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Clinical Medicine 4 > Lecture 1 (GI)- Exam 1 > Flashcards

Lecture 1 (GI)- Exam 1 Flashcards

1
Q

Esophageal Symptoms: Odynophagia
* What is it?
* usually decribed as what?
* Seen commonly with disorders causing what?

A
  • Pain with swallowing
  • Usually described as a “sharp pain”
  • Seen commonly with disorders causing inflammation to the esophagus mucosa

True dysphagia – when food gets stuck. Odynophagia – just painful swallowing.

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2
Q

Esophageal Symptoms: Odynophagia
* What is dysphagia? What are the causes? (5)

A

Patients experiencing only pain with swallowing and no sensation of obstruction do not have true dysphagia but rather odynophagia
* Highly associated to infectious etiologies (i.e. herpes, CMV, HIV ulcers)
* Tumors (end stage)
* Foreign bodies
* Pill induced (doxy and bisphosphates)
* Less likely “functional”

FLIPT

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3
Q

Esophageal Symptoms: Dysphagia
* What is it? (2)
* What does it company?
* What happens with the food?

A
  • Inability to swallow
  • Difficult swallowing
  • Coughing/choking
  • Food “sticks”
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4
Q

Esophageal Symptoms: Dysphagia
* How does it feel? Usually due to what?
* Different what?
* Not an entity upon itself but what?

A

Feels “tight”
* Usually due to neuromuscular dysfunction, obstructing lesion in the esophagus, or an inflammatory process in the esophagus.

Different etiologies pending if is to solids, liquids or both

Not an entity upon itself but a symptom that will get you to the right one

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5
Q

Dysphagia
* What are the DDXs?

A
  • Neuromuscular disorders
  • Systemic Causes
  • Extrinsic Obstructive Lesions-> Thymoma or lymphoma
  • Esophagitis – Infectious or Pill Induced
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6
Q

Dysphagia
* What are the DDXs due to obstructive lesions? (7)

A
  • Zenker’s diverticulum (dysfunction of the UES)
  • Strictures
  • Achalasia
  • Esophageal webs
  • Schatzki ring
  • Benign tumors (leiomyoma)
  • Carcinoma (SCCA, Adenocarcinoma)
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7
Q

Systemic Cause - Scleroderma
* What is it?
* What areas of the body can be involved?
* Commonly associated with what?

A
  • Chronic, degenerative, autoimmune disorder that leads to the over-production of collagen in the body’s connective tissue that leads to fibrosis involving the skin and multiple organs
  • Main area of GI tract involvement is esophagus
  • Commonly associated with Reynaud’s phenomenon
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8
Q

Scleroderma:
* Esophageal abnormality is based on what? What does that cause? (2)

A

Esophageal abnormality is based on patchy smooth muscle atrophy with fibrosis, which accounts for the decreased esophageal contractility and absence of resting LES tone (increase reflux).
* Chronic reflux due to incompetent LES
* Decrease motility

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9
Q

Scleroderma
* What happens to the distal esophagus?
* What is the txt?

A
  • Stricture of the distal esophagus (because of chronic acid exposure)
  • Treatment: PPI’s (omeprazole), promotility agents (metoclopramide), dilatation of stricture if needed
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10
Q

Infectious Esophagitis
* What are the common causes? (3)
* Seen most in who?
* Candida infections may also be associated with what? (3)

A
  • Common etiologies: Candida, herpes simplex virus (HSV), and cytomegalovirus (CMV).
  • Seen most frequently in immunosuppressed patients
  • Candida infections may also be associated with uncontrolled DM, systemic antibiotics, or inhaled corticosteroids.
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11
Q

Infectious Esophagitis
* What is the txt?

A
  • Oral or intravenous (IV) antifungal agents (for candidiasis)
  • antiviral agents (ganciclovir for CMV & acyclovir for HSV)
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12
Q

Label each one of these and also what dx test is the best?

A
  • Best test is EGD to Dx.
  • On left – white patches – candida – bleed easily when you unroof them.
  • Middle- <2cm multiple vesicular lesions that turn into shallow ulcers – HSV.
  • On right - CMV - >2cm ulcers that are usually linear and deep.
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13
Q

Pill-Induced Esophagitis
* What are the most common causes? (8)

A
  • Alendronate
  • NSAIDs
  • Antibiotics (Tetracycline&Minocycline)
  • Vitamin C
  • KCL
  • Quinidine
  • Reverse transcriptase inhibitors (Zalcitabine&Zidovudine)
  • Iron

Don’t give to bed bound patient.
VARIANT QK

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14
Q

Pill-Induced Esophagitis
* What ar ethe clinical features (4)?

A
  • Sudden retrosternal CP
  • Odynophagia
  • Dysphagia occurring several hours after taking a pill
  • Non-specific PE findings in uncomplicated cases
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15
Q

Pill-Induced Esophagitis
* What is dx test? What does it show?
* What is the management and prevention?

A

Endoscopy – discrete ulcers

Management/Prevention
* Remove offending agent
* Drink at least 4 oz of water with medications
* Remain upright at least 30 minutes after ingestion of medication

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16
Q

Zenker’s Diverticulum - esophageal diverticula
* What is it?
* What are typical sxs?

A
  • Weakness in posterior pharyngeal wall at pharyngoesophageal junction due to loss of elasticity of UES
  • Choking and halitosis are typical symptoms
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17
Q

How do you dx and tx ZD?

A

Dx: Barium Swallow (as for any dysphagia)

Treatment
* Cricopharyngeal myotomy with or without diverticulectomy
* Surgical excision of diverticula

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18
Q

Achalasia
* loss of what? What does it lead to? (3)

A

Loss of ganglion cells in the Auerbach’s plexus leads to:
* Increased resting tone of the LES
* Absent peristaltic activity in the esophageal body
* Absent or incomplete relaxation of the LES with swallowing

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19
Q

Achalasia
* What are the sxs?
* What dx test can you do?
* What is the txt?

