gastric acid
- Brain injury: Cushing ulcer

Failure of the gastric mucosal barrier

  • NSAIDs and aspirin
  • Alcohol
  • Burns: Curling ulcer
  • Helicobacter pylori

+ Uremia
+ Anisakis: worm associated with eating raw fish

118
Q

What cancers does H. pylori infection increase the risk for?

A
  • MALT lymphoma
  • Gastric cancer
119
Q

What are the two types of chronic atrophic gastritis?

A
  1. Type A
    >> Due to pernicious anemia
    >> Involves the body and the fundus
  2. Type B
    >> Due to H. pylori infection
    >> Involves the antrum and pylorus
120
Q

Name the upper GI pathology.

Stomach biopsy reveals neutrophils above the basement membrane, loss of surface epithelium and fibrin-containing purulent exudate

A

Acute gastritis

121
Q

Name the upper GI pathology.

Stomach biopsy reveals lymphoid aggregates in the lamina propria, columnar absorptive cells and atrophy of glandular structures

A

Chronic gastritis

122
Q

Name the upper GI pathology.

Diffuse thickening of gastric folds, elevated serum gastrin levels, biopsy reveals glandular hyperplasia without foveolar hyperplasia.

A

Zollinger-Ellison syndrome

123
Q

What is the pathophysiology of peptic ulcer disease?

A

Gastric acid erodes through mucosa into submucosal tissue

  • 70% due to H. pylori infection: gastric ulcer
  • 90-95% due to H. pylori infection: duodenal ulcer
  • NSAIDs/Aspirin
  • Duodenal ulcers can also be caused by Zollinger-Ellison Syndrome (rare)
124
Q

How will gastric ulcers present?

A
  • Upper abdominal and epigastric pain after eating
  • Weight loss: it hurts when they eat!
125
Q

How will duodenal ulcers present?

A
  • Pain relieved by eating
  • Pain returns several hours after eating
  • Weight gain
126
Q

What are the morphological and histological characteristics of duodenal ulcers?

A
  • Gross/endoscopic apearance: clean, smooth borders
  • Histological appearance
    >> H. pylori organisms
    >> Hypertrophy of Brunner glands
127
Q

What are the complications of PUD?

A
  • Pain
  • Weight loss or weight gain
  • Hemorrhage (treat with octreotide)
  • Perforation
128
Q

What is the triple therapy for H. pylori eradication?

A
  • Amoxicillin/Metronidazole
  • Clarithromycin
  • Proton pump inhibitors
129
Q

What is the quadruple therapy for H. pylori eradiation? What is the common indication for quadruple therapy (VS. triple therapy)?

A

Indication: when H. pylori is resistant towards clarithromycin

  • Proton pump inhibitor
  • Bismuth
  • Metronidazole
  • Tetracycline
130
Q

What are the commonly-used antacids? Name three.

A
  • Calcium carbonate
  • Magensium hydroxide
  • Aluminum hydroxide
131
Q

What are the side effects of calcium carbonate?

A

HYPERCALCEMIA

  • Stimulates G-cells to produce gastrin
  • Remember that gatrin production is stimulated by:
    >> Phenylalanine
    >> Tryptophan
    >> Calcium
  • Rebound excessive acid
132
Q

What are the side effects of magnesium hydroxide?

A
  • Diarrhea
  • Hypokalemia (from diarrhea)
  • Hyporeflexia
  • Hypotension
  • Cardiac arrest

>> Usually from IV magnesium

133
Q

What are the other indications of magnesium hydroxide (other than as an antacid)?

A
  • IV for pediatric asthmatics
  • Prophylaxis of eclampsia
  • Tocolysis
134
Q

What are the side effects of aluminum hydroxide?

A
  • Constipation
  • Hypophosphatemia
  • Proximal muscle weakness
  • Osteodystrophy
  • Seizures
135
Q

What are the side effects of cimetidine?

A
  • P450 inhibition: drug interactions
  • Anti-androgenic effects
    >> Gynecomastia
    >> Decreased libido
    >> Impotence
  • Crosses placenta and blood-brain barrier
  • Decreases methemoglobin levels
  • Decreases renal creatinine secretion
  • Thrombocytopenia (as a class effect)
136
Q

What are the side effects of proton pump inhibitors?

