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GI II Exam II AP > Esophageal disorders (Darrow) > Flashcards

Esophageal disorders (Darrow) Flashcards

1
Q

transfer dysphagia

A

problem with food getting from mouth to esophagus.

Causes: stroke, Parkinson’s, corticobulbar problems (ALS, MS)

treat- thickening agents

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2
Q

transmit dysphagia

A

Problem getting food through the esophagus to the stomach

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3
Q

SAD CREaP

A

Solids and Liquids (motility):
1- Scleroderma

2- Achalasia (watch out for “pseudoachalasia”)

3- Diffuse esophageal spasm – “corkscrew esophagus”

CREaP (for solids only):

4- Carcinoma

5- Ring(Schatski’s)*/webs**

6- Eosinophilic esophagitis
and

7- Peptic stricture

NOTE:
*distal esophagus - associated with HH and reflux symptoms
**mid or upper esophagus – congenital, epidermolysis bullosa, GVHD, pemphigus, pemphigoid,
Plummer-Vinson syndrome

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4
Q

A 35 y/o female presents to the ER with chest “pressure” and dysphagia, having not been able to finish supper one hour ago. History is positive for asthma (allergy history) as a child. She has had intermittent food (solids only) dysphagia for three years.
An EGD is performed and a meat bolus is removed. Multiple concentric rings are seen, but the mucosa is normal. A biopsy is taken as shown.

what is the diagnosis and treatment?

A

Has to be one of the “creap”
Eosinophilic Esophagitis

-rings shown in the center of the esophagus

Symptoms: GERD to food impaction
History: allergies/atopy-peripheral eosinophilia
Mucosa: normal to tapered strictures (mucosa looks normal!!) but this doesn’t mean you shouldn’t biopsy

Biopsy: eosinophilia
> 20%/HPF (High power field)

Treatment: swallowed fluticasone (steroids**)
-PPI’s don’t work as well

know this will be on test

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5
Q

A 58 y/o Costa Rican male smoker presents with a dermatitis of the palms and soles, progressive dysphagia for solid foods and liquids ***, chest pain, cough, weight loss, and nocturnal regurgitation.

A barium swallow is ordered as follows:
-distal esohpagus - looks like a bird beak- slide 6

Skin> keratoderma or hyperkeratosis (thickening, scaling)

what are the considerations in this case:

A

The possibilities in this case would mainly consist of: SAD = Scleroderma, Achalasia or Diffuse Esophageal Spasm

The patient has no other evidence of scleroderma and the barium swallow appears to be achalasia (lots of dilation) (characterized by failure of the LES to relax completely with swallowing, and aperistalsis in the smooth muscle esophagus).

Diffuse esophageal spasm would look differentially (like a rope)

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6
Q

what is pseudoachalasia caused by:

A

Chagas disease – Reduviid or kissing bug–>
Triatomine bug and Trypanosoma cruzi
-must consider this in pt’s from costa rica, central america

Cancer

May also see achalasia like motor symptoms from amyloidosis, sarcoidosis, and neurofibromatosis

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7
Q

Chagas disease?

what symptoms does it cause

A

preferentially attacks the cardiac (dysrrhythmias, CHF, emboli) and smooth muscle (megaesophagus and megacolon).

“Pseudoachalasia” – invasion of the esophagus by trypanosoma cruzi.

Megaesophagus may simulate achalasia

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8
Q

Squamous cell carcinoma of the esophagus

Versus

Adenocarcinoma

How do you tell the difference

A

Squamous - mid esophagus with “rat tail” appearance

  • men, blacks
  • mid to lower esophagus
  • risk factors alcohol, smoking, HPV, nitrates, lye, achalasia, hot liquids, tylosis >(hyperkaratosis of palms and soles), PV syndrome

Adenocarcinoma- lower esophagus

  • barret’s
  • obesity
  • GERD
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9
Q

A 58 y/o Costa Rican male smoker presents with a dermatitis of the palms and soles, progressive dysphagia for solid foods and liquids ***, chest pain, cough, weight loss, and nocturnal regurgitation.