A
  • SXS - Slowly progressive dysphagia to solids and liquids, chest pain, regurgitation
  • Barium Swallow – “bird’s beak” appearance
  • Treatment – symptomatic: pneumatic balloon esophageal dilatation or surgical lower esophageal sphincter myotomy/balloon (Heller procedure)
    * Botox injection is temporary (3mo-1yr)
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20
Q

Barium Swallow/ Upper GI - Achalasia
* What is the case? High association with what?

A

Motor problem causing structural abnormality.
* High association with cancer (pancreas, lungs and stomach)

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21
Q

Barium Swallow/ Upper GI - Achalasia
* How do you dx (including gold standard and what you see) and tx it?

A
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22
Q

Esophageal Stricture
* What area of the esophagus is affected?
* Most commonly due to what?
* What is the txt?

A

Lower third of the esophagus

Most commonly due to long-standing GERD

Treatment
* EGD w/ dilation for worsening symptomatic dysphagia
* Long-term PPI

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23
Q

Esophageal Webs/Rings
* What is it?
* What is a web and ring?

A
  • Thin projections of mucosa upon the lumen of the esophagus
  • Web is a single projection
  • Ring is a nummular projection
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24
Q

Esophageal Webs/Rings
* What are upper and lower rings associated with?
* Causes what?

A
  • Upper ring: associated with iron deficiency anemia and cancer
  • Lower rings: associated with hiatal hernias + GERD
  • Causes mechanical obstruction of the esophageal lumen -> dysphagia

Sx the same as constriction and tx is dilation

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25
Q

Lower Mucosal Esophageal Ring (Schatzki ring or B ring)
* What are they?
* Often referred to as what?

A
  • Mucosal projection that involves the most distal esophagus.
  • Often referred to as “steakhouse syndrome” and may present with non-progressive dysphagia for solids (especially steaks).
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26
Q

Plummer-Vinson Syndrome
* What are the combination of sx? (6)

A
  • Upper esophageal web
  • Iron-deficiency anemia
  • Hypothyroidism
  • Glossitis &/or cheilitis
  • Gastritis
  • Dysphagia (even without presence of a web)
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27
Q

Plummer-Vinson Syndrome
* What is the gender prodominance?
* Predominatnly where?
* What is the tx?
* Increased incidence of what?

A
  • 90% are women
  • Predominantly in northern hemisphere/ Scandinavian/Northern descent
  • Tx: Iron replacement alone may reverse some of the pathologic web changes; dilation of web
  • Increased incidence of esophageal SCCA
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28
Q

Diffuse Esophageal Spasm
* What is it?
* Often presents as what?
* What does it show on barium swallow?

A
  • High amplitude, repetitive, non-peristaltic nonfunctioning esophageal contractions
  • Often presents as chest pain/MI symptoms in a high stress patients (does not have to be with food but can worsen with food)
  • “Corkscrew/rosary bead/or Nutcracker” esophagus on barium swallow (study of choice)
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29
Q

Diffuse Esophageal Spasm
* Normal function of what?
* Intermittent what?
* What is the txt? What is a natural way to reduce spasms?

A
  • Normal function of the LES
  • Intermittent presence of normal peristaltic sequences (allows food mvt
  • Tx with NTG and CCB (to relax) + Psychotherapy (ppl with this do not like to eat so they need therapy)
  • Peppermint known to reduce spasms (NOT for ppl with poor LES)
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30
Q

Leiomyoma
* What is it? What do you need?
* Arise from what?
* What type of defect?
* What does it show with barium?
* How does the esophagus appear?

A
  • Submucosal non-malignant mass
    * Won’t know this until biopsy
  • Arise from circular or longitudinal smooth muscle
  • Round filling defect
  • Splitting of barium around tumor
  • Esophagus appears widened on AP view
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31
Q

Hiatus Hernia
* What is it?
* What does it not have to lead to?
* What are the two types?

A
  • Herniation of part of the stomach through the esophageal hiatus in the diaphragm and into the chest, and may be sliding or paraesophageal.
  • The presence of hiatus hernia will not itself lead to reflux
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32
Q

hiatus hernia
* What will give you a clue?
* What is the management?

A

Dx: Bowel sounds in chest

Management
* Typically medical (addressing GERD)
* Surgical - fundoplication

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33
Q

GERD
* What are the esophageal sxs?

A

Pyrosis or Heartburn
* “Burning” pain that radiates from the epigastrium
* Usually seen with GERD

Regurgitation
* Sudden, effortless return of small volumes of gastric or esophageal contents into the pharynx

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34
Q

GERD
* What is the pathophysio?

A
  • Transient or sustained inappropriate relaxation of lower esophageal sphincter (LES), not associated with swallowing
  • Acid-rich stomach contents reflux into esophagus, resulting in esophageal damage
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35
Q

Gastroesophageal Reflux Disease (GERD)
* Associated with what? (4)
* What are the red flags?(4)

A
  • Associated with hiatal hernia, obesity (increase abdominal weight so increase thoraic pressure) , neurological problems, medications.
  • Identify red flags : dysphagia (difficult), odynophagia (pain), weight loss (cancer) or bleeding.
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36
Q

Pathogenesis of GERD
* What are some patho causes (4)?

