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GI/Pulm > GI > Flashcards

GI Flashcards

1
Q

Murphy’s sign

A

Painful right upper quadrant, no nodules= cholecystitis
4Fs= fat, female, forty, female

  • The encounter between the examiner’s fingertips and the inflamed edge of the gallbladder causes pain and a reflex arrest in inspiration.
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2
Q

Signs of cholecystitis

A

Murphy’s sign

  • Area of hypersensitivity over the right costophrenic angle (Boas’ sign) – sensitivity only 7%.
  • At times they may also exhibit an audible rub over the edge of the gallbladder.
  • They rarely have a palpable and tender right upper quadrant mass, (see Courvoisier’s law).
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3
Q

Shifting dullness maneuver

A

Test used to diagnose Ascites:

  • Gravity- dependent shift
  • Sensitive test: 500-1000 mL of fluid (can rule out presence of GROSS ascites)
  • 50% specificity: confounder= accumulation of fluid in patients with diarrhea
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4
Q

Bulging flanks

A

Weight of intra-abdominal fluid (and effect of gravity on fluid) causing flanks to push outward while supine
- Sensitive but not specific

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5
Q

Flank dullness test

A

Percussing abdomen radiating out from umbilicus: air filled bowels vs dullness from ascites
- Sensitive but not specific

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6
Q

Fluid wave maneuver

A

Place one hand on flanks and tap on opposite flank. Have patient place ulnar hand surface vertically over umbilicus

  • Positive test= fluid wave emanating to contralateral side
  • Specific, not sensitive
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7
Q

Asterixis

A

“Liver flap”

  • Common finding of hepatic encephalopathy
  • Hands start flapping while outstretched
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8
Q

Spider telangectasias

A

Small capillary rupture- sign of liver failure

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9
Q

Palmar erythema

A

Sign of liver failure

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10
Q

Caput medusa

A

Portal hypertension causing dilatation of veins around umbilicus

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11
Q

Palpable spleen

A

Hemolytic anemia

Portal HTN, cirrhosis, obstruction

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12
Q

Foeter hepaticus

A

distinctive breath smell in liver failure (eggs)

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13
Q

Guarding

A

Diffuse or localized tension of abdominal wall

  • Involuntary (rigidity)
  • Voluntary= elicited by gentle or deep pressure
  • Localized rigidity= specific indicator of peritonitis- see absence of respiratory motion in select parts of abdominal wall
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14
Q

Carnett’s sign

A

Induced guarding= patient feels less pain when they tense abdominal wall (intrabdominal problem). If they feel more, this is abdominal wall problem

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15
Q

Abdominal wall tenderness (AWT)/ modified Carnett’s

A

Patient sits forward- at midway the physician increases pressure on tender spot. If tenderness increases–> positive abdominal wall tenderness. If tenderness decreases–> negative test

  • It should not be used in children or elderly patients (because of the risk of misinterpretation).
  • It is useless and inhumane in patients with diffuse abdominal pain who already have rigidity.
  • It is possibly dangerous in patients with an intra-abdominal abscess (straining and increased intra-abdominal pressure may cause the abscess to burst).
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16
Q

Blumberg’s sign

A

Rebound tenderness:
Severe pain of abdominal wall indirectly elicited by sudden release of hand pressure

  • Palpate area of tenderness gently, then deeper and release
  • OR, light indirect percussion over area of pain
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17
Q

Referred rebound tenderness

A

Rebound testing on side opposite to where pain reported.

ex: Rovsing’s sign

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18
Q

Abdominal hyperesthesia

A

Acute pain in abdomen due to any process in or on abdomen (organs, herpes zoster, etc)

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19
Q

The closed eye sign

A

Closed eyes + beatific smile= nonspecific abdominal pain

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20
Q

Stethoscope sign

A

Palpating abdomen using stethoscope (patient doesn’t know they are being palpated)

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21
Q

McBurney’s sign

A

Maximum tenderness/rigidity elicited by pressing finger over McBurney’s point–> appendicitis

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22
Q

Rovsing’s

A

Pain on RIGHT side by pushing on LEFT side (mirror McBurney’s point)

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23
Q

Rectal tenderness

A

Should be carried out on any patients on acute abdomen to confirm appendicitis confined to pelvis
- this sign is only helpful in case of perforation, where the rectal exam reveals a right-sided tender mass that represents the pelvic abscess.

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24
Q

Obturator test

A

Patient flexes hip, rotates internally while supine (or physician pulls ankle towards himself, pushes knee away)

  • Pain (usually referred to the suprapubic region) indicates inflammation in one of the organs surrounding the obturator internus, and is a specific but poorly sensitive sign of retrocaecal appendicitis.
  • Beside appendicitis, the obturator test may also be positive in many obstetric-gynecologic conditions characterized by the presence of pus in the pelvis.
  • In such cases the test is usually positive in both legs, whereas in appendicitis is positive only on the right leg.
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25
Q

Reverse psoas (iliopsoas) maneuver

A

Irritation of iliopsoas muscle due to retrocaecal appendicitis or other localized collections of pus/blood

  • Have patient roll to left side and hyperextend right hip–> positive when pain elicited
  • Low sensitivity, high specificity
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26
Q

VATER syndrome

A

Vertebral defects, Anal atresia, TrachEoesophageal fistula, and Renal dysplasia

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27
Q

Esophageal atresia and tracheoesophageal fistula

A

Embryologic failure of tubal esophagus to connect mouth to stomach, ending in a blind pouch; fistula may connect segment to trachea

  • Associated with VATER syndrome
  • Respiratory symptoms
  • Embyrological defect, likely due to abnormal hedgehog signaling pathway
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28
Q

Esophageal web

A

Eccentric, thin membranes of tissue in the esophagus, most commonly proximal region
Plummer-Vinson syndrome: webs + iron deficiency anemia + glossitis; women; responds to iron supplementation

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29
Q

Esophageal ring

A

Concentric, thin diaphragm of tissue in the distal esophagus, most commonly at GE junction (Schatzki’s ring)

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30
Q

Esophageal diverticula

A

Outpouchings of the esophageal wall

  • True = all layers, including muscle
  • False = mucosa & submucosa only
  • Zenker’s diverticulum = false, cervical esophagus, elderly
  • Epiphrenic diverticulum = true, any age, just above diaphragm

Reflect underlying motor dysfunction

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31
Q

Parietal cells

A

located in ruggae of gastric cardia

  • Secrete HCL, intrinsic factor
  • Stimulated by Histamine (ECL cell), Ach (parasympathetic stimulation), gastrin (G cell)
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32
Q

Chief cells

A

located in ruggae of gastric cardia

- secretes pepsinogen

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33
Q

Mechanism of gastric acid secretion

A
  1. Parasympathetic: Ach–> Ca release–> H+ release
  2. Parasympathetic–> ECL cell–> histamine release–> parietal cell acid secretion
  3. G-cell (in antrum)–> produces gastrin–> stimulates ECL cell–> histamine–> parietal cell acid secretion
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34
Q

Autoimmune vs environmental (H. pylori) atrophic gastritis

A

Autoimmune=

  • immune mediated
  • female predominant
  • body and fundus of stomach
  • < 20% have H. pylori
  • Antibodies to parietal cells and IF
  • Decreased B12, increased gastrin

Environmental gastritis=

  • H. pylori or diet
  • no sex predilection
  • antrum predominant with extension to body, multifocal
  • 90-100% H. pylori colonization
  • NO antibodies, normal B12, perhaps slight increase in gastrin
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35
Q

Odynophagia

A

Pain with swallowing:

  • Due to inflammatory (infectious) or severe reflux esophagitis
  • Seen with candida, herpes, CMV ulcers, pill induced, severe spasm, achalasia
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36
Q

Physical risk factors for GERD

A
  • Obesity
  • Delayed gastric emptying
  • Pregnancy (76% by 3rd trimester)
  • Systemic sclerosis
  • Hiatal hernia
  • Recumbency
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37
Q

Behavioral risk factors of GERD

A
  • Smoking
  • Alcohol use
  • Taking medications such as calcium channel blockers, nitrates, OCP (Progestational), Beta Adren., theophylline
  • Consuming large meals (especially before bedtime)
  • Eating certain foods such as chocolate, coffee, peppermint, or fatty foods
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38
Q

Mechanisms of sphincter incompetence

A
  • Transient Lower esophageal sphincter relaxations (majority of cases)
  • Abdominal pressure
  • Spontaneous Gastro-esophageal reflux
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39
Q

Complications of GERD

A
  • Esophagitis
  • Peptic stricture
  • Esophageal hemorrhage
  • Esophageal ulcer
  • Pulmonary symptoms
  • Barrett’s esophagus
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40
Q

Pre-esophageal dysphagia/ oropharyngeal dysphagia= “transfer dysphagia”

A

Difficulty initiating swallow due to:

  • Pharyngeal weakness, incomplete upper esophageal sphincter relaxation, obstruction
  • Neurologic, myopathic, ENT, GI disorders (CVA, polymyositis, myasthenia gravis, ALS)
  • Symptoms= nasal regurgitation, coughing, choking
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41
Q

Evaluation of esophageal dysphagia

A
  • Barium swallow
  • Esophagoscopy (biopsy) essential to evaluate for obstructing lesions (SOLID food dysphagia)
  • Esophageal manometry- look for motility disorders (SOLIDS and LIQUIDS)
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42
Q

SOLID food dysphagia

A

due to OBSTRUCTION from:

  • Carcinoma (recent, progressive dysphagia in older patients: Barretts–> adenocarcinoma or smoking/alcohol–> squamous cell carcinoma)
  • Peptic stricture
  • Web/ring (intermittent)
  • history v. important
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43
Q

Solid and liquid dysphagia causes

A
  • Achalasia (discoordinated swallowing)
  • Scleroderma
  • Diffuse esophageal spasm
  • Eosinophilic esophagitis
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44
Q

Causes of achalasia

A
  • Hypertensive LES (contracted)
  • Absent peristalsis
  • Poor relaxation of LES
  • Slowly progressive symptoms: Must R/O carcinoma invading E/G junction, neural plexus (secondary achalasia),
  • In older patients with greater weight loss, shorter duration of symptoms–> “pseudo achalasia”/secondary achalasia due to malignancy
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45
Q

Sources of esophageal pain

A
  1. Chemo receptors: H+, K+, Histamine, Serotonin
  2. Stretch receptors: submucosa, muscularis propria
  3. NO cut, tear, crush receptors

–> heartburn, odynophagia

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46
Q

Pathophysiology of GERD

A
  • Impaired acid neutralization by saliva, bicarb
  • Impaired esophageal motility
  • LES (lower esophageal sphincter) weak or inappropriate relaxation
  • Hiatal hernia- can interfere with clearance/ promote reflux but doesn’t cause GERD (exacerbates existing dysfunction, like LES dysfunction)
  • Delayed gastric emptying/ gastroparesis- unclear clinical significance- contents cause increased pressure/stress on LES
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47
Q

Clinical features of achalasia

A
  • See gradual dilation of the esophagus, smoothly tapered end (“bird beak”), air/fluid in posterior mediastinum, absent gastric air bubble
  • Nocturnal respiratory symptoms are common
  • Similar clinical picture with faster/severe onset–> rule out carcinoma
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48
Q

Plummer-Vinson syndrome

A

Esophageal webs + iron deficiency anemia + glossitis; seen in women, responds to iron supplementation

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49
Q

Barrett’s esophagus

A

Change of mucosa of distal esophagus from squamous to intestinal metaplastic columnar mucosa.