A barium swallow is ordered as follows:
-distal esohpagus - looks like a bird beak- slide 6
The patient subsequently has lab test showing a Hb of 9.5 gm with 55,000 platelets. Buffy coat exam is negative for T. cruzi. Iron and TIBC are low. Na is 128 meq/L with K of 3.5 meq/L. Bun is 12 meq/L with creatinine of 1 meq/L. Urinary Na is high with osmolality of 300 mOm/L (not appropriate for a low sodium)

This is what type of anemia?

Why might the platelets be low?

what is causing her low sodium?

What should be done next?

A

This is what type of anemia?
-anemia of chronic disease

Why might the platelets be low?
Low platelets due to ITP (antibodies), splenomegaly, bone marrow invasion, etc

What is causing the low sodium?
SIADH
-she is not hypovolemic, or hypervolemic, she is euvolemic

get a cxr

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10
Q

What should be done next?

Anemia of chronic disease
Low platelets due to ITP, splenomegaly, bone marrow invasion, etc
Low serum sodium from SIADH

A

CXR!

Chest Xray suggest a right mediastinal mass and CT is obtained which shows a mass encasing and constricting the right pulmonary artery. A brochoscopy and biopsy are carried out.

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11
Q

Chest Xray suggest a right mediastinal mass and CT is obtained which shows a mass encasing and constricting the right pulmonary artery. A brochoscopy and biopsy are carried out.

What do you expect the biopsy to show considering the
anemia, thrombocytopenia, SIADH, esophageal findings, and
chest Xray findings ?

A

expected to show small cell lung carcinoma

The biopsy returns showing small cell carcinoma with immunohistochemical staining showing CAM5.2 (a marker for neuroendocrine carcinomas, including small cell), thyroid transcription factor – 1 (marker for small cell lung cancer), chromogranin A (a neuroendocrine secretory protein), CD 56(NCAM/neural cell adhesion molecule) and anti Hu/ANNA-1 (anti- neuronal nuclear antibodies).

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12
Q

CAM5.2

A

marker for neuroendocrine carcinoma, including small cell

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13
Q

The biopsy returns showing small cell carcinoma with immunohistochemical staining showing CAM5.2 (a marker for neuroendocrine carcinomas, including small cell), thyroid transcription factor – 1 (marker for small cell lung cancer), chromogranin A (a neuroendocrine secretory protein), CD 56(NCAM/neural cell adhesion molecule) and anti Hu/ANNA-1 (anti- neuronal nuclear antibodies).

From these results how does one explain the esophageal findings? including dysphagia for solid food and liquids

A

The antineuronal nuclear antibodies (ANNA-1) destroy the myenteric plexus, simulating achalasia.

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14
Q

An HIV patient has stopped his HIV meds, but continues to take vitamin C, iron and NSAIDs for weakness and arthralgias.

He presents complaining of confusion, fever, cough, dyspnea, dyspepsia, odynophagia, anorexia, abdominal pain, diarrhea, blurred vision and weight loss.

He is asthenic and appears anxious and depressed. BP is 94/68.

His CD4 count is 48. Glucose is 70 mg/dL and Na is 130 meq/L. Dermatitis of the chest, thumb nail and mouth are shown:

  • folliculitis - red inflammation around hair cells
  • -Trichophyton rubrum (fungal infection) (proximal nail?)
  • -Candida

What are the most likely causes of the dysphagia and odynophagia, ie the esophagitis?

A
  1. GERD with peptic stricture
  2. pills - tetracycline
  3. infections:
    CMV (CD 4
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15
Q

An HIV patient has stopped his HIV meds, but continues to take vitamin C, iron and NSAIDs for weakness and arthralgias.

He presents complaining of confusion, fever, cough, dyspnea, dyspepsia, odynophagia, anorexia, abdominal pain, diarrhea, blurred vision and weight loss.

He is asthenic and appears anxious and depressed. BP is 94/68.

His CD4 count is 48. Glucose is 70 mg/dL and Na is 130 meq/L. Dermatitis of the chest, thumb nail and mouth are shown:

  • folliculitis - red inflammation around hair cells
  • -Trichophyton rubrum (fungal infection) (proximal nail?)
  • -Candida
The patient is taken for a barium swallow, EGD, colonoscopy as well 
as fundoscopic exam. Results are shown:
-large superficial ulcers 
-small ulcers 
-ulcerated friable mucosa

PCR is ordered and GI histology returns showing “owl eyes”. What is the diagnosis?

