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Gastrointestinal Flashcards

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1
Q

What is esophageal atresia with distal tracheosophageal fistula?

What are the symptoms?

How to determine if this is problem?

A

The most common Polyhydraminos in utero
The esophagus is blind end, and the lower esophagus connects to the trachea

Symptoms: Drool, choke with feeding, cyanosis due to laryngospasm

Test: Failure to pass the NG tube into the stomach

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2
Q

What is intestinal atresia?

Symptoms?

A

1) Duodenal atresia (failure to recanulize with dilatation of the stomach and proximal duodenum).
2) Jejunal and ileal atresia: disruption of the mesenteric vessels with ischemic necrosis and segmental resorption

Symptoms: bilous vomiting, abdominal distention within the first 1-2 days of life

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3
Q

What is hypertrophic pyloric stenosis?

What are the symptoms?

A

1) Cause of outlet obstruction
2) Will have a palpable olive mass with non-bilous projectile vomiting at 2-6 weeks old
3) Usually in males that were exposed to macrolides
4) Can result in hypokalemic, hypochloremic metabolic acidosis
5) Treatment is surgical incision

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4
Q

What is an annular pancrease?

A

1) Parts of the pancrease encircle the duodenum and have a ring around the duodenum which can cause vomiting

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5
Q

What is pancrease divisum?

A

1) Ventral and dorsal fail to fuse after 8 weeks

2) Usually assymptomatic, but might cause chronic abdominal pain

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6
Q

What is the histology of the esophagus?

A

squamous epithelium

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7
Q

What are cells of stomach?

A

Gastric glands

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8
Q

What are cells in the duodenum?

A

Villi and microvilli (increase absorptive surface)

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9
Q

What are cells in the jejunum?

A

Plicae circulares and crypts of Liberkuhn

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10
Q

What are cells of the ileum?

A

Peyer pathches (lymphoid)
Crypts of Lieberkuhn
Largest number of goblet cells

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11
Q

What are the cells of the colon?

A

Crypts of

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12
Q

From head to toe, what are the arteries supplying the aorta?

A

1) Celiac trunk
2) Superior mesenteric trunk
3) Inferior mesenteric trunk
4) right and left common iliac

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13
Q

Which vessel will noursih the foregut?

A

Celiac artery (lower esophagus and the proximal duoenemum) liver, gallbladder, pancrease, spleen

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14
Q

Which vessels will nourish the midgut?

A

Superior mesenteric

Distal duodenum to promximal 2/3 of the transverse colon

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15
Q

Which vessels will nourish the hindgut?

A

Distal 1/3 of the transverse colon to upper portion of the rectum

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16
Q

What are the branches of the celiac trunk?

A

1) Common hepatic
2) Spleenic
3) Left gastric

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17
Q

What are the signs of portal hypertension? And why?

A

1) esophagus (esophageal varices)
2) Umbilicus: Caput medusae (paraombilical) small epigastric veins of the anterior abdominal wall
3) Rectum: anorectal varices (superior rectal-middle and inferior rectal)

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18
Q

How to treat portal hypertension?

A

TIPS
Tranjugular intrahepatic portosystemic shunt (between the portal vein and hepatic vein) will shunt the blood into systemic circulation bypassing the liver

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19
Q

What are the differences between the internal and external hemorroids?

What type of cancer depending on the pectinate line?

A

Internal hemorroids: above the pectinate line (blood supply from the IMA( and be painfuless)

Adenocarcinoma

External: Below pectinate line (fissures) painful if thrombosed (associated with squamous cell carcinoma)

Can also be a fissure

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20
Q

What are the characterstics of anal fissure?

A

1) Pain
2) Blood
3) Posterior location (because poorly perfused) associated with constipation and low fiber diets

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21
Q

What are the zones of the liver, and what are the diseases that can affect them?

A

Zone1: periportal zone (affected by viral hepatitis and ingested toxins such as cocaine

Zone 2: intermediate zone, affected by yellow fever

Zone 3: pericentral vein ( first affected by sichemia, most sensitive to metabolic toxin)

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22
Q

Where can the gallstones be located? What is the implication?

