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GIGU Exam 1 > Clinical Notes > Flashcards

Clinical Notes Flashcards

1
Q

What is Cryptorchid testis

A

Undescended testis (increases risk of developing cancer)

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2
Q

What is it called when there’s an open connection between tunica vaginalis and the abdomen

A

Persistent processus vaginalis

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3
Q

What is hydrocele

A

Peritoneal fluid accumulation within tunica vaginalis. More common in babies.

(When illuminated will see light glow through it)

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4
Q

What is an Hematocele

A

Accumulation of blood in the tunica vaginalis

(Opaque when illuminated)

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5
Q

Describe a direct hernia.

A
  • Bulges through weakness in tranversalis fascia in Hesselbach’s triangles and pushes directly through the fascia and bulges out due to weak abdomincal structures next to the spermatic cord (in males)
  • Medial to epigastric artery
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6
Q

Describe an indirect hernia.

A
  • Through deep inguinal ring and out superficial inguinal ring
  • Lateral to inferior epigastric vessels
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7
Q

Describe a femoral hernia.

A
  • Hernia below inguinal ligament
  • more common in women
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8
Q

What is a hiatal hernia

A

Protrusion of part of the stomach into mediastinum through the esophageal hiatus (T10) of the diagphragm.

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9
Q

Para-esophageal hiatal hernia

A

Less common form of a hiatal hernia. Cardia of the stomach is in normal position but fundus goes through the esophageal hiatus. There is no regurgitation

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10
Q

Sliding hiatal hernia

A

More common form of the hiatal hernia. Cardia and part of the fundus goes through the esophageal hiatus. There is some regurgitation

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11
Q

What can cause pancreatitits

A

Bloackage of the hepatopancreatic ampulla by gall stones. This blocks the bile duct, common hepatic duct and main pancreatic duct from releasing their product into the duodenum. This can lead to a build up of bile in the pancreas

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12
Q

What causes Esophageal Varices

A

Inflammation of the submucosal venous plexuses leads to increase pressure of the portal venous system. This causes an increase in pressure of the veins in the esophagus causing the veins of the esophagus to become enlarged and dilated.

Lecture: Histology of the Esophagus & Stomach

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13
Q

What is Gastroesophageal reflux disease (GERD)/ Acid Reflux

A

Weaking of lower esophageal sphinceter resulting in backflow of gastric contents leading to chronic inflammation, ulceration & difficulty in swallowing (dysphagia).

Lecture: Histology of the Esophagus & Stomach

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14
Q

What causes Barett’s esophagus

A

Chronic GERD causing nonkeratinized stratified squamous epithelium in transition zone to become columnar mucus-secreting/glandular epithelium in the esophagus.

Lecture: Histology of the Esophagus & Stomach

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15
Q

What is a Gastric Ulcer and where does it occur

A

Painful erosive lesions of the mucosa that may extend to deeper layers. Can occur anywhere between the lower esophagus and portions of the small intestine

Lecture: Histology of the Esophagus & Stomach

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16
Q

What can cause a Gastric Ulcer

A
  • Bacterial infections with Helicobacter pylori
  • NSAIDS effects
  • Overproduction of HCl or pepsin
  • Lowered production or secretion of mucus or bicarbonate

Lecture: Histology of the Esophagus & Stomach

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17
Q

What causes Hirschprung’s Disease?

A

Mutation of the RET gene required for migration & differention of neural crest cells leading to failure of the Enteric NS to develop in the distal colon. A lack of innervation to the distal colon prevents feaces from moving out of the colon as waste.

Lecture: Histology of Small & Large Intestine

18
Q

What are the clinical presentations of Hirschprung’s Disease

A

Constipation, poor feeding, and progressive abdominal distention. Typically diagnosed < 48 hrs after birth.

Lecture: Histology of Small & Large Intestine

19
Q

What is achalasia

A

Impaired peristalsis due to incomplete relaxation of LES during swallowing resulting in the back up of food and elevation of LES resting pressure

Lecture: Motiligy of GI System

20
Q

What causes achalasia

A
  • Decreased numbers of ganglion cells in myenteric plexus
  • Degeneration of inhibitory neurons producing NO/Vasoactive intestinal peptide that produce relaxation
  • Damage to nerves in the esophagus, preventing it from squeezing food into the stomach

Lecture: Motiligy of GI System

21
Q

What are symptoms of achalasia

A

Backflow of food in the throat (regurgitation)

Difficulty swallowing both liquids and solids (dysphagia)

heartburn

chest pain

Lecture: Motiligy of GI System

22
Q

What is Gastroesophageal reflux disease (GERD)

A

Abnormal relaxing/weakening of LES resulting in reflux of stomach contents into the esophagus leading to inflammation

Lecture: Motility of GI System

23
Q

What causes GERD

A

Motor abnormalities that result in abnormally low pressures in the LES.