A
  • Increased risk for C. difficile infection
  • Increased risk for pneumonia
  • Hip fractures
  • Hypomagnesemia in chronic use
137
Q

What are the drugs that can cause gynecomastia?

A

STACKED + heroin/marijuana

  • Spironolactone
  • Testosterone
  • Alcohol
  • Cimetidine
  • Ketoconazole
  • Estrogen
  • Digitalis/Digoxin

+ HEROIN
+ MARIJUANA

138
Q

What is an important contraindication for misoprostol?

A

Pregnant women >> induces abortion

139
Q

What is Menetrier disease?

A

Gastric hypertrophy (so severe it looks like brain gyri)

  • Parietal cell atrophy >> decreased acid production
  • Enteric protein malabsorption and loss >> hypoalbuminemia >> edema

Precancerous: precusor to gastric adenoCA

140
Q

What are the risk factors for gastric intestinal adenocarcinoma?

A
  • H. pylori infection
  • Chronic gastritis
  • Nitrosamines (smoked food)
  • Cigarrette smoking
  • Achlorhydia
  • Males >50 years

>> Japanese people in Japan!

141
Q

What is a cutaneous feature associated with gastric adenocarcinoma?

A

Acanthosis nigricans

>> Other visceral malignancies
>> Insulin resistance

142
Q

What is the gross and histological characteristics of diffuse gastric adenocarcinoma?

A
  • Gross: linitis plastica
  • Histological: signet ring cells
143
Q

What are the conditions associated with signet ring cells?

A
  • Gastric adenocarcinoma
  • Krukenberg tumours
  • Lobular carcinoma (LCIS/invasive lobular CA)
144
Q

What are the classical presenting features of pyloric stenosis?

A
  • Presents 2-6 weeks of age
  • Non-bilious projectile vomiting
  • Visible peristalsis
  • Palpable olive mass in epigastric area

>> Most common condition requiring surgery in the first month of life

145
Q

What is the mechanism of odansetron?

A

5HT3 receptor antagonist

146
Q

What are the indications for odansetron?

A
  • Chemotherapy anti-emesis
  • Post-op nausea and vomiting
  • Pregnancy
147
Q

What are the side effects of odansetron?

A
  • Vasodilation
  • Headache
  • Constipation
148
Q

What are the presenting signs of duodenal atresia?

A
  • Usually in a newborn
  • Early bilious vomiting (VS. nonbilious vomiting in pyloric stnoesis)
149
Q

What is the characteristic X-ray sign seen in duodenal atresia?

A

Double-bubble sign

150
Q

What syndrome is associated with duodenal atresia?

A

Down syndrome

151
Q

What can obstruct the Ampulla of Vater?

A
  • Biliary sludge
  • Gallstones
  • Pancreatic tumour
152
Q

Name the three hormones mainly secreted from the duodenum.

A
  • CCK (cholecystokinin)
  • Secretin
  • Gastric inhibitory peptide (GIP)
153
Q

What cells secrete CCK?

A

I cells of the duodenum and jejunum

154
Q

What is the action of CCK?

A
  • Increase sphinctor of Oddi relaxation
  • Increase pancreatic secretion
  • Increase gallbladder contraction
  • Decrease gastric emptying
155
Q

What cells secrete secretin?

A

S cells of the duodenum

156
Q

What is the action of secretin?

A
  • Increase pancreatic HCO3- secretion
  • Increase bile secretion
  • Decrease gastric acid secretion
157
Q

What cells secrete GIP (gastric inhibitory peptide/glucose-dependent insulinotropic peptide)?

A

K cells of the duodenum and jejunum

158
Q

What is the action of GIP?

A
  • Exocrine: decrease gastric H+ secretion
  • Endocrine: increase insulin release
159
Q

What cells secrete somatostatin?

A

D-cells (d for decrease) throughout the GI tract and delta cells of the pancreatic islets

160
Q

What is the action of somatostatin?

A

Anti-hormone hormone

Decrease release of:

  • Gastrin
  • Secretin
  • CCK
  • GIP
  • VIP
  • Insulin
  • Glucagon
161
Q

What cells secrete VIP (vasoactive intestinal peptide)?

A
  • Smooth muscle cells of the gut
  • Parasympathetic ganglia
  • Enteric nervous system
162
Q

What is the action of VIP?