He may die if he is not placed on what treatment/meds?

A

CMV with retinitis, esophagitis, colitis, pneumonia and encephalitis.

The patient is started on appropriate therapy (ganciclovir), but may die if he is not placed on: (be familiar with the “As”) STEROIDS

NOTE:
You can see owl eyes similar in Hodgkin’s

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16
Q

what are the A’s involved in Addison Disease

and what infection might these A’s present?

A 
Anorexia and weight loss
Asthenia and weakness
Arterial hypotension and fatigue
Affect (flat)
Abdominal pain with N, V and D
Anxiety and personality change
Aglycemia, anatremia
Aching muscles
Apigmentation (vitiligo)
Axillary, areolar and anal pigmentation

CMV can cause Addison disease b/c CMV hits the adrenal glands

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17
Q

what are the main causes of infectious chronic gastritis ?

A

Helicobacter pylori***

H. Heilmanni

Mycobacterium, syphilis, histoplasmosis, mucormycosis, Blastomycosis, anisakiasis (raw fish or sushi)

Strongyloides, schistosomiasis, Diphyllobothrium

CMV, herpesvirus

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18
Q

what are the main causes of noninfectious chronic gastritis

A

Autoimmune**
Chemical **(NSAIDs, ASA, bile reflux)

Uremic
Crohn’s, sarcoid, Wegener’s, CGD, eosinophilic granuloma, etc.
Lymphocytic (Ceilac disease)
Eosinophilic
Radiation
GVHD
Ischemic
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19
Q

A 35 y/o female with a past history of Addisons disease presents with weakness and pallor She also complains of dyspepsia (indigestion)

PE shows a pale white female who has a dermopathy as shown (whitish patch on her lower limbs/shins)
Lab test show a Hb of 10.5 gm with an MCV of 115fL.

What is the dermopathy?

A

dermopathy:
destruction of the melanocytes by T cells and antibodies

Vitiligo with CD8+ cytotoxic T cells and
antibodies to tyrosinase; may be associated
with autoimmune thyroid disease, Addison’s***
PA, SLE, etc.

make sure to check TSH, 8 am serum cortisol (Addison’s) and other autoimmune markers!!

20
Q

A 35 y/o female with a past history of Addisons disease presents with weakness and pallor She also complains of dyspepsia.
PE shows a pale white female who has a dermopathy as shown (whitish patch on her limb)

Lab test show a Hb of 10.5 gm with an MCV of 115fL (high)

What is the D/D for macrocytosis?

A

Megaloblastic anemias ***(altered DNA synthesis, but RNA activity continues – macroovalocytosis and hypersegmeted neutrophils):
Includes B12 and folate deficiency, homocystinuria, antimetabolite drugs, AZT, hydroxyuria

Elevated reticulocyte count (hemorrhagic or hemolytic anemias as reticulocytes are 20% larger)

Alcohol (marrow effects or folate deficiency)

Liver disease (increased cell membrane phospholipid and cholesterol – also true in splenectomized patients)

Hypothyroidism (more commonly normocytic)

Myelodysplastic and myelophthisic anemias

COPD (excess cell water due to CO2 retention)

21
Q

A 35 y/o female with a past history of Addisons disease presents with weakness and pallor She also complains of dyspepsia.
PE shows a pale white female who has a dermopathy as shown (whitish patch on her limb)

Lab test show a Hb of 10.5 gm with an MCV of 115fL (high)

What lab test would you order now and what procedure should be done?

A

The lab studies confirm your impression and the peripheral smear and EGD is shown. A biopsy results in a positive urease test*.

*Testing for H pylori best with: stool antigen, 13C Urea breath test (rapid urease test during EGD where H pylori convert urea to ammonia and CO2). Should be off PPIs and antibiotics for 4 weeks prior to testing.

she has B12 deficiency b/c of destruction of parietal cells with loss of IF and its activation by HCL

22
Q

A 35 y/o female with a past history of Addisons disease presents with weakness and pallor She also complains of dyspepsia.
PE shows a pale white female who has a dermopathy as shown (whitish patch on her limb)

Lab test show a Hb of 10.5 gm with an MCV of 115fL (high)

The lab studies confirm your impression and the peripheral smear and EGD is shown. A biopsy results in a positive urease test*.