  • Extension of columnar mucosa > 3 cm above GEJ
  • Increased risk for adenocarcinoma–> surveillance endoscopy every 1-2 years
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50
Q

Causes of Delayed gastric emptying

A

Presentation: Postprandial bloating, nausea, vomiting

Causes:

  • Mechanical- gastric outlet obstruction (pancreatic mass, tumor, ulcer in stomach)
  • Motility disorder- gastroparesis (diabetic)

Diagnosis: EGD, Gastric emptying scan

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51
Q

Gastric outlet obstruction

A
  • Pyloric stenosis (chronic scarring from peptic ulcer disease)
  • Extrinsic compression- pancreatic cancer
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52
Q

Gastroparesis: treatment

A

Most often due to long-standing diabetes
- can also be idiopathic

Treatment:

  • Prokinetic agents- metoclopramide
  • Frequent small meals
  • Botox
  • Jejunostomy tubes
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53
Q

Chronic idiopathic intestinal obstruction

A

Rare

  • involves small bowel, sometimes colon, stomach
  • Seen with: scleroderma, diabetes
  • Presents LIKE small bowel obstruction
  • Diagnosis-required full-thickness biopsy (see abnormality of issue with NM junction)
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54
Q

Constipation

A

1-4% US population

- Women > men

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55
Q

Differential diagnosis of Chronic Constipation

A
  • Hypomotility (colonic inertia)
  • Drugs (anticholinergics, iron supplements, narcotics)
  • Colon cancer (obstruction)
  • Hypothyroidism
  • Pelvic floor dysfunction (multiparous women)–> rectocoele
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56
Q

Treatment of constipation

A
  • Diet, fluid, exercise
  • Fiber supplementation
  • Reassurance
  • Laxatives: bulking agents (cilium, fiber, cellulose), osmotic, stimulant/irritant, lubricant
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57
Q

Hirschsprung’s disease

A
  • Aganglionic section of bowel, often distal
  • Diagnosed in infancy/childhood
  • Diagnosis with: barium enema, anal manometry, rectal biopsy
  • Treatment: resection of aganglionic section
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58
Q

Irritable bowel syndrome: symptoms and etiology

A

Functional bowel disorder= “there’s nothing wrong with the bowels!”
- Unclear etiology

Symptoms:

  • Chronic
  • Relapsing
  • Abdominal pain/distension
  • Change in bowel function
  • Disordered defecation
  • More frequent stools with onset of pain
  • Passage of mucus
  • Sensation of incomplete evacuation
  • Bloating

Visceral hypersensitivity- altered perception of rectal filling, bowel movements

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59
Q

IBS- diagnosis

A

History: lactase deficiency, excessive sorbitol/fructose

  • Exclude alarm symptoms: blood in stool, weight loss, fever, pain awakening patient from sleep, pain interfering with normal sleep patterns, diarrhea awakens patient from sleep
  • Review meds
  • Psychosocial factors
  • Depression/panic disorders
  • Physical exam should be UNREMARKABLE
  • Labs: CBC, ESR, Chems, sigmoidoscopy, colonoscopy if >50 or >40 plus family history of colorectal neoplasm
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60
Q

Lactulose Breath Test

A

Administer lactulose- if patient begins digesting earlier based on exhaled products, bacteria present up in small bowel- which is a sign of inappropriate bacterial colonization

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61
Q

Inflammatory Bowel Disease (IBD)- definition and epidemiology

A

Chronic, idiopathic, uncontrolled inflammation of intestinal mucosa

  • includes Crohn Disease and Ulcerative Colitis
  • Age of onset: late teens to early 30s
  • More prevalent in Northern climates, industrialized nations
  • Similar rates in M+F
  • Slightly higher rates in Caucasians
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62
Q

Environmental triggers of IBD

A
  • Hygiene hypothesis
  • Helminth exposure–> immune system “distracted” by parasites
  • Diet: no conclusive data (?)
  • Appendectomy- increased risk of CD
  • Acute infections (C. diff) (?)
  • Meds: NSAIDs, antibiotics, OCPs (?)
  • CIGARETTES- protective
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63
Q

Overactive mucosal immune system in IBD

A

Failure to downregulate:

  1. Secretion of cytokines from activated immune cells (TNF-alpha)
  2. Activation of T cells (increased immune response)
  3. Leukocyte trafficking to colon–> cytokine production
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64
Q

Clinical presentation of Ulcerative Colitis

A 
Hematochezia
Diarrhea
Constipation
Tenesmus
Urgency
*Incontinence*
Nocturnal awakening
Lower abdominal pain
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65
Q

Clinical presentation of Crohn Disease

A

Inflammatory: fever, anorexia, weight loss, diarrhea +/- blood, abdominal pain, arthralgias, fatigue

Fibrostenotic: obstruction, diarrhea (bacterial overgrowth)

Fistulizing: perianal, rectovaginal, enterocutaneous, enteroenteric

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66
Q

Fistula

A

Abnormal passage from one epithelialized surface to another (eg between rectum and vagina)

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67
Q

Physical exam in IBD

A

General: pallor, cachexia
Vitals: high HR/ low BP, fever
Abdomen: distention, tympany, tenderness, mass
Perianal (CD): fissure, fistula, abscess, “elephant ears” skin tags
Rectal (UC): gross blood

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68
Q

Extraintestinal manifestations of IBD

A

Related to IBD:

  • Pauciarticular arthritis
  • Erythema nodosum
  • Sweet’s syndrome= neutrophilic dermatosis
  • Episcleritis

Unrelated to IBD:

  • Polyarticular arthropathy
  • Ankylosing spondylitis
  • Sacroiliitis
  • PSC= primary sclerosing cholangitis
  • Pyoderma gangrenosum
  • Uveitis
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69
Q

Lab tests supporting diagnosis of IBD

A

CBC: Anemia, thrombocytosis

CMP: hypokalemia, contraction alkalosis

Other: inflammatory proteins (ESR, CRP), serologies (pANCA= UC, ASCA= CD)

Stool: Inflammation markers (WBC, lactoferrin, calprotectin)

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70
Q

Ulcerative Colitis: colon involvement

A

Very clear demarcation of inflammation vs normal
~ 50% proctosigmoiditis
~ 35% Left-sided
~ 15% pancolitis (involve cecum)

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71
Q

Crohn Disease: colon involvement

A

Patchy “skip” lesions, rectal sparing (not always)

  • Mild: aphthoid ulcers, edema, hyperemic spots, loss of vascular pattern
  • Moderate/severe: deep, linear, stellate, coalescing “bear claw” ulcers, cobblestoning

Rule of Thirds (approx. 30% each)

  • Small bowel and colon
  • Small bowel only
  • Colon only
  • Perianal

Much less common in esophagus or gastroduodenal (except in pediatric pts)

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72
Q

Crohn disease: Surgical indications and types

A

Indications:
- Stricture, perforation, abscess, fistula, refractory disease, hemorrhage, cancer

Types: ileocecectomy, stricturoplasty, fistulotomy/setons

Lifetime incidence: 60-70%

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73
Q

Ulcerative colitis: surgical indications and types

A

Indications: refractory disease, neoplasia, fulminant colitis, toxic megacolon, hemorrhage
*Increased risk of colon cancer: colectomy with signs of dysplasia on colon biopsy

Types: total colon removal

Lifetime incidence: up to 30%

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74
Q

Colon Cancer risk in IBD

A

Increased risk in IBD pts based on: duration, extent, inflammation severity, pseudopolyps, family history, smoking

  • 5-ASA decreases risk

Surveillance: 8-10 years after onset, every 1-2 years depending on extent (4-quadrant biopsies every 10 cm)

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75
Q

Microscopic colitis

A

Subtype: lymphocytic vs Collagenous

Macroscopic: normal colon

Histology: increased epithelial lymphocytes, thickened subepithelial collagen layer

Clinical: women, 50s-60s, non-bloody diarrhea, NSAID history

Treatment: anti-diarrhea agents, bismuth salicylate, 5-ASAs, budesonide

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76
Q

Black pigment stones

A
  • Polymers of calcium bilirubinate and mucoprotein, <10% cholesterol
  • 50% radiopaque
  • Seen in patients with cirrhosis and chronic hemolytic conditions (Thalassemias, Sickle cell)
  • Migrates out of gallbladder: 80% cholesterol, 20% black pigment
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77
Q

Brown pigment stones

A
  • Calcium salts of unconjugated bilirubin with variable amounts of protein and cholesterol.
  • Primary bile duct stones.
  • Associated with biliary infection leading to bacterial deconjugation of bilirubin.
  • Asians, secretory IgA deficiency.
  • Form in bile duct as a result of stasis, above stricture, foreign body, setting of infection
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78
Q

Cholesterol gallstones

A

75-80% of gallstones in US

- 70% cholesterol by weight, radiolucent

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79
Q

Formation of cholesterol gallstones

A

Formation=

  • Cholesterol saturated bile: increased ratio of cholesterol to bile salts
  • Accelerated nucleation
  • Gallbladder hypomotility
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80
Q

Cholesterol saturation mechanisms

A

Caused by anything lowering bile salt production or recycling OR increased cholesterol levels:

  • impaired bile salt return (Crohn, small bowel resection, drugs= cholestryramine)
  • Oversensitive feedback mechanism to turn off Cholesterol-7-hydorxylase–> reduced bile acid synthesis.
  • Excessive cholesterol synthesis: HMG-CoA reductase is stimulated by insulin and food intake, obesity.
  • Combined mechanism: estrogens increase cholesterol synthesis and decrease bile acid formation.
  • Age, obesity, progesterones
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81
Q

Nucleation of cholesterol gallstones

A

Cholesterol made soluble through association with phospholipids (lecithin) and bile salts–> vesicles and micelles

  • Cholesterol saturation increases–> larger than vesicles/micelles–> precipitation
  • Nucleation promoters= mucin glycoproteins
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82
Q

Growth of cholesterol gallstones

A
  • Cholesterol crystals acquire additional cholesterol to form visible stones.
  • Alternating layers of cholesterol and mucoprotein add strength to the stones.
  • Gallbladder hypomotility facilitates stone formation.
  • Gallbladder sludge: thick mucoprotein with entrapped cholesterol crystals is thought to be a stone precursor.
  • Can be seen with fasting, TPN, octreotide and can resolve spontaneously.
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83
Q

Symptomatic gallstones

A

Only 20% gallstones

  • Biliary colic
  • Acute cholecystitis

*Asymptomatic gallstones may lead to gall bladder removal due to concerns of sickle cell disease??