A

Can reach the confluance of the common bile duct and cause blockage

This can cause cholangitis and pancreatitis

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23
Q

What are the tumors that can arise with the pancrease?

A

Can be in the head of the pancrease and cause obstruction of the common bile duct

Usually will cause painless jaunedice

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24
Q

What is the anatomy of the vessels in the femoral region?

A

NAVEL
Nerve, artery, vein, lympatics
(start at the thigh and move in)

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25
Q

What is the definition of a hernia?

A

Protrusion of the peritoneum through an opening (usually at the site of weakness)

Can become incarcerated and strangulation

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26
Q

What is a diaphgramatic hernia?

What are the causes>

A

1) Abdominal structures enter the thorax (may occur due to congenital defect of the pleuroperitoneal membrane)
2) Commonly occurs on the left side, due to the relative protection of the right hemidiaphgram by the liver

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27
Q

What is the difference between the sliding hiatal hernia, the paraesophageal hernia, and the hiatal hernia?

A

Sliding hiatal: gastroesophageal junction is displaces upwards (hourglass stomach)

Paraesophageal hernia: gastroesophageal junction is unusally normal, fundus protrudes into the thorax

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28
Q

What is an indirect hernia?

A

Goes through the internal ring, and into the scrotum
occurs within infants
Failure of the processus vaginalis to close
Covered by all 3 layers of the spermatic fascia

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29
Q

What is a direct hernia?

A

Protrudes through the inguinal triangle (bulges)

Covered by external spermatic fascia

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30
Q

What is a femoral hernia?

A

Protrudes below the inguinal ligament
More common in females
More likely to become incarcerated and herniated

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31
Q

What are structures that make up Hasselbach triangle?

A

Inferior epigastric artery
Lateral border of the retus abdominis
Inguinal ligament

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32
Q

What does gastrin do?

Source, action, regulation?

A

Source: G cells in the antrum
Action: increased H+ secretion, and growth of the mucosa
Regulation: decreases the pH

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33
Q

What happens to gastrin with increased PP1 use?

A

Decrease in gastrin

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34
Q

What happens in gastrin if have H pylori?

A

Increased in chronic atrophic gastritis

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35
Q

What happens in Zollinger-Ellison syndrome?

A

Increase in gastrin (gastrinoma)

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36
Q

What is the function, regulation, of somatostatin?

A 
D cells (pancreatic islets)
Action: decrease gastric acid and pepsinogen
Decrease pancreatic and small intestine
Decrease in gallbladder contraction 
Decrease insulin and glucagon
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37
Q

What does Cholecystokinin do?

A 
Produced by the duodenum 
Increases pancreatic secretion 
Decrease gastric emptying 
Increases sphincter of Oddi releaxation
Increased production when have fatty acids and amino acids
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38
Q

What does secretin do?

A

S cells in duodenum
Function: Increases HCo3
Decrease gastric acid secretion
Allows pancreatic enzymes to function

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39
Q

What does glucose dependent insulinotropic peptide include ?

A

K cell in the duodenum
Action: duodenum and jejunum
Decreases gastric secretion of H+
Increase secretion of insulin

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40
Q

What does motilin do?

A

Released by the small intestine
Produces migrating complexes (MMC)
It is increased in fasting state
Can be used to stimulate intestinal peristalsis

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41
Q

What do vasoactive intestinal polypetide do?

A

1) parasympathetic ganglia in sphincters, gallbladers, and small intestine
2) Increase intestinal and electrolyte secretion
3) Relaxation of intestinal smooth muscles and sphincters

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42
Q

What is a Vipoma?

A

Islet pancretic cell tumor that secretes VIP

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43
Q

What does nitric oxide do?

A

Increase smooth muscle relaxation (including the lower esophageal sphincter)

Loss of NO leads to achalasia

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44
Q

What does Grehlin do?