What is causing the nonerosive gastritis in this patient?
-just sloughing of the cells
Destruction of the gastric fundic mucosa with loss of parietal and zymogen (chief or
peptic) cells and resultant metaplasia (premalignant).

A

Pernicious anemia
AND
H. pylori

Depending on what of the above becomes predominant…..
this patient should be watched closely for development of
metaplasia and further evolution to adenocarcinoma, carcinoid
tumors and Malt B cell lymphoma

23
Q

Pernicious anemia

what is this disease process?
what are the findings- elevated substances?
what part of the stomach does it affect?
what can this disease lead to ?

how is this related to H. pylori?

A

this is an autoimmune gastritis

Pernicious anemia is associated with parietal cell antibodies,

achlorhydria,

gastric gland atrophy,

intestional metaplasia (probably sets the stage for adenocarcinoma*** ) –> Must make sure to follow these pt’s, get regular scopes

and hypergastrinemia (may stimulate gastric enterochromaffin cells to proliferate into carcinoid*** tumors).

mainly attacking corpus and fundus!! not so much the antrum, pt is not prone to an ulcer b/c you have knocked out the acid producing cells so the antrum responds by producing gastrin!

*H pylori (or aging) can cause B12 deficiency by destroying parietal cells with loss of IF and its
activation by HCl

24
Q

what are the gastric effects of H. Pylori?

A

74% - mild diffuse pangastritis (acute or chronic)

15% - antral gastritis (duodenal ulcers)

1% - fundic and corpus gastritis (atrophic gastritis, gastric ulcers, metaplasia, adenocarcinoma, and MALT **lymphoma)
-this is the worst prognosis!!

25
Q

A 66 y/o female has been on a respirator for 48 hours in the ICU for a severe pneumococcal pneumonia. Her “CURB 65” was 5 points upon admission through the ER. History is positive for chronic alcoholism and NSAID use. NG tube drainage is becoming “coffee ground” in appearance, despite a famotidine drip.

What are the causes of erosive, hemorrhagic gastritis?

A

Erosive, hemorrhagic gastritis

DASH:
Drugs:(NSAID- especially COX-1),

Alcohol

Stress

Portal Hypertensive Gastropathy

26
Q

A 66 y/o female has been on a respirator for 48 hours in the ICU for a severe pneumococcal pneumonia. Her “CURB 65” was 5 points upon admission through the ER. History is positive for chronic alcoholism and NSAID use. NG tube drainage is becoming “coffee ground” in appearance, despite a famotidine drip.

  1. What criteria are used to determine prophylaxis for stress gastritis?
  2. Why was not the famotidine successful in avoiding erosive gastritis in this patient?
A
  1. Respiratory failure***, especially on a respirator.

Platelets 1.5***
-she is already showing signs of bleeding with coffee ground coming out of her NG tube

  1. Recent NSAID use and alcohol status- these predisposed her to hemorrhagic gastritis
27
Q

what are the causes of stress gastritis

A 
Mechanical ventilation*** (> 48 hrs)
Trauma
Burns
Shock
Sepsis
Liver and kidney disease
CNS injury
Multiorgan failure
Coagulopathy*** (platelets < 50,000; 
INR > 1.5)
28
Q

prophylaxis and treatment for bleeding in stress gastritis ?

A

Prophylaxis: enteral feeding, H2 blockers,
Sucralfate suspension.

Bleeding: PPIs (esomeprazole)

29
Q

A 46 y/o male presents with complaints of nausea, vomiting, post prandial epigastric pain, weight loss, diarrhea, and pedal edema. History is positive for prior treatment for an alleged H. pylori infection. He admits to 2 high balls per day. History is negative for malnutrition, nephrotic syndrome, and chronic liver disease.
Blood test show a Hb of 12 gm with albumin of 2.1 gm/dL (3.5-5.2).
EGD and barium swallow are shown. slide 45
-Barium swallow
-Endoscopy

What causes low albumin?

A

A gastrointestinal disorder should be considered the cause of hypoalbuminemia after malnutrition, nephrotic syndrome, and chronic liver disease are excluded.

The diagnostic workup can then be focused on gastrointestinal causes.