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84
Q

Gallstones biliary colic

A
  • Steady pain
  • Transient cystic duct obstruction
  • Epigastric, postprandial, visceral-type pain
  • 1-3 hours
  • Recurrent attacks in 50%, complications 1-2%/year
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85
Q

Acute cholecystitis

A
  • RUQ pain > 3 hours, parietal-type pain
  • Bacterial infection
  • Fever
  • Murphy’s sign, Boas’ sign (Right scapula referred pain)
  • Leukocytosis, elevated LFT’s
  • Symptoms resolve in 75% in 72 hours
  • 25% symptoms persist with complications (empyema, perforation, abscess)
  • Surgery
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86
Q

Complications of gallstones

A
  • Cholangitis= fever, pain, jaundice
  • Acute pancreatitis
  • Mirizzi’s syndrome= compression of stone against bile duct–> obstruction
  • Papillary stenosis= scarring due to passage of small gall stones
  • Choledocho-enteric fistulas= stone moves through gall bladder into bowel
  • Gallstone ileus= migrates into intestine, gets stuck in ileocecal bowel (obstruction)
  • Gallbladder cancer
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87
Q

Gallstones–> gallbladder cancer

A
  • Accounts for 30-50% of gallstone related deaths.
  • 80% of patients with gallbladder cancer have gallstones.
  • 1% of patients with gallstones have gallbladder cancer at autopsy.
  • 50% of patients with porcelain gallbladder develop gallbladder cancer.
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88
Q

Diagnosis of gallstones

A
  • History and physical
  • Plain abdominal x-ray- visualize 20% of gallstones only
  • Abdominal ultrasonography
  • Hepatobiliary scan (HIDA): IV tracer–> should be taken up by gallbladder, if not= stone obstructing cystic duct
  • Endoscopic ultrasound
  • MRI/ERCP
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89
Q

Treatment of gallstones

A

Surgical removal of gallbladder (laproscopic) with:
- Recurrent biliary colic
- Acute cholecystitis
Stabilize patient with IV fluids, antibiotics, no food
#1 treatment: best to remove when symptomatic, BEFORE complications (as mortality in operation increases with complicaitons/age)

Non-surgical: reserved for patients UNFIT for surgery (dissolution therapy, lithotripsy)

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90
Q

Gallstones: Complications of treatment

A
  • Biliary strictures- treat with balloon dilatation
  • Bile leaks- stent duct to allow tissue to heal
  • Choledocholithiaisis- gallstones in common bile duct entering peritoneum
  • Transection of a bile duct- BAD- have to resect bowel loop to reattach duct to intestines
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91
Q

NOTES

A

Natural orifice transluminal endoscopic surgery

Transvaginal, transoral, transrectal surgery (no skin perforation)

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92
Q

Functional definition of diarrhea

A

Subjective= increase in stool liquidity

  • increase in stool frequency (> 3 BM/day)
  • abnormal constituents in stool
Specific: stool weight > 250 gm/day
- Western > 200 gm
- Vegetarian > 200-500 gm
Diarrheal conditions
- IBS: 250-500 gm
- Osmotic: 500-1000 gm
- Secretory > 750 gm

**Fecal incontinence not necessarily diarrhea= involuntary release of rectal contents (myogenic vs neurogenic)

  • Chronic= > 4 week decrease in stool consistency (acute < 4 weeks)
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93
Q

Pathophysiology of diarrhea

A

Osmotic= Food/nutrients not absorbed–> remain in lumen, causing water to move with osmotic gradient into lumen

Secretory= epithelial electrogenic pumps secreting excess electrolytes into lumen–> water follows

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94
Q

Fecal osmolar gap

A

Fecal osmolality (290) – (2 x (Na +K))

  • Osmotic diarrhea gap > 50
  • Secretory diarrhea gap < 50
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95
Q

Osmotic diarrhea

A

Caused by the ingestion of solutes that can not be absorbed or digested

Characteristics:

  • Stool volume < 1L/day
  • Resolves or decreases with fasting
  • Fecal Na is low as Na has been replaced by an osmotically active solute
  • Stool osmotic gap > 50
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96
Q

Cause of osmotic diarrhea

A

Lactase deficiency, carb malabsorption, disaccharidase deficiency
Steatorrhea: maldigestion/absorption of fats
- Pancreatic insufficiency–> lipase deficiency
- Bile salt deficiency due to ileal resection, disease, bacterial overgrowth–> destruction, hepatic disease
- Small bowel mucosal disease
Laxatives and antacids
Poorly absorbed carbs: sorbitol, manitol, fructose
Rapid transit (following gastric surgery, hyperthyroidism)

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97
Q

Secretory diarrhea: definition

A
  • Toxin or peptide which increases cAMP production in small bowel
  • Stool daily volume is >1 liter
  • Persists with fasting
  • Salt and water absorption is impaired
  • Stool osmotic gap <50 (as stool contains high Na content)
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98
Q

Bacterial causes of secretory diarrhea

A

Toxin producing infections:

  • Vibrio cholera (classic): Causes increase in production of cAMP and increase in Na secretion; Absorption mechanisms stay intact
  • E. coli: travelers diarrhea
  • Staph and Clostridia: preformed toxins
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99
Q

Causes of motility changes in diarrhea

A

IBS: crampy, colicky, painful–> relieved by BM; diarrhea alternates with constipation
Diabetes- nephropathy
Hyperthyroidism

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100
Q

Exudative diarrhea: causes

A

Exudative diarrhea= mucous, pus and blood in stool

Inflammatory bowel disease

  • Crohn’s disease
  • Ulcerative colitis

Malignancy

Invasive infectious organisms

  • Shigella, salmonella, campylobacter
  • amoeba
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101
Q

Fecal leukocytes: causes

A

Bacterial infections, IBD, ischemic colitis

* NOT seen in viral infections, IBS, osmotic/secretory conditions

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102
Q

Ova/parasites in stool

A

Can find:

  • Amoeba, giardia, hookworm, ova strongyloides
  • Duodenal aspirate best for suspected GIARDIA (rule out false negative in stool samples)
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103
Q

Factitious diarrhea: rule out

A

Alkalinize stool specimen:

- Add 0.1 N NaOH–> turns red if phenolphthalein (laxative) present

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104
Q

C. Difficile treatment

A
  • Antibiotics
  • Fecal transplant
  • Do NOT give Imodium/anti-diarrheals (keep bacteria in intestines)
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105
Q

Chronic diarrhea without blood

A

Lactose Intolerance
Diabetes
Infectious: HIV (microsporidia, isospora and cryptospora), Giardia
Diabetes associated with nocturnal diarrhea
Irritable bowel syndrome
Microscopic colitis

106
Q

Diagnosis of chronic diarrhea without blood

A
  • Lactose-free diet trial
  • Thyroid function tests
  • Stool for WBC’s, O+P, even culture
  • Consider colonoscopy for colonic polyps (villous adenoma), mild IBD, collagenous colitis, microscopic colitis

Fast patient for 48 hours: if malabsorption is suspected (steatorrhea):

  • 72 fecal fat collection (100gm fat diet) nl <7gm/24hours
  • D-xylose test if abnormal suggest small bowel, if nl suggests pancreatic insufficiency
  • Small bowel malabsorption celiac, Whipples, Crohn’s

Bacterial overgrowth: Hydrogen breath test, Trial of antibiotics
Schilling test for B12 absorption

107
Q

Chronic diarrhea with blood

A
  • IBD (UC)
  • Colon Cancer
  • Colon polyps
  • Colonoscopy
108
Q

Pathogenesis of diverticular disease

A

Very common in elderly (incidence correlates with age)

  • Poorly understood but is related to intestinal motility, colonic structure, diet and genetics
  • Low residue/ low fiber diet
  • May be related to muscular hypertrophy of the colon and increased intraluminal pressure
  • Prolonged colonic transit, decreased fecal fiber
109
Q

Hormonal causes of secretory diarrhea

A
  • Pancreatic cholera (increase VIP secretion–> watery diarrhea, hypokalemia, achlorydia)
  • Carcinoid syndrome (serotonin)
  • medullary thyroid cancer (calcitonin, prostaglandins)
  • Zollinger-Ellison syndrome (gastrin)
  • MIXED
110
Q

Iatrogenic causes of secretory diarrhea

A

Bile salts: ileal resection or disease

Factitious diarrhea

111
Q

Accessory pancreas

A

Pancreatic tissue present outside normal location

  • Seen in up to 14% autopsies
  • Stomach, small intestine, Meckel’s diverticulum
112
Q

Annular pancreas

A

Abnormal ring of pancreas encircling duodenum

- 1/7000 people: associated with Down’s syndrome

113
Q

Pancreas divisum

A

Failure of dorsal and ventral bile ducts to fuse (3-10% of population.
- Main drainage to duct of Santorini

114
Q

Acute Pancreatitis

A

An inflammatory condition of the exocrine pancreas that results from injury to acinar cells. Altered acinar cell protective mechanisms–> intracellular activation of digestive enzymes–> pancreatic autodigestion
Clinical presentation:
- Attacks typically very mild, about 20% of very severe.
- An attack lasts for a short time and usually resolves completely
- Severe cases lead to hemorrhagic pancreatitis with massive necrosis.

