Gastrointestinal and Nutrition Flashcards

1
Q

Uworld
Hereditary Hyperbillirubinemias: Pathophysiology
Describe Gilbert Syndrome:

A
  • Epidemiology: Mc inherited disorder of bilirubin metabolism
  • Pathogenesis: Decreased Hepatic UDP glucoronosyltransferase activity leading to decreased bilirubin conjugation
  • CF: Recurrent episodes of mild jaundice, provoked by stress
  • Diagnosis: Increase unconjugated bilirubin. Normal CBC, blood smear, reticulocyte count. Normal AST, ALT, ALP
  • Benign; no treatment required
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2
Q

Uworld: Bowel Obstruction; Anatomy
Vignette says pt with severe burns and recurrent bilious vomitting. CT showing significant reduction of the angle between the SMA and the Aorta. What is being impinged?

A

Transverse segment of the duodenum.
Severe burns brings a hyper metabolic state and lipolysis. The SMA is supported by mesenteric fat that normally cushions the transverse (third) segment of the duodenum.
Known as SMA syndrome.

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3
Q

What causes bilious vomitting?

A

Obstruction distal to the pancreatic outflow from the duodenal papilla, located in the descending (second) segment of the duodenum.

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4
Q

Uworld: Groin Hernias Anatomy
How many different types of groin hernias are there?

A

3; Indirect inguinal, Direct inguinal, and Femoral

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5
Q

Uworld: Groin Hernias Anatomy
Describe an Indirect inguinal hernia:

A

Classic presentation:
- Male infants
Pathophysiology:
- patent processus vaginalis
Anatomy:
- originates lateral to inferior epigastric vessels
- protrudes through the deep inguinal ring into inguinal canal
- may extend into the scrotum (following spermatic cord)

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6
Q

Uworld: Groin Hernias Anatomy
Describe an Direct inguinal hernia:

A

Classic presentation:
- older men
Pathophysiology:
- weakness of transversalis fascia
Anatomy:
- protrudes medial to the inferior epigastric vessels into Hesselbach’s triangle
- may pass through superficial inguinal ring
- no direct route into the scrotum

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7
Q

Uworld: Groin Hernias Anatomy
Describe a Femoral hernia:

A

Classic presentation:
- women
Pathophysiology:
- widening of the femoral ring
Anatomy:
- protrudes medial to the inferior epigastric vessels into Hesselbach’s triangle
- may pass through superficial inguinal ring
- no direct route into the scrotum

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8
Q

Uworld: Groin Hernias Anatomy
Describe an Femoral hernia:

A

Classic presentation:
- Women
Pathophysiology:
- widening of the femoral ring
Anatomy:
- emerges inferior to inguinal ligament
- protrudes through the femoral ring into the femoral canal

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9
Q

Uworld: Embryology:
What is the pathogenesis of Meckel Diverticulum?

A
  • Persistent vitelline (omphalomesenteric) duct
  • Often contains ectopic gastric mucosa -> intestinal ulceration and bleeding
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10
Q

Uworld: Embryology:
What is the epidemiology of Meckel Diverticulum?

A

Rule of 2’s
- presents often at age 2
- usually < 2 inches long
- location within 2 feet of ileocecal valve

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11
Q

Uworld: Embryology:
What is the clinical presentation of Meckel Diverticulum?

A
  • may be asymptomatic (incidental finding)
  • painless rectal bleeding +/- iron deficiency anemia
  • acute abdominal pain due to complications:
    – intussusception (recurrent, atypical)
    – diverticulitis (mimics appendicitis)
    – bowel obstruction, perforation (peritoneal signs)
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12
Q

Uworld: Embryology:
How do you diagnose Meckel Diverticulum?

A

Technetium-99m pertechnetate (Meckel) scan detects gastric mucosa (parietal cells)

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13
Q

Embryology: Spleen Rupture
Where does the blood supply for the spleen originate from?