30
Q

A 46 y/o male presents with complaints of nausea, vomiting, post prandial epigastric pain, weight loss, diarrhea, and pedal edema. History is positive for prior treatment for an alleged H. pylori infection. He admits to 2 high balls per day. History is negative for malnutrition, nephrotic syndrome, and chronic liver disease.
Blood test show a Hb of 12 gm with albumin of 2.1 gm/dL (3.5-5.2).
EGD and barium swallow are shown. slide 45
-Barium swallow - large giant gastric folds in stomach, dumping lots of protein/albumin in stomach secretions
-Endoscopy

  1. What is the suspected entity in this case?
  2. What causes the protein loss in this disease?
A
  1. Mucosal diseases without erosions or ulcerations: especially Hypoproteinemic Hypertrophic Gastropathy* – Menetrier’s disease (may be related to H pylori)
    - he is losing protein!!
  2. Hypochlorhydria, excess mucus secretion

NOTE:
*The differential diagnosis of large gastric folds includes Zollinger-Ellison syndrome,
malignancy, lymphoma, infectious etiologies (CMV, histoplasmosis, syphilis), and infiltrative disorders such as Sarcoidosis. One can also have protein losing gastroenteropathy from lymphatic obstruction, ie. Primary intestional lymphangiectasis, or diseases with mucosal erosions, ie. IBD.

31
Q

A 46 y/o male presents with complaints of nausea, vomiting, post prandial epigastric pain, weight loss, diarrhea, and pedal edema. History is positive for prior treatment for an alleged H. pylori infection. He admits to 2 high balls per day. History is negative for malnutrition, nephrotic syndrome, and chronic liver disease.
Blood test show a Hb of 12 gm with albumin of 2.1 gm/dL (3.5-5.2).
EGD and barium swallow are shown. slide 45
-Barium swallow - large giant gastric folds in stomach, dumping lots of protein/albumin in stomach secretions
-Endoscopy

What test can be used to prove whether the cause of the protein loss is from liver disease or Menetriers?

A

*** 24 hour feces for α-1-antitrypsin excretion (>13 ml/24 hr = abnormal), since it is not normally absorbed or secreted into the bowel.

listen to this again

32
Q

A 46 y/o male presents with complaints of nausea, vomiting, post prandial epigastric pain, weight loss, diarrhea, and pedal edema. History is positive for prior treatment for an alleged H. pylori infection. He admits to 2 high balls per day. History is negative for malnutrition, nephrotic syndrome, and chronic liver disease.
Blood test show a Hb of 12 gm with albumin of 2.1 gm/dL (3.5-5.2).
EGD and barium swallow are shown.

The patient is placed on cetuximab (monoclonal antibody against EGFR) and shows improvement with no vomiting and follow up EGD reveals improvement in the folds.

  1. What would most likely be the mechanism for this disease based on the response to this monoclonal antibody?
A

Overactivity of EGF

33
Q

A 48 y/o male alcoholic presents with dyspnea, weakness and near syncope. He had had an EGD six months prior because of an episode of melena. He has also had recent nausea and vomiting. No varices had been seen and no active bleeding sites were observed .

The patient appears jaundiced with the liver 4 cm below the RCM.
Palmer creases are pale. Chest findings are shown–> talangectasia (expected in cirrhosis - high estrogen levels)

Lab studies show Hb of 7.6 gm, with MCV of 101 fL, WBC of 13,000,
AST of 290 U/L, ALT of 150 U/L (points to alcohol)

bilirubin of 8.6 g/dL, creatinine of 0.8 mg/dL,
PT of 19 seconds, and triglycerides of 450 mg/dL.

  1. What is possibly causing the GI bleeding in this patient?

what is the diagnosis of the liver problem?

A

Diagnosis?
This is not cirrhosis of the liver but rather is hepatitis alcoholic

GI bleeding:
1. PUD

  1. Alcoholic gastritis (DASH causes of errosive gastritis)
  2. Esophagitis- potentially due to reflux
  3. Portal hypertensive gastropathy (PHG = “snake skin” or “mosaic stomach” - usually in fundus and body) with or without varices.
    Usually involves the stomach diffusely with dilated and twisted blood vessels
    early form of HTN
  4. Esophageal and gastric varices – usually accompanied by encephalopathy** and Spontaneous Bacterial Peritonitis.