A

Released from the stomach
Increases the appetite
Increased in fasting state
Increased in Prader-Willi syndrome

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45
Q

What does intrinsic factor do?

A

Found in parietal cells
Binds to Vitamin B12
Can have destruction of the parietal cells if have chronic gasrtis and pernacious anemia

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46
Q

What does gastric acid do?

A

Parietal cells (stomach)
Decrease the pH
Increase the Histamine, and decrease the gastrin

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47
Q

What does pepsin do?

A

Cheif cells (stomach)
Increases vagal stimulation due to local acid
Pepsinogen is converted to pepsin in the presence of H+

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48
Q

What does bicarbonate do?

A

Mucosal cells of the (stomach, duodenum, salivary glands) and Brunner glands

Serves to neutralize the acid

Increased by pancreatic and bilary secretion with secretin

Trapped the mucos that covers the gastric epithelium

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49
Q

What are the enzymes secreted by pancreatic enzymes? And what is their role?

A

1) Amylase: starch digestion
2) Lipases: fat digestion
3) Proteases: Protein digestion
4) Trypsinogen: converted to trypsin

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50
Q

How are carbohydrates absorbed? (glucose, galactose and fructose) ?

A

Glucose and galactose taken by SGLT1 (Na+ dependent)

Fructose by GLUT 5

Both are transported through the blood by GLUT-2

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51
Q

How and where is the Iron absorbed?

A

In the duodenum

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52
Q

Where is the folate absorbed?

A

In the small bowel

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53
Q

Where is the B12 absorbed?

A

In the terminal ileum along with bile slats, requires intrinsic factor

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54
Q

What are the Peyer patches?

A

Lymphoid tissue in the ileum

Secrete IgA plasma cells (antibody)

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55
Q

What is the composition of bile?

What are the functions of bile salts?

A

1) Bile salts
2) Functions: digestion and absorption of lipid and fat soluable proteins
3) Cholesterol excretion
4) Anti-microbial activity.

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56
Q

What is Bilirubin?

A

Heme that is metabolized to biliverdin which is then reduced to bilirubin

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57
Q

What happens to unconjugated bilirubin?

A

Removed from the blood by the liver, it is conjugated, and then excreted in bile

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58
Q

What happens to direct bilirubin?

A

Conjugated with glucuronic acid (water soluable)

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59
Q

What happens to indirect bilirubin?

A

Unconjugated (water insoluable)

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60
Q

What are the 3 types of salivery tumors?

A

1) Pleomorphic adenoma
2) Mucoepidermoid carcinoma
3) Warthin tumor

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61
Q

what are charactersitics of pleomorphic tumor?

A

Benign mixed tumor (most comon), reoccurs if not removed completely

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62
Q

What are characteristics of mucoepidermoid carcinoma?

A

Most common malignant tumor (has mucinous and squamous components)

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63
Q

What are the warthin tumor?

A

Benigh cyst tumor with germinal centers

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64
Q

What are the findings of achalasia?

A

Have progressive dysphagia to solids and liquids
Barium will show dilated esophagus with area of distal stenosis

Will have increased risk of squamous cell carcinoma

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65
Q

What is Boerhaave syndrome?

A

Distal esophageal rupture with pneumomediastinum, due to retching

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66
Q

What is eosinophilic esophagitis?

A

Infiltration of esonophils in the esophagus with atopic patinets
Will often have esophageal rings and linear furrows

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67
Q

What are esophageal strictures?

A

Associated with caustic ingestion and acid reflux

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68
Q

What are esophageal varices?

A

Dilated submucosal veins in lower 1/3 of esophagus secondary to portal hypertension

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69
Q

What isesophagitis?

A

Associated with reflux
Infection of immunocompromised individuals
HSV-1 punched out ulcers

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70
Q

What is GERD?

A

Presents as heartburn or regurgitation, dysphagia
May present as chronic cough
Can be associated with asthma
Can have transient decrease in LEStone

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71
Q

What is Mallory-Weiss syndrome?