A
  1. Impaired LES-low pressures or frequent transient LES relaxation
  2. Hypersecretion of acid
  3. Decreased acid clearance resulting from impaired peristalsis or abnormal saliva production
  4. Delayed gastric emptying or duodenogastric reflux of bile salts & pancreatic enzymes.
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37
Q

Factors that worsen GERD symptoms
* What are things that reduce LES Tone (LES is relaxed due to)? (8)

A
  • Fatty foods
  • Chocolate
  • Ethanol
  • Peppermint
  • Caffeine
  • Nicotine
  • Calcium channel blockers
  • Nitrates
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38
Q

Factors that worsen GERD symptoms
* What can increase intra-abdominal pressure? (6)

A
  • Pregnancy
  • Obesity
  • Bending
  • Lifting
  • Straining
  • Tight-fitting clothes
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39
Q

GERD-Clinical Features
* What is the hallmark sx?
* How is dx?

A
  • Heartburn (pyrosis) – hallmark symptom
  • Dx: Clinical via history
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40
Q

GERD Clinical Features- PAIN
* Where it is?
* Worst when?
* Relieved with what?
* 10% of pt present with what?
* Always R/O out?

A
  • Burning, substernal, radiating upward,
  • Worse 30 to 60 minutes after meals & lying supine (at night)
  • Relieved with sitting up & antacids
  • 10% of patients present with atypical “anginal” type CP
  • Always R/O MI or other cardiac causes.
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41
Q

GERD-Clinical features
* What are the ENT complatints (4)
* What is chronic?
* What are two other issues?

A
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42
Q

GERD – Clinical Features
* Severity of symptoms does not correlate well with what?
* What is nonspecific?
* Dx of GERD is best made by what?

A
  • Severity of symptoms does not correlate well with degree of esophageal mucosal damage
  • Physical Exam findings nonspecific
  • Diagnosis of GERD best made by History
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43
Q

GERD dx procedures- pH monitor test
* Prolonged monitoring of what?
* Stop PPI when?
* A pH electrode is passed where?
* When is acid reflux defined?

A
  • Prolonged monitoring of esophageal pH for 12 to 24 hours is the most reliable means of diagnosing acid reflux.
  • Stop PPI for 10 days prior to the test
  • A pH electrode is passed through the nose or mouth to 5 cm above the manometrically determined LES.
  • Acid reflux is defined when there is a decrease of esophageal pH to less than 4 (>4% of time over 24 hours).
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44
Q

What is the txt for mild and intermittent sxs of GERD?

A

Lifestyle Modifications

H2 Blockers
* Ranitidine (Zantac)
* Famotidine (Pepcid)

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45
Q

What is the txt and classification of mod/severe GERD?

A

Moderate/Severe or frequent symptoms (2+ episodes/week) or erosive esophagitis
* Proton Pump Inhibitors – 8 week therapy heals 86% of esophagitis
* Omeprazole (Prilosec)
* Lansoprazole (Prevacid)
* Pantoprazole (Protonix)
* Esomeprazole (Nexium)

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46
Q

Eosinophilic Esophagitis
* Sxs similar to what?
* hx of what? (2)
* Clinically see what?

A
  • Symptoms similar to reflux
  • History of recurrent food obstructions at younger than expected age
  • History of atopy
  • Clinically: see “Trachealization” of esophagus
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47
Q

Eosinophilic Esophagitis
* What is the histology?
* What is the txt? (3)
* If with a stricture there is high incidence what?

A
  • Histology: Needs more than 15 eosinophils in biopsy
  • Treatment: PPI’ s, trigger food avoidance, topical (inhaled) steroids
  • If with a stricture there is high incidence of complications while doing dilation
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48
Q

Barrett’s Esophagus
* What is it?
* Dx by what?
* Change in what? potential for what?

A
  • Replacement of the squamous epithelium of esophagus by columnar epithelium often due to severe esophageal reflux
  • Diagnosed by endoscopy with biopsy
  • Change in tissue has potential for esophageal carcinoma (adenocarcinoma)
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49
Q

Adenocarcinomas Arising in Barrett Esophagus
* What happens?

A
  • Distal esophagus is replaced by Barrett mucosa, producing a darker, slightly erythematous gross appearance.
  • Large ulcerating adenocarcinoma in distal esophagus that extends into upper stomach.
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50
Q

Esophageal Carcinoma
* Adenocarcinoma: Develope why? Arise where?
* Squamous Cell: What increases the risk?

A

Adenocarcinoma
* Majority develop as a complication of Barrett’s metaplasia due to chronic GERD
* Most arise in the distal 1/3 of the esophagus

Squamous Cell
* Chronic ETOH and smoking are associated with increased risk (unrelated to acid)

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51
Q

Esophageal Carcinoma Symptoms
* What is the most common sx?
* What happens with weight/
* What can occur with complete obstruction?

A
  • Dysphagia (most common)
    * Solids->Liquids
  • Weight loss
  • Regurgitation, Aspiration w/ Pneumonia may occur with complete obstruction
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52
Q

Esophageal Carcinoma Symptoms
* What are sxs if invasion of adjacenet structures? (3)

A
  • Chest pain (mediastinum)
  • Hiccups (diaphragm)-> Vagus Never
  • Hoarseness (recurrent laryngeal nerve)
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53
Q

What is going on here?

A

Esophageal cancer-> Apple core lesion

Usually find after weight loss and dysphagia.

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54
Q

Esophageal Cancer Treatment
* What are the different treatment options? (3)

A
  • Surgical resection – if there is no widespread metastasis
  • XRT (squamous cell is more radiosensitive than adenocarcinoma) - excellent palliative treatment for obstructive symptoms.
  • Chemotherapy
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55
Q

Hepatic Panel – LFT’s
* What are the tests for hepatocellular damage? (2) Chronic hepatitis? (1)

A
  • AST, ALT (found in muscle also – so MI will show higher LFT’s)
  • Chronic hepatitis – elevated LFT’s for >6months

ALT is slightly more specific for liver damage. (L for liver)

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56
Q

Hepatic Panel – LFT’s
* What tests for cholestasis (obstruction)? (3)

A

Alkaline Phosphatase, GGT and/or bilirubin

  • Alk Phos (also found in bones and placenta) – located near ducts of the liver – elevation shows obstructive type pattern. Can be due to pancreatic CA, gallstones in common bile duct.
  • GGT – helpful if only have elevated Alk Phos level and AST/ALT are normal. Can see if it’s a bone problem (Paget’s). If GGT is elevated along with Alk Phos = liver problem. If GGT is normal and Alk Phos is elevated – bone etiology.
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57
Q

Hepatic Panel – LFT’s
* What are the tests for liver synthetic function?
* What is the test for bilary excretion?