Normal portal vein to inferior vena cava gradient = 2-6mm Hg.
When > 10-12 mmHg = portal hypertension

6 . Mallory- Weiss Tear- mucosal tear

  1. Boerhaave’s syndrome
    - if you see pseudomediastinum with left pleural effusion, this suggests Boerhaave’s syndrome
  2. AV malformations – Hereditary Hemorrhagic Telangiectasia*, CREST syndrome, CRD
  3. Dieulafoy’s lesion (congenital)– erosion of an ectatic artery or a “persistent caliber vessel” into the stomach - (large and submucosal)
34
Q

what is the triad of cirrhosis?

A

varices
encephalopathy
SBP- spontaneous bacterial peritonitis

35
Q

what is the normal portal vein to inferior venal cava gradient?

what is the pressure that defines portal HTN

A

normal 2-6 mmHg

When > 10-12 mmHg = portal hypertension

36
Q

what are the AV malformations that cause GI bleeding

A
  1. AV malformations – Hereditary Hemorrhagic Telangiectasia*

CREST syndrome (calcinosis, raynauds, esophageal abnormality, sclerodactyl, telangiectasia)

CRD

NOTE:
*All genes known so far to be linked to HHT code for proteins in the TGF-β signaling pathway which promote
angiogenesis of new blood vessels out of existing ones.

37
Q

pseudomediastinum

A

Boerrhave’s syndrome

38
Q

what are the causes of Telangiectasia

A

alcohol

Osler weber randu (hereditary hemorrhagic telangiectasia)- linked with TGF-b pathway overactivity

39
Q

Dieulafoy’s lesion

A

(congenital)– erosion of an ectatic artery or a “persistent caliber vessel” into the stomach - (large and submucosal)

acid gets too close to the surface

40
Q

what is watermelon stomach

GAVE

A

(GAVE – gastric antral vascular ectasia)

– older women with ectasia of antrum associated with scleroderma, DM, CRF, and cirrhosis (rarely)

There is only antral involvement in “watermelon stomach” (GAVE or gastric antral
vascular ectasia/telangiectasia*) which is reported in Scleroderma, DM and CRF.
It is less responsive to TX than PHG (portal hypertensive gastropathy) and less associated with portal hypertension.

know this for the test

41
Q

Pseudoxanthoma elasticum

A

degeneration and calcification of elastic fibers in connective tissue related to mutations in the ABCC6 – ATP binding cassette which doesn’t allow vitamin K to reach peripheral tissue.

Involves midlaminar layer of the dermis, Bruch’s membrane in the eye, and midsized arteries ( premature atherosclerosis)

plucked chicken appearance -ridging and nodularity of the skin- effects the elastic fibers and they degenerate and calcify

42
Q

Aging ROTS MILK

causes of gynecomastia!!

A

Aging, Adolescence

Refeeding (UC, hemodialysis, etc)

Obesity

Thyrotoxicosis, Testicular tumors (HCG)

Secondary to testicular failure (hemochromatosis, increased LH = increased estrogen)

Meds: (THC, flutamide, finasteride, bicalutamide, spironolactone, digitalis, phenothiazines, ketoconazole, cimetidine, nifedipine)

Idiopathic

Liver disease

Klinefelters (47,XXY)

43
Q

how is the diagnosis of achalasia made?

A

esophagography showing birds beak

endoscopy

manometry (absent peristalsis, elevated LES pressure, intraesohpageal pressure > gastric pressure)

Decreased numbers of neurons (ganglion cells) in the myenteric plexuses

Degeneration
preferentially involves the nitric oxide-producing, inhibitory neurons that effect the relaxation
of esophageal smooth muscle; the cholinergic neurons that contribute to LES tone by
causing smooth muscle contraction are relatively spared

44
Q

GIST (gastrointestinal stromal tumors)

A
  • mesenchymal tumors with KIT mutation (CD117)

interstitial cells of Cajal

treat with imatinib

submucosal mass

45
Q

Snake skin or mosaic stomach

A

portal hypertensive gastropathy

usually involves the fundus and body with dilated and twisted blood vessels

causes GI bleeding

GI II Exam II AP (4 decks)

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