A

Mucosoal lacerations at the gastroesophageal junction due to severe vomiting

Leads to hematoma

Can be found in alcoholics and bulimics

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72
Q

What is Plummer-Vinson syndrome?

A

Triad: Dysphagia, Iron deficiency anemia, Esophageal webs (increased risk of esophageal squamous cell carcinoma)

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73
Q

What is scleordermal esophageal dysmotility?

A

Smooth muscle atrophy
Decreased LES pressure and dysmotility
Have acid reflux and dysphagia leading to stricture

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74
Q

What is Barrett’s esophagus?

A

Intestinal metaplasia, with squamous epithelium

Due to GERD

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75
Q

What are the types of esophageal cancer?

A

Squamous cell carcinoma: upper 2/3 (risk factors ETOH, hot liquids, strictures and smoking)

Adenocarcinoma: Lower 1/3 chronic GERD, Barrett esophagus, smoking (more common in the Amercian)

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76
Q

What are the causes of acute gastritis?

A

1) NSAIDS ( decrease PGE), decrease gastric mucosa
2) Burns (Curling ulcer) hypovolemia leading to intestinal ischemia
3) Brain injury (Cushing ulcer) increase vagel stimulation (increase ACh and increase H+)

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77
Q

What are the causes of Chronic gastritis?

A

H. Pylori (most common) increased risk of peptic ulcer disease, MALT lymphoma

Autoimmune: Autoantibodies to parietal cells and intrinsic factor

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78
Q

What are the most common types of gastric cancer?

A

Adenocarcinoma and lymphoma

GI stromal tumor carcinoid (rare)

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79
Q

What are some clinical signs of gastric cancer?

A

Virchow node: involvement of left supraclavicular node by mets from the stomach

Krukenberg tumor: bilateral mets to the ovaries, abundant mucin secreting cells

Sister Mary Joseph: subcutaneous periumbilicus metastasis

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80
Q

How to tell the difference between a gastric and duodenal ucler?

A

Gastric ulcer:

1) Pain is greater with meals
2) H pylori in 70%
3) Mechanism: decreased mucosal protection against gastric acid
4) can be caused by NSAIDS
5) Increased risk of carcinoma
6) Need to biospy the margins to rule out malignancy

Duodenal ulcer:

1) Decreased pain with meals
2) 90% association
3) Other causes can be Zollinger-Ellison syndrome
4) Generally benign
5) Hypertrophy of the Brunner glands

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81
Q

what are possible complications of ulcers?

A

1) Hemorrage
2) Obstruction
3) Perforation

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82
Q

What are the symptoms of malabsortion syndrome?

A

1) Diarrhea
2) Steatorrhea
3) weight loss
4) Weakness
5) Vitamin and mineral deficiency

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83
Q

What are the signs of celiac disease?

How is celiac disease diagnosed?

A

1) Gluten sensitive enteropathy
2) Celiac sprue
3) European descent
4) Increased chance of malignancy
5) D-xylose test: absorbed in the small intestine (blood and urine level decreased with mucosa defects)

Treatment is gluten free diet

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84
Q

How to test for lactose intolerance?

A

Lactose hydrogen breath test (+ for lactose malabsorption if postlactulose breath hydrogen value rises above 20 ppm compared to baseline

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85
Q

What are some causes of pancreatic insufficency?

A

1) Chronic pancreatitis
2) cystic fibrosis
3) Obstructing cancer

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86
Q

what is tropical sprue?

A

Similar to celiac sprue (affects the small bowel) however, it requires antibiotics. Unknown cause

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87
Q

What are the symptoms and the cause of Whipple disease? How is it treated?

A

1) Caused by infectionTrophyerma whipplie
2) Symptoms include lymph node
Cardiac symtoms
Arthalgias
Neurological symptoms

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88
Q

What are the differences between Crohn’sand Ulcerative Colitis?