Lecture: Motility of GI System

24
Q

What are symptoms of GERD

A

Heartburn and acid regurgitation

gastrointestinal bleeding

irritation of esophageal lining

scar tissue in esiphagus

Barrett’s esophagus

Lecture: Motility of GI System

25
Q

What is gastroparesis

A

Slow emptying of the stomach/paralysis of the stomach in the absecnce of mechanical obstruction

Lecture: Motility of GI System

26
Q

What are causes of gastroparesis

A

Diabetes mellitus (Type 1)

Injury to Vagus nerve

Lecture: Motility of GI System

27
Q

What are symptoms of gastroparesis

A

Nausea, vomiting, early feeling of fullness when eating, weight loss, abdominal bloating, abdominal discomfort

Lecture: Motility of GI System

28
Q

What is Hirschsprung disease

A

Low levels of VIP leads to smooth muscle constriction and loss of coordinates movement in the LI. This causes colon contents to accumulate

colon equivalent of achalasia

Lecture: Motility of GI System

29
Q

What are symptoms of Hirschsprung disease

A

Failure to pass stool. Poor feeding, vomitting, constipation, swollen belly, malnutrition.

Lecture: Motility of GI System

30
Q

Where is Vitamin B12 absorbed?

A

Distal ileum

31
Q

How does pernicious anemia occur?

A

Failure to secrete IF leading to lack of B12 absorbed

32
Q

What can lead to disruptions in the absorption of Vitamin B12?

A
  1. Gastrectomy - leads to loss of parietal cells (source of IF)
  2. Gastric bypass
33
Q

Describe Zollinger-Ellison syndrome.

A

Increased secretion of gastrin by duodenal or pancreatic tumors leading to gastrinomas

  • increased H+ and parietal cells
  • inhibition of sodium and water absorption
  • ulcers formed by increased hydrogen overwhelming bicarbonate
  • damage of intestinal epithelial cells/villi
34
Q

How can you test for Zollinger-Ellison syndrome?

A

Secretin stimulation test

-injecting secretin will lead to unexplained increase of gastrin. Under normal conditions, secretin inhibits gastrin release.

35
Q

What causes peptic ulcer disease?

A

In the U.S. Helicobacter pylori and use of NSAIDs are the predominant causes

36
Q

What are the two most common types of ulcers?

A

Gastric ulcer: defective mucosal barrier

Duodenal: increased H+ secretion rates

37
Q

How does H. pylori work?

A

1) Releases cytotoxins to breakdown mucosal barrier
2) Uses urease to convert urea to ammonia, which alkalinizes local env
3) NH4+ buildup can lead to cytotoxicity

38
Q

How does H. pylori work?

A

1) Releases cytotoxins to breakdown mucosal barrier
2) Uses urease to convert urea to ammonia, which alkalinizes local env
3) NH4+ buildup can lead to cytotoxicity

39
Q

What are the two most common types of ulcers?

A

Gastric ulcer: defective mucosal barrier

Duodenal: increased H+ secretion rates

40
Q

What causes peptic ulcer disease?

A

In the U.S. Helicobacter pylori and use of NSAIDs are the predominant causes

41
Q

Differentiation gastric vs duodenal ulcers

A

Gastric: Decresed H+ secretion = increased gastrin levels = damage to protective barrier of gastric mucosa

Duodenal: Increased H+ secretion = increased gastrin = increased parietal cell mass due to increased gastrin levels. MORE COMMON

42
Q

What is cystic fibrosis

A

Mutation in the cystic fibrosis transmembrane conductance regulator gene (CFTR) results in a defect in Cl- channels. It is associated with a deficiency of pancreatic enzymes resulting in malabsorption and steatorrhea.

HCO3-/Cl- pump can also be affected

Lecture: Secretions of the GI tract

GIGU Exam 1 (25 decks)

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