A

Tests for Liver synthetic Function
* Albumin, PT/INR

Tests for Biliary excretion
* Bilirubin

  • Total – direct bili = indirect bili
  • CMP gives you all but GGT and direct bili. Can order those separately.
  • Albumin – liver makes it – low albumin in cirrhosis.
  • All clotting factors except factor 8 are made by liver. PT checks factor 7 – most sensitive.
  • Elevated indirect bili – not really a liver problem – could be hemolysis.
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58
Q

Serum Transaminases
* What are the two?
* Elevations in those mean what?

A
  1. Aspartate Aminotransferase (AST) also known as serum glutamic oxaloacetic transaminase (SGOT)
  2. Alanine Aminotransferase (ALT) also known as serum glutamic pyruvic transaminase (SGPT)
  3. Elevation of the aminotransferases indicates inflammation and/or injury to hepatocytes.
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59
Q

Common Patterns of Serum Transaminase elevations in Liver Disease

Alcoholic Hepatitis and Alcoholic Cirrhosis
* Mild to moderate elevations of what?
* What is higher?

Extrahepatic obstruction (def look for GGT and Alk Phos)
* What do you look for?

A

Alcoholic Hepatitis and Alcoholic Cirrhosis
* Mild to moderate elevations of ALT and AST (usually to <500 IU) with
* AST greater than ALT (ratio >2:1)

Extrahepatic obstruction (def look for GGT and Alk Phos)
* Moderate elevations of ALT and AST to <500 IU

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60
Q

Common Patterns of Serum Transaminase elevations in Liver Disease

Viral, toxic, or ischemic hepatitis
* What do you see in labs?

AST and ALT may be normal in who?

A

Viral, toxic, or ischemic hepatitis
* Extreme elevations of ALT and AST >500 IU

AST and ALT may be normal in some patients despite significant disease (i.e. hemochromatosis)

61
Q
A

big jumps in acute infections and toxicity

62
Q

Alkaline Phosphatase
* Present where? (4)
* Measure what to determine a hepatic orgin?
* Elevation of GGTP/GGT indicates what?

A
  • Present in liver, bone, placenta, and intestine
  • Measure serum γ-glutamyltranspeptidase (GGTP) {also known as gamma-glutamyl transferase (GGT)} to determine if the elevated alkaline phosphatase is from a hepatic origin
  • Elevation of GGTP/GGT indicates a hepatobiliary source
63
Q

Significant elevations of hepatic alkaline phosphatase occur in what? Give examples (5)

A

Significant elevations of hepatic alkaline phosphatase occur in HEPATIC OBSTRUCTION
* Strictures
* Neoplasm
* Pancreatitis
* Primary Biliary Cirrhosis/Cholangitis (PBS)
* Primary Sclerosing Cholangitis (PSC) – R/O Crohn’s or UC

64
Q

Approach to identifying the cause of elevated LFT’s
* How can you tell the difference between acute vs chronic in labs?
* What are the identifying clues? (4)

A
65
Q

Approach to identifying the cause of elevated LFT’s
* What are list of meds that can cause elevated LFTs?(7)
* What should you look at for cholestatic?

A
  • Statins, ACE, antibiotics specially Augmentin, acetaminophen( only if an overdose), Imuran, Isoniazid, anti seizures medications, etc.
  • Cholestatic (Alk phos/GGT)
66
Q

Serum gamma-glutamyl transferase (GGT)/γ-glutamyltranspeptidase (GGTP)
* Elevated in what? (2)

A
  • Elevated in chronic alcoholic liver disease
  • Elevated in cholestatic disease (Primary Biliary Cirrhosis/Cholangitis, Primary Sclerosing Cholangitis)
67
Q

Serum Lactate Dehydrogenase (LDH)
* Significantly elevated in what?
* Slight elevation may be seen in what?

A
  • Significantly elevated in metastatic disease to the liver
  • Slight elevations may be seen in hepatitis, cirrhosis, extrahepatic obstruction, and congestive hepatomegaly
68
Q

What are the 2 MEASURES OF SYNTHETIC LIVER FUNCTION?
* Explain if they are high and low

A

1) PROTHROMBIN TIME (PT, INR)
* Elevated in severe liver damage and indicates a poor prognosis( Because PT/INR reflects hepatic synthesis of factors I, II, V, VII, X)

2) SERUM ALBUMIN
* Low in Significant liver disease

To R/O cause of elevated PT INR give them Vit K. If Vit K deficient – it will improve their PT/INR. If liver cause, Vit K wont do anything.

69
Q

What does not does not immediately affect synthetic function?

A

Acute insult with elevated transaminases does not immediately affect synthetic function

70
Q
  • What else will cause hypoalbuminemia?
  • What else will cause an elevated PT/INR?
A

What else will cause hypoalbuminemia?
* Nephrosis, malabsorption (sprue or bacterial overgrowth, Cancer).

What else will cause an elevated PT/INR?
* Coumadin, malabsorption of Vit K (Fat soluble), High amounts of ABX.