A

Location (always Crohn vs Ulcerative)

1) Locaton: any portion of the GI tract vs. colon with rectal involvement
2) Gross morphology: transmural vs submucosal
3) Microscopic: non caseating granulomas vs bleeding crypt ulcers
4) Complications: malabsorption (colorectal cancer) fistulas, recurrent UTI vs Cancer, toxic megacolon, perforation
5) Intestinal manisfestations: diarrhea that may or may not be bloody vs bloody diarrhea
6) External manifestations: Rash, ulcerations in the mouth vs. uvertits, episcelritis, spondylotitis, P-ANCA and scleorising cholangitis
7) Crohn’s is cobblestone lesions, while the ulcerative colitis is the continuous

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89
Q

What are signs of irritable bowel syndrome?

A

Recurrent abdominal pain that is associated with

1) Pain that improves with defecation
2) Change in stool frequency
3) Change in appearance of the stool

90
Q

What are the characteristics of appendicitis?

A

Initially have diffuse ombilical pain that migrates to McBurney’s point (1/3 the distance from the right anterior obturator)
Can have Roving signs, which is guarding and rebound tenderness

91
Q

What is diveritculum?

A

Blind pouch protruding from the alimentary tract

Communicates with the lumen of the gut

92
Q

What is the difference between a true and false diverticulum?

A

True has all three walls of the gut

False is only the mucosa and the submucosa

93
Q

What are complications of diverticulosis?

A

Painless bleeding

Diverticulitis

94
Q

What are the symptoms and treatement for diveriticulitis?

What are the complications for diverticulitis?

A

1) Left lower quadrant pain
2) Fever
3) Leucocytosis

Complications of diverticulitis:
Abcess
Pneumonia
Obstruction 
Perfortation with peritonitis ( treat with percutaneous drainage or surgery)
95
Q

What is Zenker’s diverticulum?

A

Pharynesopageha; false diverticulum
Presents with dysphagia, obstruction, gurgling, aspiration, foul breath and neck mass

Sticks out through Killian triangle

96
Q

What is Meckel’s diverticulum?

A

True diverticulum caused by persistence of vitelline duct

Can have ectopic acid secreting gastric mucosa

Can lead to Melena, RLQ pain, intussusception, volvulus or obstruction

97
Q

What are the classic 6 signs of Meckel’s diverticulum?

A

1) 2 times more likely in males
2) 2 inches long
3) 2 feet from ileoccecal valve
4) 2% of the population

Commonly presents in the first 2 years of life

98
Q

What is Hirschsprung’s disease?

A

Congenital megacolon with lack of ganglion cells and enteric nervous plexus

Presents with:

1) Bilous emesis
2) Abdominal distention
3) Failure to pass meconium within 48 hours
4) Chronic constipation

Treatment: resection

99
Q

What is malrotation of the stomach?

A

Anomaly of the midgut rotation during fetal developpement

Improper positioning of bowel with formation of fibrous bands

Can lead to volvulous or duodenal obstruction

100
Q

What is a volvulus?

A

1) Twisting of the bowel around the mesentery can lead to obstruction and infarction

Sigmoid volvulus are more common in the elderly

101
Q

What is intussception?

A

Telescoping of the proximal bowel segment into the distal segment

Compromised blood supply

Will have intermittent abdominal pain with currant stools

102
Q

What are the causes of acute mesenteric ischemia?

A

1) Have critical blockage of intestinal blood flow (usually due to embolic occlusion of the SMA)

Will have abdominal pain out of proportion with physical findings

103
Q

What are the causes of chronic mesenteric ischemia?

A

Intestinal angina

Artherosclerosis of the celiac artery (SMA or IMA) with intestinal hypoperfusion

104
Q

What is colonic ischemia?

A

Reduction in intestinal blood flow causing ischemia
Crampy, abdominal pain followed by hemtochezia
Commonly occurs at watershed areas (splenic flexure)

Typically occurs within the elderly

105
Q

What is angiodysplasia?

A

Torturous dilatation of the blood vessels (hematochezia)
Most often found in the cecum, terminal ileum and ascending colon
Confirmed by angiography

106
Q

What are adhesions?