115
Q

Parietal cell

A

Neck of gastric gland–> bulges into gastric lumen

Resting state (sleeping): prominent cytoplasmic tubulovesicles, apical canaliculus

Active state: tubulovesicles disappear, canaliculi coalesce–> elongated microvilli–> acid into lumen (active transport)

116
Q

Gastric gland

A

Mucous neck cells: Secrete mucin and bicarb; precursor cells of other epithelial cells

Chief cells: secrete pepsinogen

Endocrine cells:

  • G cells= gastrin
  • D cells= somatostatin
  • ECL cells (enterochromaffin-like)= Histamine
117
Q

Stimulants to parietal cell

A

Vagus–> Ach–> parietal cell Ach receptor

Stomach stretch, digested food, vagus–> G-cells in stomach–> Gastrin

Ach + Gastrin–> ECL cell–> Histamine–> parietal cell–> acid release

118
Q

Ach release in stomach

A

Sight/Smell/Taste of food causes the Vagus nerve to release acetylcholine and stimulate the parietal cell by binding to the AcH receptor

119
Q

Gastrin release

A
  • Released by the G-cells in the stomach
  • Stimulants of gastrin: Stretching of the stomach, Digested food, Vagus nerve
  • Binds to gastrin receptors on the parietal cell
120
Q

Histamine release

A
  • Released by ECL cell
  • Stimulants of histamine release: gastrin, Ach
  • Binds to parietal cell–> activation–> acid secretion
121
Q

Gastric defense mechanisms

A

Pre-epithelial (luminal)- Mucous-bicarb barrier, surface phopholipids, mucoid cap

Epithelium- tight junctions, rapid turnover, surface cells maintain intracellular pH

Subepithelial- mucosal blood flow

122
Q

Duodenal defense

A

Bicarbonate gradient along proximal to distal duodenum prevents acid from damaging epithelium

123
Q

Acid overproduction states

A 
Gastrin: 
- Gastrinoma (sporadic or MEN-1)
- G cell hyperplasia (H pylori-associated)
H pylori:
- Direct parietal cell stimulation 
Histamine:
- Systemic Mastocytosis
ICU stress ulceration:
- Head trauma (Cushing Ulcer)
- Burns (Curling Ulcer)
Idiopathic hypersecretion
124
Q

Diseases/iatrogenic damage to gastric defense

A

NSAIDs
H. pylori (duodenal ulcers)
Other (ischemia, neoplasia)

125
Q

Pathogenesis of H. Pylori ulceration

A

Virulence factors:

  • Urease neutralizes acid in lumen (survival)
  • Decreased acid–> decreased mucous production–> Penetrates mucous–> inflammation
  • Stimulates parietal cell secretion–> hyperchloridia

Hypergastrinemia
- Antrum infection–> Decreased D-cell mediated secretion of somatostatin–> lack of gastrin inhibition–> increased acid

Decreased mucosal bicarb–> duodenal ulcer (90% correlation with h. pylori)

  • Gastric acid hypersecretion–> acid to duodenum
  • Gastric metaplasia in duodenum + excess acid overwhelming duodenal defenses–> ULCER
126
Q

NSAID induced ulceration

A

Direct effects:

  • Gastric pH maintains hydrophobicity of drugs–> diffuse across cell membranes
  • Neutral cellular pH- drug loses proton–> trapped intracellularly–> toxic to epithelial cells (effect mitigated by enteric coating)

Systemic effects:

  • Mucous bicarbonate: Thins mucous bicarbonate layer (quantity and quality of mucous)
  • Epithelial layer: Reduces epithelial cell proliferation (can’t repair)
  • Subepithelial layer: NSAIDs reduce mucosal blood flow by blocking prostaglandings–> weakened defenses, ulceration
127
Q

Diagnosing gastric ulcers

A

Barium: Visualize central mucosal defect
- No ability to obtain tissue or perform therapy

Endoscopy

  • Direct visualization of ulcer
  • Apply hemostatic therapies
  • Sample tissue to determine etiology of ulcer
  • Sample gastric pH
  • Evaluate for hypersecretory states
128
Q

Complications of peptic ulcer disease

A

Bleeding (15%): seen with age, comobidities, antiplatelets/coagulants, NSAIDs

Perforation (7%): Duodenal–> anterior wall; Gastric–> anterior lesser curve

Penetration: Ulcer bores into adjacent organs

  • Gastric: left hepatic lobe, colon
  • Duodenal: posterior to pancreas (gastroduodenal artery–> exsanguination)

Obstruction (2%): functional or mechanical (scarring)

129
Q

Non-healing ulcer: causes

A
  • Failure to eradicate H pylori (85-90% eradication with therapy)
  • Noncompliance with medication
  • Malignant etiology
  • Recurrent NSAID use (May not be purposeful)
  • Tobacco use
  • Hypergastrinemic states
  • Other etiology (Crohn’s…)
130
Q

Types of Gross (overt) GI bleeding

A

Red per rectum: lower GI bleeding or brisk bleeding from upper GI sources

Melena (black, tarry, malodorous stool= oxidation of heme): upper GI tract blood due to small bowel, proximal colon bleeds

131
Q

Clinical presentation of overt bleeding

A
  • Hemetemesis: Red blood and/or coffee grounds, Upper digestive tract bleed
  • Symptoms of anemia
  • Syncope, chest pain, pallor, dyspnea
132
Q

Clinical presentation of occult bleeding

A 
Symptoms of anemia: 
- Iron deficiency anemia
- Pallor
- Dyspnea on exertion
- Fatigue/lightheadedness
Positive hemoccult test
133
Q

Shock

A

Class 1: HR < 100
Class 2: HR > 100
Class 3: Decreased BP
Class 4: Confused mental state

134
Q

NG aspiration and Stool color

A

NG clear + Brown/red stool= 6% mortality

NG coffee ground + Black = 8.2%
NG coffee ground + red= 19.1%

NG bright red + brown stool= 12.3%
NG Bright red + black= 19.4%
NG bright red + red= 28.7%

135
Q

Hemodynamic shock resuscitation

A
  1. IV O2 monitor
  2. IV access: 2 large bore 14/16 g catheters, antecubital or femoral

Replete volume:

  1. Saline
  2. RBC/ blood product
  3. Measure hemodynamics, URINE output (adequate resuscitation)

EKG

136
Q

Sites of GI bleeding

A

Esophagus:
- Esophagitis, ulcer, Mallory-weiss tear (retching induced), varices, cancer

Stomach:
- Gastritis, ulcer, varices, portal gastropathy (liver failure), cancer, angiodysplasia, Dieulafoy lesion (tortuous lesion in stomach that quickly recedes)

Duodenum:
- duodenitis, ulcer, cancer, angiodysplasia, aortoenteric fistula, hemobilia (biliary tree bleed), hemosuccus pancreatitis (bleeding from pancreas)

Small bowel:
- ulceration, angiodysplasia, tumors, Meckel’s diverticulum

Colon:
- Diverticulosis, angiodysplasia, cancer, colitis/colopathy (IBD), hemorrhoids/ fissures

137
Q

Diagnosis of Lower GI bleed

A
  1. Rectal exam

Small bowel:

  • Capsule enteroscopy (obscure bleeds after endoscope negative, while still bleeding)
  • Meckel scan
  • Small bowel barium x-ray
  • Enteroscopy

Colonic:
Colonoscopy:
- early: localize site, administer therapy
- can’t see anything during ACTIVE bleed

Red cell scintigraphy:

  • Technetium-labeled RBCs
  • detects 0.5-1 mL/min bleeds
  • DOESN’T ID bleed site

Tc=99 Sulfur colloid scan

  • 0.1 mL/min bleed
  • used with pertechnetate for Meckel’s
  • Low specificity

Angiography:

  • 0.5-1 mL/min bleed
  • Highly accurate, can intervene during scan
  • Rare complications: arterial thrombosis, contrast reactions (allergic, ARF), pseudoaneurysms
  • Cannot define structure of bleeding lesion
138
Q

Gastric Pre-epithelium

A

Luminal barrier

  • Mucous-bicarbonate: produced by mucous neck cells, defends against H+, mechanical barrier
  • Surface phospholipids: increase viscosity, hydrophobicity of mucous layer
  • Mucoid cap: response to injury–> second mucous layer with neutral pH–> microenvironment for mucosal repair
139
Q

Gastric epithelium

A

Tight junctions between epithelial cells
Rapid turnover of damaged cells:
- Reconstitution: migration of cells from along pit to repair small defects
- Regeneration: cellular proliferation to repair larger defects
Surface cells: maintain intracell pH even when exposed to gastric acid (mucous layer absent)

140
Q

Gastric subepithelium

A

Layer preserving mucosal blood flow:

  • Provides nutrients to support cell turnover (in epithelium)
  • Supplies bicarb for mucous layer
  • Buffer of H+ ions
141
Q

Non-NSAID/h. pylori causes of mucosal disruption

A
  • Cancer (ulceration)
  • Adrenocorticosteroid use
  • Alcohol use
  • Tobacco: inhibits healing of ulcers (decreased blood flow), but doesn’t cause ulcers
142
Q

Diagnosis and Therapy for upper GI bleed

A

Diagnosis:

  1. NG lavage
  2. Endoscopy (esophagus, stomach, duodenum, proximal jejuneum with enteroscope)

Treatment:
Endoscopic:
- Injection of epinephrine, saline, slerosant, alcohol (shrink vessles, replenish fluids)
- Electrothermal
- Band ligation (varices)
- Argon plasma coagulation
- Endoscopic clips
- Minnesota tube
- Interventional radiology: embolization, transjugular intrahepatic portosystemic shunt (TIPS) for varices
- Surgery: uncontrolled ulcer bleeds, massive bleeding (aortoenteric fistulae)

143
Q

Hereditary pancreatitis

A

AD disease with 80% penetrance

  • Cationic trypsinogen gene (PRSS1) and serine protease inhibitor gene (SPINK1) mutations–> trypsinogen autoactivation
  • Labs identical to hereditary pancreatitis
  • Earlier age of onset, less pancreatic calcification, DM
  • 40% develop pancreatic ductal adenocarcinomas
144
Q

Non-neoplastic pancreatic cysts

A

Simple= sporadic, or part of AD polycystic kidney disease or Von Hippel Lindau disease

Pseudocysts= complications of chronic pancreatitis, not true cyst (no epithelial lining)

145
Q

Acute Pancreatitis: cellular/glandular events

A

Dissolution of organelles and membranes:

  • Release of cellular components (phopholipase, lysolecithin, elastase)
  • Release of cytokines (PAF, TNF-alpha, IL-1b…)

Increased vascular permeability (influx, activation of inflammatory cells

Formation of reactive metabolites

  • Dissolution of bloods vessels and extracellular matrix
  • Thrombosis, hemorrhage (third space losses–> patient dehydrated due to internal hemorrhage)
  • Tissue necrosis (fat necrosis, pancreatic and peripancreatic necrosis)
146
Q