71
Q

Serum Bilirubin
* What is unconjugated and conjugated bilirubin? (Think: bound to and stored)

A

Total Bilirubin

Unconjugated Bilirubin = Indirect Bilirubin
* Bound to albumin and gets conjugated in liver

Conjugated Bilirubin = Direct Bilirubin
* Stored in liver, excreted to colon (which converts to urobilinogen-> causes the brown color of stool) or bile

72
Q

Under notes

  • Indirect bili elevation in blood will have normal what? What is elevated?
  • Unconjugated hyperbilirubinemia usually results from what?
  • Elevated direct bili (liver problem) – spills out into blood – will have
A
  • bili in urine (tightly bound to albumin) but elevated urobilinogen in urine (liver cant keep up with too much and its not bound to albumin or there is not enough albumin secondary to liver disease).
  • Unconjugated hyperbilirubinemia usually results from dysregulation in the bilirubin metabolism that includes increased production, impaired hepatic uptake, and decreased conjugation of bilirubin.
  • Elevated direct bili (liver problem) – spills out into blood – will have elevated bili and urobilinogen in urine.
73
Q

Urine bilirubin
* Present only with what? What are the examples? (3)

A

Present only with elevated direct bilirubin (not bound to albumin – gets excreted)
* Hepatitis
* Hepatocellular jaundice
* Biliary Obstruction

74
Q
A

You need to ask what they eat
* Carrots contain beta carotene which can discolor the skin

75
Q

Causes of Jaundice – Elevated Bilirubinemia
* How do you get unconjugated bilirubin? What is another name?
* What is another name of conjugated bilirubin?

A

Unconjugated Bilirubin = Indirect Bilirubin (usually not given, so you have to calculate)
* I=T-D

Conjugated Bilirubin = Direct Bilirubin

76
Q

What are the history questions you need to ask when a patient is jaudice?

A
77
Q

A post op cholecystectomy presenting with jaundice – suspect what?

A

suspect nicking or accidental removal of common bile duct due to bad visibility.

78
Q

Physical Exam in a patient with Jaundice
* What will be shown in a patient with liver disease?(3)

A

Portal HTN
* Palmar erythema
* Caput Medusae (round ligament revasclularized)

79
Q

Stigmata of liver disease
* What causes encaphalopathy?
* What can happen to hands?
* What happens to breath?
* What happens to skin? (2)
* What about fluid consumption?

A
  • Encephalopathy (increased ammonia NH3)
  • Asterixis (asynchronous flapping – liver flap/ also ESRD)
  • Fetor hepaticus (halitosis)
  • Bruising (clotting factors low and platelets can be trapped in liver) and Spider Nevi
  • Ascites (low albumin)

Spider nevi – blanch – higher pressure in BV

80
Q

Stigmata of Liver Disease
* What is enlarged?
* What about edema?
* What happens to muscles?
* What happens to breast tissue
* What happens to testes?

A
  • Splenomegaly
  • Lower extremity edema
  • Muscle wasting (Temporalis muscle, interosseous muscles)
  • Gynecomastia (high estrogen state)
  • Testicular Atrophy (estrogen high)
81
Q

Physical Exam in a patient with Jaundice
* What are the signs of biliary tract obstruction/infection?

A

Fever, RUQ pain, with the jaundice (Charcot’s Triad)

82
Q

Physical Exam in a patient with Jaundice

Physical exam clues to a specific disease
* What do you see with hereditary hemochromatosis
* IV drug use?
* Copper metabolism problem?

A
  • Bronzed skin of Hereditary Hemochromatosis
  • Track marks (IV drug use)
  • Kayser-Fleischer ring of Wilson’s Disease->Copper metabolism problem
83
Q

Elevated Unconjugated Bilirubin
* What is going on here?
* What are examples?(4)

A

“Pre-hepatic jaundice” - occurs when there is a fault somewhere upstream of conjugation.
* Hemolysis
* Gilbert’s Disease
* Neonatal Jaundice
* Crigler-Najjar Syndrome

84
Q

Hemolysis
* Common cause of elevated what?
* known as what?
* What is the patho behind this?

A
  • Common cause of elevated unconjugated bilirubin
  • Known as hemolytic jaundice
  • RBC cell lysis leads to overload of unconjugated bilirubin that is not excreted/CONJUGATED through liver fast enough
85
Q

Hemolysis
* What are the differentials? (5)
* What is the txt (2)

A

Differentials:
* Sickle cell anemia, hereditary spherocytosis, TTP, autoimmune hemolytic anemia, thalassemia minor

Treatment
* Geared towards cause
* Phototherapy or exchange transfusions may help

86
Q

Neonatal jaundice:
* What is it due to? (3)
* What may increase the risk?(3)

A

Due to:
* Excess fetal destruction of red cells
* Immature uptake and conjugation pathways in the neonatal liver
* Absence of gut flora to metabolize bile pigments.

Prematurity, dehydration, and breast feeding may increase neonatal jaundice

87
Q

Neonatal Jaundice
* When does jaundice peak? When does it subside?
* What is the main concern?

A
  • Jaundice peaks between the second and fifth day of life, and should subside within two weeks
  • Main concern is kernicterus
88
Q

Gibert’s Disease
* What type of cause? Elevated what?
* What is it? What does ti cause?

A
  • Completely benign cause of jaundice with elevated total and unconjugated bilirubin
  • A congenital defect in the liver’s uptake and conjugation pathways causing elevation of unconjugated bilirubin, but normal LFT’s
89
Q

Gilbert’s Disease
* Occurs in who?
* Usually identified following what?
* Not what?

A
  • Occurs in about 4-16% of the population, usually in adolescence; M>F.
  • Usually identified following illness, starvation/dehydration, or surgery.
  • Not a liver problem and work-up is rarely required unless other causes of hyperbilirubinemia are being worked up.
90
Q

“Pre Hepatic” Bilirubinemia
* There is no what?
* What is normal?
* What is the issue?

A
  • There is no bilirubin in the urine, which remains its usual color
  • There is more than the usual trace of urobilinogen in the urine
  • The bilirubin in the blood is unconjugated (preliver problem – hemolysis or Gilbert’s)
91
Q

Conjugated Bilirubin Problems
* Inherited disorders in what?
* What are the different examples?