A

Fibrous bands of scar tissue after surgery (most common cause of small bowel obstruction)

Can have well demarcated necrotic zones

107
Q

What is ileus?

A

Intestinal hypomotility without obstruction
Have constipation and flatus

Usually associated with abdominal surgery, opiates, hypokalemia, and spesis

Treatement: bowel rest, electrolyte correction, anc cholinergic drugs

108
Q

What is meconium ileus?

A

cystic fibrosis, necrosis of the intestinal mucosa leads to perforation and pneumotosis intesinalis

109
Q

What are the colonic polyps?

A

Growths of tissue within the colon (may be neoplastic or non neoplastic( can be flat, sessile, or pedunculated with protrustion into the colonic lumen

110
Q

What is a hyperplastic polyp?

A

Non neoplastc (smaller, and in the rectosigmoid region)

111
Q

What is a hamartous polyp?

A

Non neoplastic, solitary lesions without significant risk of malignant transformation

Growths of normal colonic tissue with distorted architecture

112
Q

What is adenomatous polyp?

A

Neoplasm (chromosome abnormality through APC and KRAS) tubular histology has less malignant potential then villous

Usually assymptomatic (may present with occult bleeding)

113
Q

What is serrated polyp?

A

Premalignant via CpG, hypermethylation phenotype. Has a saw tooth pattern on biospy

Is involved in 20% of sporadic CRC

114
Q

What are the polyposis syndromes?

A

1) Familial adenomatous
2) Gardner
3) Turcot
4) Peutz-Jeghers
5) Juvenile polyposis
6) Lynch syndrome

115
Q

What is familial adenomatous?

A

Autosomal dominent mutation of the APC (chromosome 5q2hit) , many polyps arise after starting puberty.
Always involves the rectum
Need colectomy

116
Q

What is GArdener syndrome?

A

FAP with osseus and soft tissue tumors

Have retinal pigment epithelium

117
Q

What is Turcot syndrome?

A

FAP with malignant CNS tumor

118
Q

What is Peutx-Jeghers syndrome?

A

Autosomal dominent with hamartomas throughout the GI tract, can have hyperpigmented mouth, lips, hands, genitalia

Associated with increased risk of breast and GI cancer

(Colorectal, stomach, small bowel)

119
Q

What is juvenilepolyposis syndrome?

A

Autosomal dominent in children (less then 5 years old)

Harmatomatous polyps in the colon, stomach, small bowel. Associated with increased risk of CRC

120
Q

What is lynch syndrome?

A

Hereditary non-polyposis colorectal cancer
Autosomal dominant mutation
80% progress to CRC
Proximal colon involved
Associated with endometrial, ovarian, and skin cancer

121
Q

What is the epidemiology, risk factors, presentation, and diagnosis of colon cancer

A

Epi: most patients are over 50 years old (only 25% family history)

Risk factors: adenomatous and serrated polyps and familial cancers, IBD, tobacco, and diet of processed meats and low fiber

presentation: Rectosigmoid > ascending> descending
Ascending: exophytic mass, iron deficiency anemia , weight loss
Descending: infiltrating mass, partial obstruction, colicky pain, hematochezia
Can sometimes present with streptococcus bovis bacteriemia
Diagnosis: Iron deficiency anemia in males > 50 years old
Apple fore lesion seen on the barium enema

CEA tumor, good for monitoring, but not for screening

122
Q

What is the molecular basis of the colorectal cancer?

A

Mutation in the APC gene can cause FAP

123
Q

What is cirrhosis?

A

Diffuse fibrosis hat disrupt the normal archtecture of the liver
Increase risk of hepatocellular carcinoma

ETOH most commun cause in 60-70% of the cases

124
Q

What are the types of non-alcholic cirrhosis?

A 
Steatohepatitis
Chronic viral hepatitis
Autoimmune hepatitis
Bilary disease 
Genetic/metabolic
125
Q

what are the causes of portal hypertension other then cirrhosis?