A
  • Increase relaxation of intestinal smooth muscle and sphincters
  • Increase water and electroyte secretion in the gut

>> Excess VIP causes cholera-like excessive/copious watery diarrhea

163
Q

What cells secretion motilin?

A

Small intestinal cells

164
Q

What is the action of motilin?

A

Produces migratory motor complexes (MMCs) to promote massive peristalsis during fasting

165
Q

What substances can accentuate the action of motilin?

A

Motilin receptor agonists – macrolides

166
Q

What are the drugs that are pro-kinetic and can treat ileus (e.g. post-op ileus)?

A

Increase ACh action (parasympathetic: rest and digest)

  • Cholinergic agonists: bethanachol
  • Cholinesterase antagonists: neostigmine

Increase 5HT or decrease dopamine action
- Metoclopramide
>> 5HT4 receptor agonist
>> D2 receptor antagonist
>> Often used to treat diabetic gastroparesis
>> Side effects include seizures

Increase motilin action
- Macrolides
>> Erythromycin, clarithromycin etc.
>> Stimulate smooth muscle motilin receptors

167
Q

What is the function of Brunner glands?

A

Secrete alkaline mucus

168
Q

Where are Brunner glands found?

A

Duodenum ONLY

169
Q

What condition is associated with hypertrophy of Brunner glands?

A

Peptic ulcer disease (esp. duodenal ulcer)

170
Q

Name the retroperitoneal structures.

A

A DUCK PEAR

  • Adrenal glands
  • Duodenum
  • Ureter
  • Colon: ascending and descending
  • Kidneys
  • Pancreas: except the tail
  • Esophagus: abdominal part beyond the diaphragm
  • Aorta
  • Rectum
171
Q

Which ligaments are excised in splenectomy?

A
  • Gastrosplenic ligament
  • Splenorenal ligament
172
Q

Which ligament can be passed through or excised to reach the lesser sac of the abdomen?

A

Gastrohepatic ligament

173
Q

Which ligament can be clamped to stop bleeding from the proper hepatic artery or portal vein?

A

Hepatoduodenal ligament

174
Q

Name the pathology.

Small intestinal mucosa laden with distended macrophages in the lamina propria, which are filled with PAS(+) granules and rod-shaped bacilli seen by electron microscopy

A

Whipple disease

175
Q

Name the pathology.

Defect in chylomicron exportation

A

Abetalipoproteinemia

176
Q

Name the pathology.

Cramping associated with milk products

A

Lactase deficiency

177
Q

Name the pathology.

Weight loss, diarrhea, fever, adenopathy, hyperpigmentation, cardiac symptoms, arthralgias, and neurological symptoms

A

Whipple disease

CAN

  • Cardiac symptoms
  • Arthralgia
  • Neurological symptoms
    + Hyperpigmentation
178
Q

What are the possible causes of pancreatic insufficiency?

A
  • Cystic fibrosis
  • Chronic pancreatitis
  • Obstructing lesions such as cancer
179
Q

What antibodies are found in celiac sprue?

A
  • Anti-gliadin antibodies
  • Anti-tissue transglutaminase antibodies
  • Anti-endomysial antibodies
180
Q

Which organism is associated with Whipple disease?

A

Tropheryma whipplei

181
Q

Which genes are associated with celiac sprue?

A

HLA-DQ2 and HLA-DQ8

182
Q

Patients with celiac sprue are at increased risk of developing which cancers?

A
  • T-cell lymphoma
  • GI cancer
  • Breast cancer
183
Q

What is a positive lactose tolerance test for lactase deficiency?

A
  • Administation of lactose produces symptoms
  • Glucose rises <20mg/dL
184
Q

What is the pathophysiology of abetalipoproteinemia?

A

Inability to synthesize apoB lipoproteins (e.g. Apo-B48, Apo-B100) >> unable to make chylomicrons, VLDL or LDL >> accumulation of lipids in enterocytes

185
Q

What are the presenting features of abetalipoproteinemia?

A
  • Steatorrhea
  • Stunted growth
  • Failure to thrive
  • Ataxia
  • Night blindness
  • Acanthocytosis
186
Q

Where is iron absorbed?

187
Q

What conditions will decrease iron absorption?