A

Inherited disorders resulting in conjugated hyperbilirubinemia and normal LFTs (typically asymptomatic)
* Dubin-Johnson Syndrome
* Rotor Syndrome
* biliary atresia in newborns

92
Q

Conjugated Bilirubin:
* What is the issue with dubin johnson syndrome?
* What is the issue with rotor syndrome?
* Consider biliary atresia in newborns who develop what?

A
  • Dubin-Johnson Syndrome: Mutation in the transporter gene that moves the bilirubin from the hepatocyte to the bile canaliculus -> Asymptomatic elevations in conjugated bilirubin
  • Rotor Syndrome: Defect in the ability of the hepatocyte to store bilirubin -> Asymptomatic elevations in conjugated bilirubin
  • Consider biliary atresia in newborns who develop clay colored stools (no bili in stool) and have elevated direct bili

For Dubin and rotor, you need to do genetic testing

93
Q

What are the INTRAHEPATIC Causes of Cholestasis? (6)

A
94
Q

Primary Biliary cirrhosis/cholangitis
* Also known as what?
* Seen more commonly in who?
* What is affect?

A
  • Also known as Primary Biliary Cholangitis
  • Seen more commonly in women ages 30-65 y/o
  • Progressive, immune mediated destruction of the interlobular bile ducts only
95
Q

Primary Biliary Cirrhosis/Cholangitis
* What are the sxs?
* What are the labs?

A
  • SXS: fatigue and pruritis-> Jaundice, xanthomas, skin hyperpigmentation, steatorrhea (floating stool), bone pain from osteoporosis complications (i.e. compression fractures)
  • Labs: cholestatic picture – elevated alkaline phosphatase and GGT.
96
Q

Primary Biliary Cirrhosis/Cholangitis
* How do you dx it?
* What does the liver biopsy show?
* What is the txt?

A
  • Diagnosis – Elevated Antimitochondrial antibody (AMA); Elevated serum IgM levels
  • Liver Biopsy – destructive lesions of the bile ducts
  • Treatment – Ursodeoxycholic acid (replaces toxic bile acids) improves pruritis, slows progression of disease, and delays the need for liver transplant.

Do AMA test and do liver Bx.

97
Q

Primary Sclerosing Cholangitis (PSC)
* What is it?
* 70% of patients have what? What is elevated?
* May lead to what?
* What is the tx?

A
  • Inflammation of the Extrahepatic ducts OR Intrahepatic ducts leading to fibrosis
  • 70% of pts with PSC have IBD ->Cholestatic picture: elevated alk phos and GGT
  • May lead to cirrhosis
  • TX - liver transplant if severe
98
Q

Primary Sclerosing Cholangitis
* What imaging can be done? What does it show?

A

ERCP image shows mural irregularity of the cystic duct (arrows) due to primary sclerosing cholangitis

99
Q
A
100
Q

What are the EXTRAHEPATIC Causes of Cholestasis? (4)

A
  • Primary Sclerosing Cholangitis
  • Gallstones
  • Pancreatic Cancer (causing extrahepatic compression of bile ducts)
  • Cholangiocarcinoma (causing bile duct obstruction)
101
Q

What is the work up of cholestatic jaundice?

A
102
Q

Viral Hepatitis A Transmission
* How is it spread?
* Direct contact with what?
* Ingestion of what?

A
  • Primarily spread fecal -> oral route
  • Direct contact with HAV infected person
  • Ingestion of HAV contaminated water or food
103
Q

What are the sxs of acute hepatitis signs and symptoms? (10)

A
104
Q

Hep A serology:
* What is present in acute infection and past infection?

A

Acute Infection
* Hepatitis A Antibody IgM (HAV-Ab IgM)
* Total HAV Ab is positive (includes IgM too)

Past infection = Immunity (vaccine)
* Total Hepatitis Antibody (+Total HAV Ab) w/ a negative HAV Ab IgM – patient is vaccinated

105
Q

Hep A
* Does not have what?
* What is positive in acute and immune cases?
* Can measure what?

A
  • Hep A doesn’t have a chronic stage.
  • IgM is positive in acute – MAC +M and Acute
  • IgM is negative in immune or if no disease is present. But there is no chronic stage in Hep A so it’s a vaccine.
  • Can measure IgG (immune) IgM (acute) or total Ab’s.
106
Q

What is the timeline for hep A?

A
107
Q
A

  • Acute, Immune/vaccinated or at risk (no disease)
  • Total is really never tested unless you’re looking for vaccination.
108
Q

Hepatitis A
* What is the incubation period?
* What is the onset? What are the sx?
* What is the txt?
* What is the course of the disease?

A
  • Incubation period: Average 30 days
  • Onset:Acute with Malaise, nausea, vomiting, jaundice, dark urine, diarrhea, etc
  • Treatment: Supportive (hydration and anti-nausea meds)
  • Course: Usually self-limiting (recovery within 6-12 months). No associated carrier state or chronic hepatitis.
109
Q

Hepatitis A Prevention: Vaccine and Immunoglobulin (IG)
* Who should get pre exposure?

A

Pre-exposure (vaccine and/or IG)
travelers to intermediate and high HAV-endemic regions
Individual risk setting

110
Q

Hepatitis A Prevention: Vaccine and Immunoglobulin (IG)
* Who should get post exposure?

A

Post-exposure: vaccine or IG (within 14 days)

Routine
* household and other intimate contacts

Selected situations
* institutions (e.g., day care centers)
* common source exposure (e.g., food prepared by infected food handler)

111
Q

Hepatitis B Virus Risk Transmission
* how is it transmitted? (3)

A
  • Parenteral exposure to HBV infected blood
  • Sexually/Salivary transmitted (except breast milk)
  • Perinatal

In horizontal transmission, viruses are transmitted among individuals of the same generation, while vertical transmission occurs from mothers to their offspring

112
Q

Hepatitis B Virus Risk Transmission
* What is the incubation period?
* What is the acute vs chronic situation?
* Chronic patients may develop what?