A

1) Portal vein thrombosis
Budd chiari syndrome
Schistosomiasis

126
Q

What are the signs of portal hypertension

A

1) Esophageal varices
2) Hemtamesis
3) Gastric varices
4) Melena
5) Spleenomegaly
6) Caput medusa
7) Ascites
8) Anorectal varices

127
Q

What are some signs of cirrhosis?

A

1) Jaunedice, spider angiomas, palmer erythema, purpura, petechiae
2) Testicular atrophy
3) Gynecomastia
4) Amenorrhea
5) Hepatic encephalopathy
6) Asterixis
7) Anorexia
8) nausea.vomiting
9) abdominal pain
10) Fetor hepaticus
11) Thrombocytopenia/anemia
12) Metabolic: hyperbilirubinemia, hyponatremia
13) Cardiovascular: cardiomyopathy, periphereal edema

128
Q

What are the liver markers for disease?

What happens to them in the liver disease?

A

Aspartate increased in most liver disease ( ALT more then AST)
Aminotransferase Increased in ETHOH AST> ALT
Alanine aminotransferase AST > ALT means advanced fibrosis
Alkaline phosphatase increased in cholestasis, infiltrative disorders, bone disease
Glutamyl-transpeptidase: increased in liver and bilary disease (not in bone disease)

129
Q

Why is bilirubin increased?

A

Liver disease, bilary obstruction, ETOH, and vrial hepatitis

130
Q

What happens to albumin in the liver disease?

A

Decreased

131
Q

What happens to prothrombin in liver disease?

A

Increased in liver disease

Decreased production of clotting factors

132
Q

What happens to platelets in liver disease?

A

Decreased thrombopoietin
Decreased liver sequestration
Causes portal hypertension

133
Q

What is Reye’s syndorome?

A 
Fatal hepatic encephalopathy
Fatty liver
Hypoglycemia
Vomiting
Heptomegaly
Coma
Viral infection (treated with ASA)
134
Q

What is hepatic steatosis?

A

Macrovesicular fatty changes (maybe reversible with ETOH cessation)

135
Q

What is ETOH hepatitis?

A

Long term ETOH
Swollen and necrotic heptocytes (neutrophil infiltration)
Mallory bodies

136
Q

What is ETOH cirrhosis?

A

Final and irreversible
Micronodular and shrunken liver
Scelrosis
Manifestations of chronic liver disease

137
Q

What are non-ETOH fatty liver diseases?

A

Due to metabolic syndrome
Fatty infiltration of hepatocytes
Cellular ballooning

138
Q

How does hepatic encephalopathy occur?

Signs?

A 
Portosystemic shunts, that decrease the NH3 metbolism and cause neuropsyhciatric dysfunction
Signs:
disorientation
Asterix
different arousal or coma
139
Q

What are the triggers of metabolic encephalopathy?

A

Increased NH3 production and absoprtion (Dietery protein, GI bleed, constipation, and infection)

140
Q

What causes decreased NH3 removal?

A

Renal failure, diuretics, bypassed hepatic blood flow (post TIPS)

141
Q

How to treat hepatic encephalopathy?

A

Lactulose
rifaximin
neomycin

142
Q

What are the associations with hepatocellular carcinoma?

A

Most comon malignant tumor of the liver

Usually associated with HCV, ETOH, and non-ETOH (fatty liver), hemochromatosis, alpha antitrypsin

143
Q

What are findings associated with hepato cellular carcinoma?

A 
Jaundice
Hepatomegaly
Anorexia
Ascites
Polycythemia
144
Q

How is the diagnosis of the heptocellular carcinoma made?

A

Elevated alpha-fetoprotein
Ultrasound
CT or MRI

145
Q

What is a cavernous hemangioma?

A

Common, benign tumor

Typically occurs between 30-50 years of age.

146
Q

Should a hemangioma be biospied?

A

There is risk of hemorrage (contra indication)

147
Q

What are characteristics of hepatic adenoma?