A

Foregut (Splenic artery from the celiac trunk)

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14
Q

Pancreas physiology
What is the response to secretin secreted by duodenal S-cells?

A

The increase H+ concentrations ( decrease in pH ) increases pancreatic bicarbonate secretion. Pancreatic- Chloride secretions decrease compared to bicarbonate.

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15
Q

Pathology: Gastritis and Peptic Ulcers
Pt presents with burning epigastric pain, weight loss, frequent belching, and EGD reveals ulcers in the gastric antrum, what is the causal organism?

A
  • Helicobacter pylori; a curved flagellated, gram-negative rod that colonizes Tha antrum of the stomach causing gastritis and ulceration.
  • increased gastrin production via destroying somatostatin-producing D cells. No somatostatin
    -> gastrin produces -> acid secretion from parietal cells -> ulcer formation.
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16
Q

Pathology:
Describe Zollinger- Ellison syndrome:

A

Phenomena caused by a gastrin-secreting tumor in the duodenum.
- causes recurrent ulcers, abdominal pain, and diarrhea
- EGD will reveal duodenal ulcerations and hypertrophic gastric folds

17
Q

Pathology:
What are conditions associated with HIV/AIDS found in the mouth?

A
  • Hairy leukoplakia: an inflammatory condition caused by Ebstein-Barr virus
  • Oral candidiasis (thrush)
  • Herpetic stomatitis and herpes esophagitis: caused by HSV
18
Q

Pathology:
What is Lichen planus?

A

A benign lesion of the mouth and jaw that is self-limited. Classically shows Wickman striae, which are white, lace-like like patterns on top of papule or plaques. It commonly manifests on wrists, elbows, and oral mucosa and is associated with chronic Hepatitis C.

19
Q

Pathology:
What is oral candidiasis?

A

Yeast infection in the mouth; it is commonly seen in breast-feeding infants or immunocompromised hosts. Exam will show cottage-cheese like lesions.

20
Q

Pathology:
What is leukoplakia?

A

Pemalignant lesion of squamous cell hyperplasia. Can also be seen in other inflammatory conditions.
Hairy leukoplakia is distinct affecting immunocompromised pts (pre-AIDS defining condition)

21
Q

Pathology:
What is the most common oral cancer?
What are its risks factors?

A

Squamous cell carcinoma, risk factors include chronic cigarette and alcohol use.

22
Q

Pathology:
For SCC, how does it present, how would you diagnose. how would you treat, and what is the prognosis?

A
  • presents with persistent papule, plaques. erosions, and ulcers
  • biopsy with TNM staging
  • treat with surgery, radiation, and chemotherapy, depending on stage
  • prognosis related to stage; often diagnosed at late stage and recurs, even if caught early.
23
Q

Pathology:
For Melanoma, how does it present, how would you diagnose. how would you treat, and what is the prognosis?

A
  • presents with oral lesion with asymmetry, irregular borders, color changes, increasing diameter
  • diagnosis via biopsy
  • treat via surgical resection with negative margins; radiation if negative margins are not obtained
  • prognosis depends on stage, including tumor thickness and ulceration
24
Q

Pathology:
For Leukoplakia, how does it present, how would you diagnose. how would you treat, and what is the prognosis?

A
  • presents with white patches or plagues on oral mucosa that cannot be scraped off
  • diagnosis vis biopsy
  • treatment is surgery, cryotherapy ablation, carbon dioxide laser ablation
  • prognosis: 1-20% of lesions progress to malignancy in 10 years
25
Q

Pathology:
For HSV-1 herpetic stomatitis, how does it present, how would you diagnose. how would you treat, and what is the prognosis?

A
  • presents with vesicular lesions with erythematous bases
  • presents with multinucleate cells on Tzanck smear
  • treat with acyclovir, pain management, and fluids
  • recurs some patients. have success with chronic suppression
26
Q

Pathology:
For aphthous ulcers, how does it present, how would you diagnose. how would you treat, and what is the prognosis?