Acute pancreatitis: Renal effects

A
  • Lack of adequate fluid intake
  • Capillary leak with massive intraabdominal fluid loss
  • Hemorrhage
  • Kallikrein-mediated peripheral vasodilation
  • Pain with inspiration–> low tidal volume
  • Hemorrhage–> reduced O2 carrying capacity
147
Q

Acute pancreatitis: Pulmonary effects

A
  • Phospholipase A2 (from pancreas) degrades surfactant and alveolar membranes
  • diaphragmatic excursion restricted by subdiaphagmatic inflammation
148
Q

Acute pancretitis: DIC

A

Systemic efffect of released cellular mediators leading to diffuse activation of fibrinolyitic and coagulation pathways

149
Q

Acute pancreatitis: Systemic effects

A
  • Renal failure
  • Pulmonary failure
  • DIC
  • Shock (vascular collapse)
150
Q

Etiology of acute pancreatitis

A
  • 50%: bile duct stones= obstruct both gall bladder and pancreatic duct at sphincter of Oddi–> ductal hypertension
  • 30%: alcohol (more commonly chronic pancreatitis)
  • 13%: other= obstructing tumor, dysfunction with sphincter of Oddi, helminths, pancreatic pseudocyst/stone/stricture, pancreas divisum, annular pancreas (anything causing partial obstruciton), medications, hyperlipidemia, hypercalcemia, trauma, toxins, vascular injury, autoimmune, infection (parasites, mumps, viruses), genetic
  • 7%: idiopathic
151
Q

Presentation of acute pancreatitis

A

Abdominal pain, back pain (pressing against spine)
Nausea, vomiting
Low grade fever (up to 101)
Dehydration

Exam: mild distention, decreased bowel sounds, tenderness

152
Q

Lab tests for Acute pancreatitis

A

Amylase (80-90% sensitive, 70% specific)
Lipase (90% sensitive, 90% specific)

  • Magnitude of elevation is NOT of prognostic significance
153
Q

Imaging in acute pancreatitis

A

CT= method of choice (92% sensitive, 90% specific)

  • Can give severity of pancreatitis
  • First scan should be done WITHOUT contrast (as they’re dehydrated- protect the kidneys!)
  • 72 hours after hydration, start IV contrast scanning

MRI is NOT better for acute pancreatitis (better for OTHER pancreatic diseases)- BUT, use with contrast allergies, pregnancy

154
Q

Prognosis of acute pancreatitis

A

80% mild

20% severe (9% total die from disease- multi-system organ failure, infection)

155
Q

Diagnosis of acute pancreatitis

A

Bedside assessment= underestimates severity of disease
CT criteria: fluid collections, necrosis, calcifications
Scoring systems: Ranson, Glasgow, Apache II
Serum markers: CRP, trypsinogen activation peptide (TAP), monocyte chemotactic protein (MCP-1)

Histo: fat saponification (think vegetable cell), calcification

156
Q

Treatment for acute pancreatitis

A

No therapy interrupts acute autodigestion/inflammatory process

Therefore:

  • Assess severity/assign level of care
  • Provide supportive care
  • Prevent and treat complications

Seek etiology

157
Q

Supportive care for acute pancreatitis

A

Aggressive fluid, electrolyte replacement (25 cc/kg NS bolus, follow 3 cc/kg/hr infusion)
NPO
Monitoring (intravascular volumes)
Analgesics, anti-emetics
Antibiotics: ONLY with sign of infection
Nutritional support (enteral preferred- feed the gut to enhance immune function in intestines)
Organ failure support (mechanical ventilation, dialysis, pressors)

158
Q

Chronic pancreatitis

A

Persistant, progressive disease
- Changes in pancreatic structure/function precede symptoms, always persist even after precipitating cause corrected

  • Reduced acini, increased islet cells
159
Q

Pathophysiology of chronic pancreatitis

A
  • Increased permeability: increased intraductal Ca and proteins–> protein plugs and stones
  • Low-grade ductal obstruction
  • Ductal atrophy, disruption
  • Glandular inflammation and fibrosis (fibroblasts, lymphocytes, plasma cells)
  • Loss of exocrine/endocrine tissue
  • Develop hard, fibrotic gland
160
Q

Etiology of chronic pancreatitis

A

1) Alcohol (95%):
- Direct acinar cell toxicity
- Alters membrane infrastructure–> increased permeability
- Increased basal protein secretion
- Decreases trypsin inhibitor
- Alters lithostatin–> precipitation of Ca

2) Non-alcohol etiologies (5%):
- Chronic partial duct obstruction
- Hereditary (Abnormal trypsinogen gene, Abnormal trypsin inhibitor gene, Cystic fibrosis, Other CFTR mutations)
- Autoimmune

161
Q

Presentation of chronic pancreatitis

A

Recurrent :
- 50% present with recurrent attacks of acute pancreatitis

Insidious:

  • 35% present with the insidious onset of abdominal pain
  • 15% present with the insidious onset of: malabsorption, diabetes, jaundice
162
Q

Symptoms of chronic pancreatitis

A 
Acute pancreatitis
Chronic pain / nausea: Constant, dull, radiates to back, worse with food
Malabsorption: Diarrhea, steatorrhea
Diabetes 
Weight loss
163
Q

Diagnosis of chronic pancreatitis

A

MRI/MRCP= GOLD standard
- Shows parenchymal fibrosis, ductal abnormalities
CT: irregular contour, calcifications, dilated duct, cysts
Endoscopic ultrasound
Plain X-ray film: shows calcifications

164
Q

Complications of chronic pancreatitis

A
  • Narcotic addiiction
  • Malnutrition
  • Pseudocyst formation
  • Common bile duct obstruction
  • Duodenal obstruction
  • Splenic vein thrombosis–> gastric varices (bleeding complications)
165
Q

Physical appearance with liver pathology

A

General appearance:

  • Muscle wasting
  • Paucity of body hair (axillary, pubic)
  • Parotid enlargement
  • Testicular enlargement, gynecomastia

Skin:

  • Excoriations (itching)
  • Echhymoses, petechiae, spider angiomata, palmar eythema
  • Pallor, abnormal pigmentation
  • Needle tracks (IVD use)
  • Scarring
  • Dupuytren’s contractures
  • Peripheral edema

HEENT:
- Scleral icterus, Kayser-Fleischer rings (copper rings= Wilson’s disease)

Abdomen:

  • Liver tenderness, englargement, firmness
  • Ascites, splenomegaly, prominent abdominal collateral vessels

Neuropsychiatric:
- Confusion, depression, memory loss, inappropriate/unusual behavior, asterixis (hand flap), fetor hepaticus (acetone scented breath)

166
Q

Bilirubin

A
  • Relative index of the efficiency of hepatic capacity for transport and metabolism
  • Degradation product of RBCs processed in liver–> conjugated and excreted
  • Jaundice is often the first clinical sign detected in patients with liver disease
  • Jaundice becomes clinically apparent when the serum bilirubin exceeds 3 mg/dL (normal 0.2-1.0 mg/dL)

Abnormalities:

  • Obstruction
  • Liver can’t conjugate (liver failure)
167
Q

Unconjugated Hyperbilirubinemia

A

Diagnosed if more than 80% of an elevated total bilirubin is indirect

Elevation results from either:

  1. Increased bilirubin production
    - Hemolytic anemia (bilirubin rarely > 4 mg/dL)
    - Hematoma
    - Ineffective erythropoiesis (thalassemia, pernicious anemia)
    - Neonatal (physiologic) jaundice
  2. Reduced hepatic ability to conjugate bilirubin= Glucuronosyltransferase deficiency in:
    - Gilbert’s syndrome (young men)= jaundice in times of stress/illness- not fatal
    - Crigler-Najjar syndrome (rare)
    - Neonatal (physiologic syndrome)
  3. Reduced uptake by hepatocytes due to: drugs/toxins, neonates, hepatocellular injury
    - May present with elevated conjugated bilirubin as well
168
Q

Conjugated hyperbilirubinemia

A

Diagnosed if more than 50% of elevated bilirubin is direct. Elevation results from:

  1. Impaired flow through canaliculus/bile duct (uptake/storage/secretion):
    - Intrahepatic hepatocellular canalicular, ductular damage (hepatitis)
    - Dubin-Johnson syndrome (pigmentation)
    - Rotor’s syndrome (benign process)
  2. Extrahepatic biliary obstruction (stones, tumors, stricture):
    - Choledocholithiasis
    - Tumor
    - Primary sclerosing cholangitis
169
Q

Aminotransferases

A

Enzymes involved in the transfer of amino groups to ketoglutaric acid
- Aspartate Aminotransferase (AST)
- Alanine Aminotransferase (ALT)
AST and ALT are elevated in syndromes of hepatocellular injury

  • Aminotransferase elevation is often the first biochemical abnormality detected in a patient with viral, drug-induced or alcoholic hepatitis
170
Q

AST

A

Aspartate Aminotransferase

  • Present in liver tissue
  • Present in heart, skeletal, kidney, brain, pancreas, lung, WBCs, RBCs (therefore not specific for liver disease)
171
Q

ALT

A

Alanine aminotransferase
- Almost exclusively elevated in liver disease (more specific than AST)

ALT> 1000 U/L due to:

  • Acute viral hepatitis
  • Drug toxicity
  • Shock liver (severe hypotension)
  • Autoimmune hepatitis
172
Q

AST/ALT ratio

A

> 2: sensitive (not specific) for alcoholic hepatitis

- Aminotransferases rarely elevated greater than 10 times upper limit of normal in alcoholic liver disease

173
Q

ALT predominance

A 
Chronic viral hepatitis
Nonalcoholic fatty liver disease (NAFLD)
Metabolic diseases (Hemochromatosis, Wilson’s disease, alpha-1-antitrypsin deficiency)
Medications
Autoimmune hepatitis
174
Q

AP (Alkaline phosphatase)

A 
Alkaline phosphatase
Present in: 
- liver, bone (80%) 
- intestine, kidney, placenta 
Liver vs. Bone
- increased gamma-glutamyltransferase (GGT)= liver
- AP isoenzymes= bone

AP elevation connotes either:

1) Cholestasis/ obstruction
- Gallstones
- PSC
- PBC
2) Infiltration of the liver parenchyma:
- fibrosis
- Sarcoidosis