A

Decreased acidity

  • Antacids
  • Quinolones, tetracyclines
  • Cereal, fibre, tea, coffee, eggs, milk
  • Gastric bypass surgery
188
Q

What conditions will decrease folate absorption?

A
  • Poor nutrition
  • Alcoholism
  • Goat’s milk in children
189
Q

Where is folate primarily absorbed?

A
  • Duodenum
  • Jejunum
190
Q

What conditions will decrease B12 absorption?

A
  • Autoimmune destruction of parietal cells >> decreased amount of intrinsic factor >> pernicious anemia
191
Q

Where is B12 absorbed?

192
Q

How does irritable bowel syndrome (IBS) present?

A
  • Chronic abdominal pain
    >> Crampy
    >> Improves with defecation
  • Altered bowel habits
    >> Diarrhea
    >> Constipation
    >> Alternating diarrhea and constipation
  • Other GI symptoms: GERD, dysphagia, early satiety, nausea and chest pain
  • Non-GI symtpoms: urinary frequency and urgency, dysmenorrhea, dyspareunia and fibromyalgia
193
Q

What is the treatment for IBS?

A
  • Dietary modification
  • Fibre supplement
  • Antispasmotics: dicyclomine, hyoscyamine
  • Antidepressants: TCA, SSRI
  • Guanylate cyclase agonists, especially for IBS with constipation
194
Q

What embryological structure is Meckel’s diverticulum derived from?

A

Vitelline duct

195
Q

How is Meckel’s diverticulum diagnosed (without OT)?

A

Technetium scintigraphy for uptake by ectopic gastric mucosa

196
Q

What site is most common for intussusception?

A

Ileocecal junction

197
Q

How does intussusception present?

A
  • Intermittent severe abdominal pain
  • Current jelly stools

>> The most common abdominal emergency in children <2 years of age

198
Q

What are the most common causes of intussusception, espeically in children?

A
  • 75% idiopathic
  • 25% causes known
    >> Adenovirus infection
    >> Meckel’s diverticulum
199
Q

What are the common causes of small bowel obstruction?

A

ABC

  • Adhesions, especially from previous surgeries
  • Bulge/hernia
  • Cancer/tumours

+ Intussusception
+ Volvulus
+ Crohn’s disease
+ Gallstone ileus
+ Bezoar
+ Bowel wall hematoma from trauma
+ Inflammatory stricture
+ Congenital malformation
+ Radiation enteritis

200
Q

What are the most common causes of meconium ileus?

A
  • Cystic fibrosis
  • Hirschsprung disease
201
Q

What are the classical radiograph findings in necrotizing enterocolitis?

A
  • Distended bowel with air
  • Paucity of gas
  • Pneumatosis intestinalis
  • Aerobilia
  • Free gas in the abdomen in case of perforation
202
Q

What is a defining feature in the presentation of ischemic colitis?

A

Pain out of proportionally severe compared to physical examination findings

203
Q

What are the presenting features of carcinoid tumours/syndrome?

A

BFDR

  • Bronchospasm
  • Flushing
  • Diarrhea
  • Right heart murmurs
204
Q

What are the GI problems associated with Down syndrome?

A
  • Duodenal atresia
  • Hirschsprung disease
  • Annular pancreas
  • Celiac disease
205
Q

Where does volvulus most commonly occur?

A
  • Cecum
  • Sigmoid colon

>> A twisting of the gut on its own mesentery

206
Q

Where does angiodysplasia most commonly occur?

A
  • Terminal ileum
  • Cecum
  • Ascending colon
207
Q

What is the most abundant bacterium in the large bowel?

A

Bacteroides fragilis

208
Q

What are the normal gut flora?

A
  • Bacteroides fragilis
  • Escherichia coli
  • Klebsiella pneumoniae
  • Salmonella
  • Shigella
  • Proteus mirabilis
  • Proteus vulgaris
209
Q

What are the risk factors for colon cancer?

A
  • Genetic mutations
    >> APC
    >> K-RAS
    >> Loss of p53
  • Inflammatory bowel disease (IBD)
  • Villous adenoma
  • Smoking
  • Alcohol
  • High-fat, low-fibre diet
  • Obesity
210
Q

What are the presenting features of carcinoid syndrome?