A
  • Incubation period 1-3 months
  • Acute vs chronic. 90% will get through symptoms and will recover. 10% will become chronic. Most likely in patients with vertical transmission.
  • Chronic patients may develop HCC without going through cirrhosis
113
Q

What are the sxs of Hep B? (10)

A
114
Q

What are the different antibodies and antigens for hep b?

A

Most will spontaneously recover but some will go to chronic stage.

115
Q

KNOW

Hep B Serologies
* HBsAg (+) =
* HBsAb/Anti-HBs (+) =
* HBcAb(IgM) =
* HBcAb/Anti-HBc(IgG) =

A
  • HBsAg (+) = chronic carrier or active disease
  • HBsAb/Anti-HBs (+) = immunity (vaccinated) or previous disease (recovered)
  • HBcAb(IgM) = acute disease exposure or active infection
  • HBcAb/Anti-HBc(IgG) = previous disease exposure

  • HBsAg is used to make vaccines
  • Test core – Anti-HBc – to see if its acute or chronic Hep B. If Anti-HBs is positive, test Anti-HBc for acute (+ IgM) or chronic (IgM negative; IgG positive).
  • Core antibody does not provide any protection from the disease.
116
Q

Hepatitis B Serologies
* HBeAg (+) =
* HBeAb (+) =
* HBV-DNA < 105 =
* HBV-DNA > 105 =

A
  • HBeAg (+) = active viral replication
  • HBeAb (+) = strong viral suppression (i.e. seroconversion)
  • HBV-DNA < 105 = chronic carrier or well suppressed
  • HBV-DNA > 105 = active chronic infection (Higher HBV DNA levels = higher risk of Cirrhosis or hepatocellular carcinoma)

  • Hbe – for envelope – measures the amount of infectivity. HBe Ag positive – high infectivity. Anti HBeAg negative – low infectivity
  • HBV-DNA unreliable and tests a viral load
117
Q

Serology Summary
* What are antigens for?
* What are the different types of antibodies and what are they for? (3)

A

Antigens – acute infection

Antibodies
* Surface (Ag or Ab) – Immunity via vaccine or recovery from infection with immunity
* Envelope (Ag or Ab) – Measures degree of infectivity
* Core (IgM or IgG) – Discriminates Acute vs Chronic infection

118
Q
A
119
Q
A
120
Q
A
121
Q

Fill in

A

HBe to see infectivity

122
Q

What are the clinical outcomes in hep B virus?

A

Don’t treat Acute HepB and wait until chronic stage because they have a chance to recover. Don’t start them on toxic interferon meds yet.

123
Q

What is the timeline for Hep B?

A
124
Q

What is the timeline for acute HBV to chronic?

A
125
Q

Who gets txt for chronic Hep B? What are the examples? (6- excluding combo therapy)

A

Treatment options for Chronic Hepatitis B who are serum HBsAg+, HBeAg/HBV-DNA-positive pts with symptoms, elevated AST, ALT levels & Liver biopsy evidence of chronic hepatitis
* Pegylated Interferon
* Lamivudine
* Adefovir
* Entecavir
* Telbivudine
* Tenofovir

126
Q

What does combo therapy result in for the txt of hep B?

A

Results in anti HBe seroconversion with clinical, biochemical, & histologic improvement in 40% of cases

127
Q

Management of Chronic Hepatitis B
* Vaccinate against what?
* Avoid what?
* Screen for what? How?
* Manage what?

A
  • Vaccinate against Hepatitis A (don’t want to damage the liver anymore than already have)
  • Avoid hepatotoxic medications & Alcohol
  • Screen for Hepatocellular Carcinoma: AFP + RUQ US (Q6-12 months)
  • If Portal HTN is present, manage complications.

They arent more susceptible to Hep A but they will probably die if they do get it.

128
Q

HBV Prevention
* What is reccommeded in the US?
* Check for what?

A
  • Universal vaccination of all children and adults is recommended in US
  • Check anti-HBs titers 1-2 months after completion of the vaccine (not all respond to vaccine)
129
Q

HBV Prevention
* Vaccinate who? (7)

A

Vaccine targeted to high-risk groups
* Health care workers
* Men who have sex with men
* Persons who use IV drugs
* Hemodialysis pts
* Patients with hemophylias
* Household & sexual contacts of HBsAg carriers
* Neonates in endemic areas or high-risk neonates in lower-risk areas

130
Q

What if a person does not develop a protective concentration of anti-HBs (<10 mIU/mL) after receiving the hepatitis B vaccine series ?

A

Repeat the 3 vaccine doses & repeat anti-HBs 1-2 months after completion

Persons who do not have a protective concentration of anti-HBs after revaccination should be tested for HBsAg.

You want it >10. Less than 10 – did not develop protection so repeat the vaccine.

131
Q

Persons who do not have a protective concentration of anti-HBs after revaccination should be tested for HBsAg.
* If the HBsAg test result is positive, the person should receive what?
* Persons who test negative for HBsAg should be considered for what?

A
  • If the HBsAg test result is positive, the person should receive appropriate management, and any household, sex, or needle-sharing contacts should be identified and vaccinated
  • Persons who test negative for HBsAg should be considered susceptible to HBV infection and should be counseled about precautions to prevent HBV infection and the need to obtain HBIG postexposure prophylaxis for any known or likely parenteral exposure to HBsAg-positive blood
132
Q

Hepatitis D Virus
* What does it require?
* Coinfected with what?
* What is the txt?