175
Q

Diagnosis of extrahepatic biliary obstruction

A
  • Synthesis of AP by biliary epithelial cells is increased

- Imaging by ultrasound, CT or MRI will demonstrate biliary dilatation

176
Q

Causes of extrahepatic biliary obstruction

A
  • Gallstones (choledocholithiasis)
  • Tumor (pancreas, ampulla of Vater, bile duct, lymph nodes)
  • Stricture, especially primary sclerosing cholangitis (PSC)
  • Inadvertent surgical ligation of biliary structures
  • IgG4-associated cholangitis
177
Q

Causes of Intrahepatic cholestasis

A
  • Primary biliary cirrhosis (PBC: autoimmune destruction of microscopic bile ducts)
  • Medication-induced- block ATPases that allow bile secretion
  • Cellular rejection: ductular-type (liver transplant patients)
  • Graft-versus-host disease
  • Rare: small duct primary sclerosing cholangitis
  • Congenital ductopenic syndromes (rare)
178
Q

Infiltrative disorders causing bilirubinemia

A
  • Granulomatous hepatitis (sarcoidosis, mycobacterial)
  • Malignant infiltration, especially lymphoma
  • Amyloidosis
179
Q

Albumin

A
  • Major plasma protein, synthesized exclusively by the liver
  • Albumin can be decreased in any chronic illness
  • In the setting of chronic liver disease, low albumin is indicative of liver synthetic dysfunction
180
Q

INR

A

International normalized ratio

  • A measure of prothrombin (clotting factor)
  • Early/sensitive marker of synthetic dysfunction
  • Acute liver injury: increased INR: worse prognosis
  • Chronic liver disease: increased INR: advanced disease
  • Cholestatic liver disease: increased INR may be due to malabsorption of fat-soluble Vitamin K
  • Antibiotic use and malnutrition can lead to Vitamin K deficiency
181
Q

Risk factors for cholesterol stones

A
  • Reproductive age women (estrogen)
  • Obesity
  • Oral contraceptives
  • Genetics (Pima indians)
  • Diet/metabolic abnormalities (cholesterol)
  • Drugs (fibrates)
182
Q

Gallbladder neoplasms

A

Benign tumors (papillomas) associated with GALLSTONES

Carcinoma (adenocarcinoma) associated with CHOLELITHIASIS, CHRONIC CHOLECYSTITIS

183
Q

Hepatitis A virus

A

Non-enveloped single-stranded RNA virus

  • Acquired from food ingestion (enteric)
  • Causes acute infection (no envelope= no chronicity): nausea, vomiting, jaundice

Labs:

  • Spilling HAV in feces for 1-2 months before symptoms
  • ALT elevation
  • IgM anti-HAV= fighting off current Hep A infection
  • IgG anti-HAV= history of Hep A infection (neutralizing)
  • Elevated bilirubin (jaundice)

Prognosis: All patients recover (NEVER chronic)

Vaccine:

  • Passive= pooled donor IgG
  • Active= HAV vaccine
184
Q

Hepatitis B virus

A

Enveloped, dsDNA virus
Acute= nausea, vomiting, fever, jaundice
- Acute illness in 35%
- Prognosis: 0.5% fulminant hepatitis–> necrosis, mortality
- Labs:
1) serum HBsAg = beginning of infection
2) IgM anti-HBc (core)= current infection
3) Total anti-HBc= history of infection
4) anti-HBs= immunity (neutralizing antibody)

Chronicity: Progresses to chronic disease in 90% of infants infected (vertical transmission–> immune tolerant phase), only 5% in adults

  • Histo: “ground glass” appearance

Vaccine:

  • Pre-exposure= vaccinate those at risk
  • Post-exposure= HBIG (hep B immune globin) and vaccine
185
Q

Hepatitis C virus

A

Enveloped, ssRNA virus
Labs:
1) HCV RNA
2) anti-HCV+

  • Seldom seen in acute phase (recognized years later in setting of chronic infection
  • 85% chronically infected (enveloped)–> 20% develop cirrhosis
  • 10% cirrhotic individuals develop hepatocellular carcinoma
  • Histo: tightly-formed lymphoid aggregate
  • Vaccine: none
186
Q

Hepatitis D virus

A

Envelope (from HBV infection), ssRNA virus
- Can ONLY Infect HBV-infected cells (chronic HBV infection)

1) Co-infection: aggressive (2-20% mortality) due to simultaneous infection with HBV
- Severe acute disease, low risk of chronic infection

2) Superinfection: Chronic HBV with worsened condition (due to HDV)= 30% mortality
- Decompensation of previously stable chronic HBV

  • Higher risk of acute liver failure, cirrhosis, no clear association with HCC
  • Associated with drugs, dependent on B

Vaccine: vaccinate against HBV

187
Q

Bile salts

A

Component of bile from cholesterol metabolism

  • Secreted in zone 1: stimulates flow of bile towards zone 1 via osmotic gradient
  • Maintains cholesterol homeostasis
  • Emulsifies/ enhances abosorption of dietary lipids in intestine
188
Q

Bilirubin

A

Component of bile from heme breakdown

- Secreted in Zone 3 as bile pigment (yellow-green-brown color)

189
Q

Composition of Bile

A

Bile salts
Bilirubin
Copper

190
Q

Canal of Hering

A

Stem cell area outside of portal tract (biliary system)

191
Q

Ductule (cholangiole)

A

Periphery of portal triad

192
Q

Urobilinogen

A

Bilirubin in colon modified by bacteria
Enters portal blood:
- enterohepatic circulation
- small portion escapes–> urobilin in urine (light yellow color)

Most urobilinogen excreted in feces–> stool color

95% bile salts reabsorbed in terminal ileum–> portal blood; 5% lost in feces

193
Q

Clinical manifestations of biliary disease

A

Bile salt accumulation–> pruritis
Bilirubin–> jaundice (icterus)
Conjugated bilirubin–> dark urine
Extrahepatic biliary obstruction–> pale stool

194
Q

Clinical manifestations of extrahepatic biliary obstruction

A

Jaundice
Pruritis
Dark urine
Pale stools

195
Q

Clinical manifestations of Primary Biliary cholangitis/cirrhosis (PBC)

A

Female
Early signs:
- Asymptomatic with elevated alkaline phosphatase (out of proportion to bilirubin)
- Pruritis without Jaundice
- Malabsorption of fat-soluble vitamin ( can lead to elevated INR in absence of end-stage liver disease due to decreased Vit K absorption)

Later signs:

  • Xanthomas
  • Osteoporosis (Vit D malabsorption)
  • Jaundice, ascites, portal HTN (liver failure)
196
Q

Clinical manifestations of Primary Sclerosing Cholangitis (PSC)

A

Disease of extrahepatic/hilar (large) bile ducts; may involve intrahepatic ducts.
Rule of 7s: 70% male, 70% associted with Ulcerative Colitis/ IBD (rare Crohn association), 7% develop cholangiocarcinoma

Early clinical symptoms

  • Pruritis
  • Jaundice
  • Fever due to ascending cholangitis, abdominal pain
  • Increased Alk Phos

Late signs:

  • End stage liver disease (portal HTN)
  • Cholangiocarcinoma (primary adenocarcinoma of bile ducts)
197
Q

Steatohepatitis

A

Lipid accumulation and fibrotic changes in hepatocytes (vs steatosis)

Alcoholic steatohepatitis (ASH)= chronic alcohol abuse

  • Labs: AST/ALT ratio > 1 (generally > 2), GGT increased
  • Histo: Mallory bodies, giant mitochondria more common, neutrophilic inflammation

Non-alcoholic steatohepatitis (NASH)= no excessive alcohol use. Associated with diabetes, obesity, metabolic syndrome, hyperlipidemia, drugs (corticosteroids), malnutrition

  • Labs: AST/ALT ratio < 1
  • Histo: Glycogenated nuclei
198
Q

Acute hepatitis

A

Clinical evidence of liver disease < 6 months
- Clinical: malaise, low grade fever, nausea, vomiting, RUQ abdominal pain, jaundice

Biochemical:

  • Elevation of aminotransferases (AST/ALT exceed 1000)
  • Bilirubin elevations later, may persist, Jaundice if severe
  • Elevated INR- uh oh!

*Hospitalization indicated for poor PO intake, elevated prothrombin time, encephalopathy

199
Q

Hepatitis E infection

A

Epidemiology similar to HAV: India, Asia, Africa, Central America

  • Infection enteric, usually waterborne
  • Raw deer, undercooked boar
  • Person-to-person spread is rare
  • Recovery is rule EXCEPT in pregnancy–> can lead to chronic infection in 10-20% (only patients with poor prognosis)

Vaccine:

  • Passive= Ig role unknown
  • Vaccine under development (Asia)
200
Q

Chronic hepatitis

A

Liver disease > 6 months
Clinical:
- Early: Fatigue, jaundice, pruritis, cachexia
- End stage: ascites, edema, GI bleed, coagulopathy, encephalopathy, hypersplenism, HCC

Biochem:

  • Hyperbilirubinemia, hypoalbuminemia, (synthetic liver dysfunction)
  • Coagulopathy (elevated prothrombin, elevated INR)
  • Elevated ALT, AST
201
Q

Chronic HBV infection

A
  • Labs:
    1) elevated ALT
    2) HbeAg (immune active phase)
    3) Anti-HBe seroconversion
    4) HBV DNA
  • Increases risk for hepatocellular carcinoma (even outside of cirrhosis)
  • Most common cause of chronic infection worldwide= vertical transmission; in USA= sexual
202
Q

Chronic HCV infection

A

Often asymptomatic, can present 20-30 years post-exposure with symptoms cirrhosis. Screen “baby boomers”
Risk: IVD, blood transfusion prior to 1992
*leading cause of liver tansplantation in US, increased risk of HCC
Natural history:
- Exposure
- 15% resolve spontaneously, 85% chronic
- Chronic: 80% stable, 20% cirrhosis
- Cirrhosis: 75% stable, 25% death
- 4% total die of acute hepatitis

Labs: Hep C antibody, HCV RNA tests

203
Q

Treatment of chronic hepatitis

A 
Interferons
- 70% success in HCV
- Flu-like symptoms
Nucleoside/tide analogs
- HBV active chronicity

Hep C: + Ribavirin

204
Q

Symptoms of fulminant hepatitis

A

Fulminant hepatic failure, acute liver failure

  • Liver failure (encephalopathy and synthetic dysfunction) within 8 weeks onset of disease
  • Cerebral edema: leading cause of mortality
  • Consider liver transplantation immediately
205
Q

Non-alcoholic fatty liver disease (NAFLD)