A

BFDR

  • Bronchospasm
  • Flushing
  • Diarrhoea
  • Right-sided heart murmurs
211
Q

What are the associated conditions found in infants presenting with annular pancreas?

A
  • Polyhydramnios
  • Down syndrome
  • Esophageal/duodenal atresia
  • Imperforate anus
  • Meckel diverticulum
212
Q

What is the most common presenting feature of annular pancreas?

A

Two-thirds of patients remain asymptomatic throughout their life

213
Q

What hormones stimulate pancreatic secretions?

A
  • CCK
  • CNX
  • Secretin – for bicarbonate secretion
214
Q

What is the mode of inheritance of cystic fibrosis?

A

Autosomal recessive >> CFTR gene on chromosome 7 – Phe508 deletion

215
Q

What are the causes of acute pancreatitis?

A

GET SMASHED

+ Idiopathic

  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune disease
  • Scorpion sting
  • Hypercalcemia, Hypertriglyceridemia
  • ERCP
  • Drugs: didanosine, zalcitabine, stavudine, protease inhibitors and sulfa drugs
216
Q

What are the possible complications of acute pancreatitis?

A
  • Multi-organ failure
  • DIC
  • Hemorrhage into the pancreas
  • Necrosis of the pancreas
  • Hypocalcemia
  • Saponification
  • Chronic pancreatitis
  • Pancreatic pseudocysts – lined with fibrous scar tissue and granulation tissue from the ongoing inflammation; filled with pancreatic juices and enzymes)
217
Q

What is the histology of a pancreatic pseudocyst?

A
  • Lined by granulation tissue and fibrous scar tissue
  • Filled with pancreatic juices and enzymes
218
Q

What are the risk factors for pancreatic cancer?

A
  • Chronic pancreatitis
  • Tobacco use
  • Diabetes
  • Age >50 years
  • Jewish-American or African-American males
219
Q

How can pancreatic cancer present?

A
  • Weight loss
  • Abdominal pain radiating to the back
  • Obstructive jaundice with an enlarged/palpable NONTENDER gallbladder – Courvoisier’s sign
  • Trousseau’s syndrome
    >> Hypercoagulability
    >> Venous thrombosis
    >> Migratory thrombophlebitis
220
Q

What is the most common location for pancreatic adenocarcinoma?

A

Head of the pancreas

221
Q

What is the rate-limiting enzyme in carbohydrate digestion?

A

Oligosaccharide hydrolases

  • Maltase
  • Isomaltase
  • Sucrase
  • Lactase
222
Q

What is the treatment for esophageal variceal bleeding?

A
  • Octreotide: analog of somatostatin
  • Propranolol/nadolol
  • Endoscopic banding of varices
  • TIPS (Transjugular intrahepatic portosystemic shunt)
223
Q

What are the three stages of alcoholic liver disease?

A
  1. Steatosis
  2. Hepatitis
  3. Cirrhosis
224
Q

What are the histological features of alcoholic hepatitis?

A
  • Swollen and necrotic hepatocytes
  • Neutrophilic infiltration
  • Mallory bodies: intracytoplasmic eosinophilic inclusions of keratin
225
Q

What is the liver enzyme profile for alcoholic hepatitis?

A

AST > ALT ration >1.5 (usually 2 or higher)

226
Q

What are the symptoms of liver cirrhosis?

A

A. Liver failure
- Coagulopathy, elevated PT and PTT
- Edema
- Ascites
- Hepatic encephalopathy
>> Confusion, delirium, hypersomnia
>> Coma and death
>> Asterixis/Liver flap
>> Fetor hepaticus
- Gynecomastia
- Testicular atrophy
- Spider naevi
- Palmar erythema
- Scleral icterus
- Jaundice
- Decreased LDL and HDL

B. Portal hypertension
- Varices: esophageal, gastric, caput medusae, anorectal varices (portosystemic shunts)
- Hepatomegaly
- Splenomegaly
- Ascites >> spontaneous bacterial peritonitis (SBP) — the ascites fluid is an excellent culture medium!
>> Diuretics
>> Paracentesis

227
Q

What are the drugs that a patient with hepatic cirrhosis may have?