A
  • presents with localized, shallow, round ulcers with gray bases that heal in 7- 14 days
  • presents clinically
  • tx involves symptomatic relief with oral analgesics
  • some patients have recurrent aphthous stomatitis
27
Q

Pathology:
For Oral candidiasis (thrush), how does it present, how would you diagnose. how would you treat, and what is the prognosis?

A
  • presents with white plaques that can be scraped off
  • dx via KOH prep
  • Tx is Nystatin mouthwash for 7-10 days
  • can be recurrent if pt immunocompromised
28
Q

Pathology:
For Lichen planus, how does it present, how would you diagnose. how would you treat, and what is the prognosis?

A
  • presents with Wickham stile: white, lace-like patterns on top of papule or plaques
  • dx with bx
  • tx involves symptomatic relief with topical corticosteroids
  • self-limited, can recur
29
Q

Pathology:
What is the cause/presentation, diagnosis, treatment, and prognosis for Mumps?

A
  • cause/presentation: Prarmyxovirus (parotitis, fever, myalgias, headache, anorexia, orchitis)
  • diagnosis: positive IgM mumps antibody, rise in IgG titers, isolation of mumps virus
  • Tx: symptomatic: analgesics and antipyretics
  • Prognosis: vaccination has decreased the incidence of mumps infections
30
Q

Pathology:
What is the cause/presentation, diagnosis, treatment, and prognosis for hypertrophy?

A
  • can be caused by eating disorders (bulimia), kwashiorkor, alcoholism, and metabolic disease
  • dx via clinical observation
  • tx: tx underlying
  • null prognosis
31
Q

Pathology:
What is the cause/presentation, diagnosis, treatment, and prognosis for Sialolithiasis (salivary stones)?

A
  • Cause/presentation: Submandibular glands; more common in men. Forms when saliva rich in calcium is stagnant. Some association with gout and nephrolithiasis.
  • dx: fine-needle aspiration with TNM staging bx, CT, MRI
  • Tx: benign: surgical excision. Malignant: wide margin surgical excision with or without chemo/radiation therapy.
  • prognosis: high rate of recurrence
32
Q

Pathology:
What is the hallmark of Sjögren Syndrome (Xerostomia; Keratoconjunctivitis Sicca)?

A

Abnormal lymphocytic infiltration of exocrine glands (notably the salivary and lacrimal glands) resulting in dry mouth and dry eyes.

33
Q

Pathology:
Sjögren Syndrome (Xerostomia; Keratoconjunctivitis Sicca) has an increased risk for what?

A

B-cell lymphoma, which presents as unilateral parotid swelling.

34
Q

Pathology:
How do you diagnose Sjögren Syndrome (Xerostomia; Keratoconjunctivitis Sicca)?

A
  • presence of anti-Ro/SSA or anti-La/SSB antibodies
  • Schirmer test to measure tear production
  • Rose Bengal stain to show epithelial cell damage
  • salivary gland biopsy from lip may show focal collections of lymphocytes
35
Q

Pathology:
How would you treat Sjögren Syndrome (Xerostomia; Keratoconjunctivitis Sicca)?

A
  • symptomatic: eye drops and manic acid containing compounds to stimulate saliva production
  • Good oral hygiene and dental care
  • more severe cases may require pilocarpine, a muscarininc agonist that stimulated salvation, AE includes sweating abdominal cramping, and flushing.
36
Q

Pathology:
Describe a Pleomorphic Adenoma:

A

Most common salivary gland tumor. Presents as painless, mobile mass. Benign but will recur if incompletely excised or ruptured intraoperatively.

37
Q

Pathology:
Describe Mucoepidermoid Carcinoma:

A

Most common malignant salivary gland tumor. Painless, slow growing mass with mutinous and squamous components.

38
Q

Pathology:
Describe Warthin tumor:

A

Benign, lymphocyte-rich tumor of parotid gland