A
  • It requires the hepatitis B virus to survive and replicate
  • Coinfection with Hepatitis B
  • No specific treatment or vaccine available for Hepatitis D. Vaccinate patients for Hepatitis B
133
Q

Hepatitis C (HCV)
* What is it the MCC of?
* What are the Viral properties?

A
  • Most common cause of liver transplant and chronic hepatitis in the US
  • Viral Properties: Caused by flavi-like virus with RNA genome of > 9,000 nucleotides(similar to yellow fever virus, dengue virus)
134
Q

Hepatitis C (HCV)
* What is the incubation period?
* What does the CDC recommend?

A

Incubation Period
* 2-8 weeks
* 85-90% will develop chronic hepatitis

CDC recommendation to screen all baby boomers, because that is the highest risk group, and 75 % does not know they have it.

135
Q

Under slide

Hep C
* More common than what?
* What are their labs?
* What is a really common cause?

A
  • More common than Hep B (resolves more quickly).
  • Their LFT will be border line elevated with HCAg is positive.
  • IV drug abuse is really most common cause.
136
Q

HCV-Epidemiology
* What is the transmission?
* What accounts for 50% of cases?
* Little ecidence for what?
* Often asymptomatic and presents frequently when?

A
  • Percutaneous transmission accounts for > 90% of transfusion associated hepatitis cases
  • IV drug use accounts > 50% of reported cases
  • Little evidence for frequent sexual (horizontal) or perinatal (vertical) transmission
  • Often asymptomatic and presents frequently in the chronic phase with borderline consistent elevated LFTs
137
Q

Hep C sxs
* New onset?
* Patients usually present in the chronic stage with what?

A
  • New onset Hepatitis C is usually asymptomatic
  • Patients usually present in the chronic stage with mild persistent elevation of LFTs or sequella of liver disease
138
Q

What is the CDC HCV Screening Guidelines with HCV Ab test? (2)

A
  • Individuals at an increased risk for HCV (i.e. patients with a history of injection drug use, homelessness)
  • Individuals born in the United States between 1945 and 1965 (*New recommendation)
139
Q

What is the clinical course of hep C?

A
140
Q

Hepatitis C Serologies

A

Measure Ab because RNA is not reliable

  • Test to order Anti-HCV or HCV Ab
  • RNA test isnt very reliable. If negative – cant say patient doesn’t have Hep C.
141
Q

What is the timeline for hep c?

A

Hep C acute is less severe than Acute Hep B.

142
Q

What are some other tests you can do for Hep C? (2)

A
  • Viral Genotyping (some types are worse than others)
  • Liver biopsy to see severity and prognose treatment
143
Q

Conditions Associated with HCV
* What are the conditions/what are they? (5)

A
  • Diabetes mellitus occurs three times more frequently in HCV-infected persons
  • Glomerulonephritis
  • Essential mixed cryoglobulinemia, a condition involving the presence of abnormal proteins in the blood
  • Porphyria cutanea tarda, an abnormality in heme production that causes skin fragility and blistering
  • Non-Hodgkins lymphoma may occur more frequently
144
Q

Newer Treatment Options for Hep C
* What are the Options for Hepatitis C for Genotype 1 ? (3) What are the MC SE?

A

Options for Hepatitis C for Genotype 1 (most difficult to treat) are protease inhibitors
* Ledipasvir/sofosbuvir (Harvoni) – once daily
* Boceprevir (Victrelis) – PO three times a day
* Telaprevir (Incivek) – PO every 8 hours
* Most common side effects: Anemia (that may respond to Epogen) and Skin Rash (may be life threatening in telaprevir)

  • 65-75% cure rate (double to triple that of standard therapy)
  • Most patients only need 8-24 weeks rather than the usual 48 weeks
145
Q

Older treatment option for chronic Hepatitis C
* What is the older treatment? What is the issue with it?
* What are common SE?

A
  • Pegylated interferon in combination with ribavirin SQ x 24-48 weeks
  • Contraindications to therapy: LOTS OF THEM (see below)
  • Common adverse events: influenza-like symptoms. Psychiatric side effects (depression, irritability, insomnia)

Major uncontrolled depressive illness, organ transplant, autoimmune hepatitis or other autoimmune condition known to be exacerbated by peg - interferon and ribavirin, untreated thyroid disease , pregnant or unwilling to comply with adequate contraception , severe concurrent medical disease (severe hypertension, heart failure, significant coronary heart disease, poorly controlled diabetes, chronic obstructive pulmonary disease), Age less than 2 years, known hypersensitivity to drugs used to treat HCV.

146
Q

Management of Chronic Hepatitis C
* What s the management? (4)

A
  • Vaccinate against Hepatitis A & B
  • Avoid hepatotoxic medications & Alcohol
  • Screen for Hepatocellular Carcinoma: AFP + RUQ US (Q6-12 months)
  • If Portal HTN is present, manage complications.
147
Q

Hepatitis E
* Similar to what and how?
* Highly _
* Differs from what and how?

A
  • Similar to hepatitis A in its mode of transmission (fecal-oral) and in the involvement of contaminated water.
  • Highly contagious
  • Differs from hepatitis A : a high incidence of mortality, particularly in pregnant women
    * Increased incidence of fetal demise

Similar to HepA and more severe in pregnants. Seen in 3rd world Countries.

148
Q

Clinicians who may encounter pediatric patients with hepatitis of unknown etiology to consider what? What is the test?

A

Clinicians who may encounter pediatric patients with hepatitis of unknown etiology to consider adenovirus testing.
* Adenovirus 41 type was noted in 5 children in Alabama with acute live failure

Nucleic acid amplification testing (NAAT, e.g. PCR) is preferred for adenovirus detection and may be performed on respiratory specimens, stool or rectal swabs, or blood.

Clinical Medicine 4 (13 decks)

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