A
  1. Diuretics: to get rid of ascitic fluids
  2. Beta-blockers: to prevent variceal bleeding
  3. Vitamin K: to enhance coagulation
  4. Lactulose: to trap ammonia in the gut for stool excretion and prevent hepatic encephalopathy from hyperammonemia
228
Q

What are the possible causes of an elevated ALP level?

A
  • Biliary diseases (gallstones, cancer)
  • Bone diseases
    >> Childhood – high bone turnover
    >> Paget disease
    >> Bone cancer
229
Q

What are the presenting features of Reye syndrome?

A

Hepatoencephalopathy

  • Fatty liver: microvesicular fatty change
  • Hepatomegaly
  • Hypoglycemia
  • Vomiting
  • Coma
230
Q

What is the pathophysiology of Reye syndrome?

A

Aspirin metabolites decrease beta-oxidation by reversible inhibition of mitochondrial enzymes

231
Q

What organs are affected in Wilson disease?

A
  • Liver
  • Brain
  • Cornea
  • Joints
  • Kidneys
232
Q

What are the presenting features of Wilson disease?

A
  • Decreased ceruloplasmin
  • Cirrhosis
  • Hepatocellular carcinoma
  • Hemolytic anemia
  • Basal ganglia degeneration >> Parkinsonism
  • Asterixis
  • Dementia, Dyskinesia, dysarthria
  • Kayser-Fleisher rings
  • Fanconi syndrome: proximal tubular dysfunction of the kidneys
233
Q

What is the treatment for Wilson disease?

A
  • Penicillamine
  • Trientine
234
Q

What are the presenting features of hemachromatosis?

A

The clinical triad:
1. Hepatic cirrhosis
2. Diabetes mellitus
3. Skin pigmentation
>> “Bronze diabetes”

+ Congestive heart failure
+ Testicular atrophy
+ Increased risk for HCC

235
Q

What is the mode of inheritance of primary hemachromatosis?

A

Autosomal recessive

236
Q

Describe the iron profile of a patient suffering from hemochromatosis.

A
  • Increased ferritin
  • Increased total serum iron
  • Decreased iron-binding capacity
  • Increased transferrin saturation
237
Q

What is the treatment for hemochromatosis?

A
  • Repeated phlebotomy
  • Deferoxamine or deferasirox (iron chelating agents)
238
Q

What is the mode of inheritance of alpha-1-antitrypsin?

A

Autosomal recessive

239
Q

What are the presenting features of alpha-1-antitrypsin deficiency?

A
  • Cirrhosis
  • Early-onset panacinar emphysema

>> Due to uninhibited elastase activity from misfolded alpha-1-antitrypsin’s lack of activity

240
Q

What is the histological feature of alpha-1-antitrypsin deficiency?

A

PAS (+) globules in the liver + cirrhosis

241
Q

What are the risk factors of hepatic adenoma?

A
  • OCP use (esp. women aged 20-44 years)
  • Anabolic steroid use
  • Glycogen storage diseases types I and III
242
Q

What is the treatment for hepatic adenomas?

A
  • Discontinue OCPs
  • Serial imaging monitoring
  • Serial AFP monitoring
  • Resection, especially if adenoma is >5cm
243
Q

What are the risk factors for hepatic angiosarcoma?

A
  • Vinyl chloride
  • Arsenic
244
Q

What are the risk factors for HCC?

A
  • Viral hepatitis B and C
  • Alcoholic cirrhosis
  • Carcinogen exposure: e.g. aflatoxin from Aspergillus
  • Wilson disease
  • Hemochromatosis
  • Alpha-1-antitrypsin deficiency

>> HCC can lead to Budd-Chiari syndrome

245
Q

What are the presenting features of HCC?

A
  • Jaundice
  • Tender hepatomegaly
  • Polycythemia (decreased breakdown of EPO)
  • Ascites
  • Anorexia
    >> Elevated AFP
    >> Mass/lesion on USG/Contrast CT
246
Q

What conditions are associated with Budd-Chiari syndrome?

A
  • Hepatocellular carcinoma
  • Hypercoagulable states
  • Polycythemia vera
  • Pregnancy
247
Q

What is Budd-Chiari syndrome?

A

Occlusion of IVC or hepatic veins

248
Q

What are the possible causes of hepatitis?