A

Resembles alcoholic liver disease
Risk factors:
- Diabetes (Type 2), obesity, dyslipidemia
- Affects 10-25% population
- 50-75% incidence in obese individuals
- Most common cause of elevated LFTs in blood donors
- “Cryptogenic cirrhosis”- leading cause

Types:

  1. Steatosis: fat without inflammation, no fibrosis, non-progressive
  2. NASH: fat and inflammation, central hyaline sclerosis, progressive
    * can only determine type by liver biopsy
206
Q

Diagnosis and treatment of NAFLD

A

Diagnosis:

  • Hepatomegaly
  • Ultrasound, CT, MRI: bright (fat in liver)
  • Biopsy: steatosis vs steatohepatitis

Treatment:

  • Underlying risk factors (DM, hyperlipidemia, obesity)
  • Pharmacotherapy hasn’t reversed it yet
207
Q

Autoimmune hepatitis

A

Chronic inflammatory condition of liver: hepatocellular inflammation, necrosis, fibrosis
- “Chronic active hepatitis”, “lupoid hepatitis”, plasma cell hepatitis

Labs:

  • elevated ALT > 1000
  • AMA positive, ANA
  • increased IgG
  • Liver biopsy: portal inflammation, plasma cells

Treatment: responds very well to steroid therapy
- Azathioprine: immune-suppressive helps to withdraw steroid therapy

Pathogenesis: cell-mediated immune attack of hepatocytes. Lymphocytes sensitized to hepatocyte membrane proteins

Features: similar to viral hepatitis (fatigue, myalgia, RUQ pain, jaundice)

  • Rapid recognition, treatment essential
  • Can progress to cirrhosis in months
  • Untreated severe AIH–> 40% mortality
208
Q

Hepcidin

A

Produced by hepatocytes, encoded by HAMP gene, regulated by HFE, TfR2, HJV proteins
Normal function: feedback to liver of iron levels–> inhibits iron absorption

Hemochromatosis: no feedback inhibition of iron absorption (hepcidin defective) due to mutations in HFE (or TfR2, HAMP, or HJV)

209
Q

Hemochromatosis symptoms

A 
Cirrhosis
Bronzing skin
Diabetes
Testicular atrophy
Conduction abnormalities in heart
210
Q

Diagnosis of hemochromatosis

A 
Genetic: GOLD standard
- Homozygous C282Y/C282Y
- Compound heterozygous C282Y/H63D
Serum tests: 
- iron (high > 175)
- iron binding capacity (low < 300)
- transferrin saturation (high > 50%)
- ferritin levels (high > 300)
Radiographs: T2 weighted MRI, lower than normal intensity of liver
Liver biopsy: 
- Stainable iron (prussian blue) from Zone 1 hepatocytes--> Zone 3
- Hepatic iron index (> 5600 compared to 1800)
Response to phlebotomy

** high risk of HCC (first degree relatives should be screened by transferrin saturation, ferritin)

211
Q

Alpha-1 antitrypsin deficiency (A1AT): diagnosis

A 
A1AT elastase inhibitor
- Autosomal co-dominant inheritance
One allele (Pi) from each parent: 
- Normal is PiMM
- Disease: PiMZ, PiZZ (associated with liver disease)

Biopsy findings: globules stained with PAS and diastase (to eliminate glycogen staining)

212
Q

Alpha-1 antitrypsin deficiency: symptoms and treatment

A

Liver disease (abnormal protein stuck in hepatocytes)-

  • Seen in 10-15% of PiZZ genotypes (mostly Europeans, Scandinavians)
  • Neonatal jaundice in 10% PiZZ
  • Adult presentation: chronic hepatitis, cirrhosis
  • Increased risk of HCC

Emphysema: alpha-1 antitrypsin blocks elastase in lungs–> excess lung tissue breakdown

Treatment: Liver transplant cures disease

213
Q

Wilson’s disease: symptoms

A

Rare
Disorder of copper excretion through bile canaliculus

Symptoms:

  • Kayser-Fleisher rings
  • Neuropsychiatric disorders
  • Cardiomyopathy
  • Hepatitis, Cirrhosis
  • Fanconi syndrome
  • Hemolysis
  • Osteopenia, arthropathy
214
Q

Wilson’s disease: presentation

A
  • YOUNGER patient with cirrhosis
  • Abnormal liver tests
  • Acute hepatitis
  • Fulminant hepatic failure
  • Chronic active hepatitis
  • Cirrhosis
  • Portal HTN
215
Q

Wilson’s disease: diagnosis

A

Ceruloplasmin (low)- < 20 mg/dL
Slit lamp exam for Kayser-Fleisher rings
Urine copper > 100 ug/ 24hr

If positive for any of three above, liver biopsy with quantitative copper

216
Q

Wilson’s disease: treatment

A

Chelation of excess circulating copper
- Trientine
- D-penicillamine
Zinc: diminishes copper absorption
Liver transplantation is curative
First degree relatives should be screened
- ceruloplasmin level, slit-lamp examination

217
Q

Treatment of PBC- Primary biliary cirrhosis

A

Ursodeoxycholic acid (Ursodiol)

  • replaces hepatotoxic bile salts
  • Symptomatic/biochemical improvement
  • transplant-free survival advantage

Cholestyramine

  • Binds bile acids, can relieve pruritis
  • No effect on natural history of disease

Liver transplantation (curative but can RECUR)

218
Q

Diagnosis of PSC

A

Labs:

  • Elevated alkaline phosphatase
  • Atypical P-ANCA (reaction with nuclear envelope proteins of neutrophils)

Histologic features:

  • onion skin fibrosis (small duct involvement), ductopenia, fibrosis
  • Periductal inflammation and fibrosis

Imaging:

  • Cholangiogram
  • Endoscopic retrograde cholangiopancreatography (ERCP)= diagnostic, potential to apply therapy (shunting)
  • MRI with MRCP
219
Q

Treatment of PSC

A

Therapy:

  • NONE
  • treat for cholangitis
  • open strictures, monitor for cancer
  • Liver transplant curative, can recur
220
Q

Alcoholic liver disease: demographics

A
  • Less than 80 g of alcohol/day: mild hepatic changes (10g/drink)
  • 100-150 g or more/day is associated with severe liver disease
  • Women more susceptible to develop severe alcoholic liver disease (20g/day)
221
Q

Clinical picture of Alcoholic hepatitis

A
  • Asymptomatic to critically ill
  • Jaundice, RUQ pain, anorexia
  • PE: fever, jaundice, ascites
  • Lab: AST/ALT > 2, elevated bilirubin (20 vs 4-5 in liver failure pts), elevated WBC
  • Liver biopsy: fat, inflammation, Mallory bodies, central fibrosis
222
Q

Diagnosis of PBC

A

Testing:

  1. Elevated Alkaline phosphatase
  2. Ultrasound of liver/gallbladder (look for obstruction)
  3. AMA blood test
  4. Liver biopsy

Labs:

  • AMA (antimitochondrial antibodies)- 90%
  • Elevated Alkaline phosphatase without liver failure

Histo:

  • Involves intrahepatic bile ducts (MICROscopic)
  • See bile duct lesions (lymphocytic infiltration/granulomatous inflammation)
  • Chronic non-suppurative destruction cholangitis
  • Leads to ductopenia/fibrosis
223
Q

Pathophysiology of portal hypertension

A

Liver has dual circulation:
- 2/3 portal vein, 1/3 hepatic artery
Portal HTN results from:
- Increased resistance to portal outflow (flow of blood into liver)
- increase in flow of blood into portal circulation

EKG needed to rule out cardiac failure (R-sided) causing liver failure

224
Q

Pre-hepatic portal hypertension

A

Increased flow from spleen to liver–> increasd portal pressure

225
Q

Intra-hepatic portal HTN

A

Cirrhosis

- Microscopic: portal venule, hepatic venule

226
Q

Post-hepatic portal HTN

A

Blockage of post-hepatic veins (thrombosis)
IVC obstruction
R-sided heart failure (hepatic outflow obstruction)

227
Q

Portal hypertensive hemorrhage

A

Gastropathy (mildest form)
- Increased vascularity of stomach mucosa
Esophageal varices
- Leading cause of death in patients with portal hypertension
- 60% of patients with cirrhosis
- 25% risk of bleeding within 2 years of dx
- 40-70% mortality from initial variceal bleed

228
Q

Pharmacologic treatment of esophageal varices (with no bleeding)

A

Lowering of portal pressure (non-selective beta-blockade)
Vasopressin and Somatostatin analogues (octreotide, terlipressin):
- Reduce portal inflow
Non-selective beta-blockers (natolol, timolol, carbetolol
- Primary and secondary prophylaxis
- No role in acute bleeding

229
Q

Treatment of ACUTE portal HTN bleed

A
  1. ABCs
    - Tranfuse hemoglobin
    2, Pharmacological therapy
    - Somatostatin analogues: octreotide
    - Prophylactic antibiotics
  2. Endoscopic therapy – band ligation (put band at base of varice
  3. If unsuccessful, then tamponade – Sengstaken-Blakemore or Minnesota tube
  • Shunt= transjugular intrahepatic porto-systemic shunt (moves flow from portal vein to hepatic vein)–> risk for HEPATIC ENCEPHALOPATHY, ischemia of liver (bypassing liver metabolic processes, depriving liver blood flow)
  • Decompressive shunt: portocaval, mesocaval (mesenteric vein to IVC), distal splenorenal
  • Advanced liver disease- poor prognosis with surgical intervention
230
Q

Portal-systemic (hepatic) encephalopathy

A

Changes in metal status related to hepatic dysfunction

  • Products of liver portal system breakdown released into general circulation
  • Excess nitrogenous compounds in systemic circulation (ammonia, aromatic amino acids, GABA?)

Stages:

1) Confusion
2) Drowsiness
3) Somnolence
4) Coma

231
Q

Formation of Acites

A

Accumulation of fluid in abdominal cavity due to portal hypertension
- Transudation of fluid from viscera
- Ascites in cirrhosis- 50% 2-year survival
Other causes:
- Neoplasm, CHF, infection (intraabdominal)

232
Q

Systemic circulation effects of portal hypertension

A

Portal HTN–>
Arterial splanchnic Vasodilation–>
Decreased “effective arterial blood volume” (more blood in splanchnic circulation–> body perceives less blood elsewhere)–>
Activation of:
1) Renin-angiotensin system–> renal vasoconstriction
2) Sympathetic nervous system–> hyperdynamic circulation
3) Arginine vasopressin–> sodium/water retension

  • Ascites forms because renal system continues to retain sodium and water in spite of fluid accumulation due to less perceived fluid in circulation
233
Q

Diagnosis of Ascites

A

Abdominal paracentesis
Shifting fluid:
- Lying on back
- Shift to one side- dullness should shift with abdominal movement (fluid moving around)

234
Q

Serum-ascites albumin gradient (SAAG)

A

SAAG= (serum albumin)- (ascites albumin)
SAAG >= 1.1 (ascites likely from portal HTN)
SAAG < 1.1 (infection or neoplasm)

235
Q

Treatment of ascites

A

Determine underlying cause: portal HTN, R heart failure, cirrhosis?