A
  • Viral infections
  • Chronic alcohol use
  • Toxins
  • Autoimmune causes
  • Other diseases
249
Q

What is the definition of chronic hepatitis?

A

Hepatitis lasting for more than 6 months

250
Q

What are the laboratory results for hepatitis?

A
  • Bilirubinuria
  • Increased AST and ALT
    >> AST > ALT = alcoholic hepatitis (A Scotch and Tonic)
    >> ALT > AST = viral hepatitis
  • Increased bilirubin
  • Increased ALP (alkaline phosphatase)
251
Q

What genetic material does HAV contain?

A

ssRNA (picornavirus)

252
Q

What is the route of transmission of HAV?

A

Fecal-oral

253
Q

How long is the incubation period for HAV?

254
Q

How does one diagnose HAV?

A

Serum IgM antibodies

255
Q

What genetic material does HEV contain?

A

ssRNA (hepevirus)

256
Q

What is the route of transmission of HEV?

A

Fecal-oral route

257
Q

Which virus has 20% mortality for pregnant patients?

A

HEV - E for Expectant mothers

258
Q

What genetic material does HDV contain?

A

ssRNA – DEFECTIVE/INCOMPLETE GENOME

>> Needs HBsAg to be infective

259
Q

What is the route of transmission of HDV?

A
  • Sexual
  • Parenteral
  • Transplacental
260
Q

What genetic material does HCV contain?

261
Q

What is the route of transmission of HCV?

A
  • Parenteral: IV drugs, tattoos, blood transfusion
  • Sexual
  • Transplacental
262
Q

How does one diagnose HCV?

A

Anti-HCV Antibodies

263
Q

What is the most frequent cause of transfusion-mediated hepatitis?

A

Hepatitis C

264
Q

What is the treatment for HCV?

A
  • Interferon-alpha
  • Ribavirin

>> Vaccination is NOT available for HCV (but available for HBV and HAV)

265
Q

What genetic material does HBV contain?

A

dsDNA - the only hepatitis virus that is not ssRNA

266
Q

What is a Dane particle?

A

Intact HBV particle

267
Q

What is the route of transmission?

A
  • Sexual
  • Parenteral
  • Transplacental
268
Q

How long is the incubation period for HBV?

A

60-90 days

269
Q

What is the chance for HBV(+) patients to progress into chronic hepatitis?

A
  • 10% adults
  • 80-90% if acquired as an infant or if immunocompromised
270
Q

What are the possible treatments for hepatitis B?

A
  • Interferon-alpha
  • Lamivudine
  • Telbivudine
  • Entecavir
  • Adefovir
  • Tenofovir
271
Q

Name the serological markers for HBV.

A
  • HBsAg: surface antigen indicating active disease
  • Anti-HBsAg antibody/HBsAb: indicates immunity against HBV (good!)
    >> Immunization/Vaccination
    >> Previous infection
  • HBcAg: core antigen, undetectable in serum studies
  • Anti-HBcAg antibody/HBcAb
    >> IgM: active disease
    >> IgG: chronic or previous disease
  • HBeAg: indicates active viral replication and thus high transmissibility
  • Anti-HBeAg antibody/HBeAb: low transmissibility
272
Q

When will the patient be HBsAg positive (relative to exposure)?

A

~1 month after exposure
>> The first serum marker to appear
>> Decreases and disappears at 5-6 months after exposure

273
Q

What is the window period?

A

1-2 weeks after HBsAg is undetectable and Anti-HBsAg antibodies have not yet risen to detectable levels yet (~5-6 months after exposure)

>> The stalemate period

274
Q

What are the types of autoimmune hepatitis, and what are the antibodies associated with them?

A
  • Type I autoimmune hepatitis
    >> ANA(+)
    >> Anti-smooth muscle antibody
  • Type II autoimmune hepatitis
    >> Liver/kidney microsomal antibody
    >> Liver cytosol antigen
275
Q

What antibody is associated with primary sclerosing cholangitis?

A

Up to 80% of patients with PSC have positive p-ANCA

276
Q

What conditions are associated with primary sclerosing cholangitis?

A
  • Ulcerative colitis
  • Cholangiocarcinoma
277
Q

What is the treatment for primary biliary cirrhosis?

A
  • Ursodiol
  • Liver transplant

USMLE Step 1 (14 decks)

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