  • Sodium restriction (2.0g/day)
  • Fluid restriction ONLY if serum Na+< 120mmol/L (hyponatremic)
  • Diuretics: K+ sparing (spironolactone, amiloride, triamterene), loop (furosemide, bumetanide, torsemide)–> get body to dump Na
236
Q

Refractory Ascites

A

Ascites not responsive to maximal conventional therapy

  • 5-10% ascites patients
  • High volume paracentesis (4-12 liters), repeated for comfort
  • TIPS
  • Surgical mesocaval shunt
237
Q

Spontaneous bacterial peritonitis (SBP)

A

Infection in cirrhosis due to transudation of bacterial from bowels (ascites complication)

  • Suspect when ANY decompensation in patient with stable cirrhosis
  • Monomicrobial infection: e.coli, klebsiella, s. pneumonia
  • Diagnosis: ascites with > 250 PMN/ mm3
  • Treatment: 3rd gen cephalosporin (ceftriaxone) until transplant
  • 50% 6-month survival (need to transplant)
238
Q

Hepatorenal syndrome:
Type 1
Type 2
Treatment

A

Rapidly progressive renal failure in cirrhosis with no morphologic kidney abnormalities (Ascites complication)

  • Due to vasoconstriction of renal circulation
  • Low urinary Na despite adequate intravascular volume

Type 1: anuria, rapid, high mortality
Type 2: slowly progressive
Without liver transplant–> pre-morbid event

Treatment: reverse peripheral vasodilation

  • Volume resuscitation/replacement
  • Splanchnic vasoconstriction (midodrine)
  • Inhibition of vasodilation (octreotide)
239
Q

Diagnosis of portal systemic encephalopathy

A
  • Changes in state of arousal in chronic liver disease patient
  • Investigate other causes
  • Venous ammonia
  • Presence of asterixis (“liver flap”)
  • Neuropsychiatric testing (trail-making test: connect the dots)
  • EEG
240
Q

Treatment of portal systemic encephalopathy

A

Correct underlying factors: bleeding, infection, carcinoma

  • Decrease dietary animal protein, increase dietary vegetable protein
  • Lactulose (hydrolyzed by colonic bacteria, reduces colonic pH–> trap nitrogenous waste)–> 2-3 semi-solid BM/day
  • Rifamixin: poorly absorbed oral antibiotic that eradicates colonic bacteria
241
Q

Child-Pugh score

A

Grading scale for cirrhosis
Formerly used for liver transplant
A= 5-6, B= 7-9, C= 10-15

242
Q

MELD score

A

Model for end-stage liver disease
Multimeric regression calculation for survival with end stage liver disease (how likely is it patient will die in 3 months)- higher score, sooner to transplant

243
Q

Hemosiderosis

A

Accumulation of iron in tissues, generally acquired (secondary) due to:

  • Blood transfusions
  • Hemolytic anemia
  • Ineffective erythropoiesis (thalassemia)
  • Liver disease (decreased hepcidin- Hemochromatosis)

First involves Kupffer cells, bone marrow, spleen–> moves to parenchyma throughout body

244
Q

Liver iron accumulation

A

1) Primarily in hepatocytes= Hereditary hemochromatosis
2) Primarily in Kupffer cells= blood tranfusions, ineffective erythropoeisis
3) Mild accumulation in Kupffer cells/hepatocytes= chronic hepatocyte injury causing lower hepcidin (Hepatitis)

245
Q

Causes of chronic vomiting in pediatric patients

A
  • GI infection (more commonly acute)
  • Metabolic diseases
  • Increased intracranial pressure
  • Gastroesophageal reflux
  • Allergic gastroenteritis
  • Esophageal atresia
  • Pyloric stenosis
  • Duodenal atresia/stenosis/ annular pancreas
  • Malrotation/volvulus
  • Intestinal atresia
246
Q

GI infection in children

A

More likely to present as acute condition
- Can be due to parasites
Chronicity seen due to other infections in body:
- Otitis media
- UTI

247
Q

Metabolic diseases in children

A
  • Renal tubular acidosis
  • Methylmalonic acidemia
  • Propionic acidemia
248
Q

Causes of Increased intracranial pressure

A

Hydrocephalus
Meningitis
Brain tumors
Ventricular hemorrhage (traumatic birth, shaken baby)

249
Q

Presenting signs and symptoms of GERD in infants

A
  • Recurrent vomiting/irritability
  • Recurrent vomiting/ poor weight gain
  • Dysphagia, feeding refusal
  • Esophagitis
  • Apnea/ ALTE (apparent life-threatening events= blue baby, cease breathing, choking)
  • Wheezing/asthma
  • Pneumonia (aspiration- poor gag reflex)
  • Upper airway symptoms
250
Q

Diagnosis and treatment of GERD in infants

A

Diagnosis:

  • history (non bilious vomit, may contain thready blood due to irritation)
  • UGI (upper GI series): delineates anatomy, can’t distinguish cause (physiologic vs non-physiologic)
  • Nuclear medicine scintiscan/milk scan: 60 minute scan; baby ingests labeled milk- scanned every 6 seconds
  • 24-hour pH probe/endoscopy: GOLD STANDARD; probe 2-3 cm above LES–> look for pH over 24 hour period
  • Multiple intraluminal electrical impedance measurements
  • Endoscopy

Treatment:

  • Conservative: positioning, feeding alterations
  • Medications
  • Surgery
  • Natural history of reflux resolves in most cases by 2 years
251
Q

Allergic gastroenteritis in infants

A 
Types:
- Mucosal enteropathy
- Eosinophilic esophagitis
- Eosinophilic gastritis
- Serosal eosinophilic enteritis
Due to: 
- Cow's milk
- Soy protein
Seen with family history of atopic allergies (food, eczema, asthma)

Symptoms: food impaction (due to swelling)

Diagnosis: clinical, allergy testing, endoscope
Treatment: dietary

252
Q

Esophageal atresia in infants

A

1/3000-5000 births: associated with tracheo-esophageal fistula
- Blind esophageal pouch with distal tracheo-esopheal fistula
Symptoms:
- 50% present with polyhydramnios
- Emesis, swallowed secretions, aspiration
- Later vomiting/respiratory symptoms

Treatment: surgical

253
Q

Pyloric stenosis in infants

A

Narrowing of pyloric outlet due to hypertrophy of pyloric muscle
- 1/1000 births, M:F 5:1
Symptoms:
- Emesis (non-bilious, projectile) in 3-6 weeks
- Poor weight gain, dehydration (hypochloremic alkalosis)

Diagnosis: palpate “olive”, pyloric sonograms, UGI series

Treatment: surgical: pyloromyotomy (open up pyloris muscle)

254
Q

Duodenal atresia, stenosis, annular pancreas in infants

A 
1/10,000 infants
- 50% premature
- 20-30% Down's syndrome
Symptoms:
- Emesis within first 2 days of life
- Non-bilious above ampulla of vater (30%)
- Bilious in 70%

Symptoms:

  • Poor feeding
  • Abdominal distention
  • Double bubble (dilated stomach, duodenal blub on scan)

Treatment: surgical

255
Q

Malrotation in infants

A
  1. 2% of population- seen in first few weeks of life
    - Defect in intestinal lengthening/rotation in 8th week of gestation
    - Narrow base of attachment for small bowel mesentery–> twisting (VOLVULUS)

Symptoms:

  • Bilious emesis, pain
  • Vomiting, distention

Complications: Bowel ischemia, necrosise

Treatment: surgical

256
Q

Intestinal atresia

A

Complete obstruction of lumen in bowel or stenosis

  • Jejunem/ileum more common (1/2700)
  • Idiopathic, may stem from ischemic events to bowel

Symptoms:

  • Bilious emesis
  • Growth failure
  • Abdominal distension

Treatment: Surgical

257
Q

Manning criteria

A

Used to diagnose IBS:

  1. Onset of pain linked to more frequent bowel movements
  2. Looser stools associated with onset of pain
  3. Pain relieved by passage of stool
  4. Noticeable abdominal bloating
  5. Sensation of incomplete evacuation more than 25% of the time
  6. Diarrhea with mucus more than 25% of the time
258
Q

Rome criteria

A

Used for classifying symptoms of Irritable Bowel syndrome

259
Q

ALT > 1000

A

Shock
Acute viral hepatitis
Autoimmune hepatitis
Drugs

260
Q

Celiac Sprue

A

Symptoms:
Chronic diarrhea without blood
Abdominal pain- colic

Gold standard diagnosis:: response to gluten-free diet

Testing:

  • Gluten-containing diet before biopsy, response to gluten-free diet
  • Serology: Anti-tTG IgA (anti-tissue transglutaminase; high sensitivity, specificity), serum IgA (to rule out IgA deficiency= false negative), anti-endomysial IgA, anti-Gliatin, HLA testing of DQ2/DQ8
  • Thyroid function tests
  • Stool (WBCs, ova, parasites, culture)
  • Colonoscopy for: colonic polyps, IBD, collagenous colitis, microscopic colitis
  • Be careful with biopsies from duodenal bulb: subjected to physiologic peptic injury–> broader, shorter villi and increased PMNs in normal physiologic state

Fast patient for 48 hours: If malabsorption is suspected (steatorrhea), workup includes:

  • 72 fecal fat collection (100gm fat diet) nl <7gm/24hours
  • D-xylose test if abnormal suggest small bowel, if nl suggests pancreatic insufficiency
  • Small bowel malabsorption celiac, Whipples, Crohn’s
  • Bacterial overgrowth: Hydrogen breath test, trial of antibiotics
  • Schilling test for B12 absorption

Histo: increased intraepithelial and lamina propria lymphocytes, lamina propria plasma cells, severe villous blunting, crypt elongation- Marsh 3 classification. Other conditions with histologic pattern of increased IEL/ villous blunting:- Disorders of immune regulation (common variable immunodeficieny, HIV, enteropathy, autoimmune)

  • Infections (H. pylori, tropical sprue, bacterial overgrowth, parasites)
  • NSAID injury

GI/Pulm (7 decks)

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