A

Rare, bengin tumor
Related to oral contraception or anabolic steroids
Can spontaneously rupture

148
Q

What is angiosarcoma?

A

Malignant tumor of endothelial origin

Associated with exposure to arsenic and vinyl chloride

149
Q

What are common mets to the liver?

A

GI malignancies
Breats
Lung cancer

150
Q

What is Budd Chiari syndrome

A

Thrombosis of the hepatic veins with congestion and necrosis

Results in hepatomegaly, ascites, varices, abdomingal pain, liver failure, and JVD

Associated with hypercoagulable states, polycythemia, postpartum.

151
Q

What are characteristics of alpha antitrypsin deficiency?

A

1) Misfolding gene prodyct protein aggregates in hepatocellular ER

Results in cirrhsis with PAS globules

152
Q

What are manifestations of alpha antitrypsin defieciency in the lungs?

A

Uninhibited elastase in alveoli
Decrease elastic tissue
Leads to panacinar emphysema

153
Q

What are the characteristics of Jaunedice?

A

Abnormal yellowing of the skin or sclera

Caused by Bilirubin deposition

154
Q

What are the causes of hyperbilirubinemia?

A

1) Increased production
2) Decreased hepatic uptake
3) Increased conjugation
4) Decreased excretion

155
Q

What are causes of unconjugated (indirect hyperbilirubinemia)?

A

Hemolytic
Crigler-Najaar
Gilbert syndrome

156
Q

What are causes of elevated direct hyperbilirubinemia?

A

Bilary obstrcution: gallstones, cholangiocarcinoma, liver cancer, liver fluke

Bilary tract disease
Scleorosing cholangitis
Biliary Cirrhosis
Excretion defect: Dubin-Johnson Syndrome

157
Q

What are the causes of mixed hyperbilirubinemia?

A

Hepatitis

Cirrhosis

158
Q

What is the cause of physiologic neonatal jaundice?

A

At birth have immature UDP-glucuronosyltrasnferase
Leads to unconjugated hyperbilirubinemia
Leads to jaunedice and kernicterius

159
Q

How to treat physiologic neonatal jaundice?

A

Usaully occurs 24 hours after life
Usually resolves 1-2 weeks
Treatment is with phototherapy (non-UV light)

Changes the non-conjugated bilirubin to water soluable form.

160
Q

What is Gilbert’s syndrome?

A

Mildly decreased UDP glucronosytransferase conjugation and impaired bilirubin uptake

Asymtomatic of mild jaunedice

Bilirubin increases with fasting and stress

Increase in unconjugated bilirubin without overt hemolysis

161
Q

What is Crigler-Najjar syndrome?

A

NO UDP-glucuronosyltrasnferase
Presents early in life
Findings:kernicterus, increase unconjugated bilirubin

Treatement: plasmapheresis, phototherapy

162
Q

What is the Dubin-Johnson syndrome?

A

Hyperbilirubinmia due to liver excretion
Will have a grossly black liver
Benign

163
Q

What is rotor syndrome?

A

Milder then presentation of the Dublin-Johnson, has no black liver
Due to impaired hepatic uptake and excretion

164
Q

What are characteristics of Wilson’s disease?

A

Recessive mutation in ATPase (copper transporting)
Inadequate copper excretion
Presents before age of 40 with liver disease (hepatits, acute liver failure, cirrhosis) neurological disease

Treatement: chelation with penicillamine

165
Q

What are charcteristics of hemochromatosis?

A

Recessive HFE gene
Increased intestinal absorption of ferritin, increased iron, decreased TIBC
Have iron overload and accumulates in the liver, pancrease, skin, heart, etc
Can have hemosiderin on MRI
Biospy with prussian stain

166
Q

What is presentation of hemochromatosis in women?

A

1) Presents before 40 (because iron is loss through mentrusation)

167
Q

what is classic triad of hemochromatosis?

A

Cirrhosis
DM
Skin pigmentation (bronze)

Can also cause:
Cardiomyopahty
Hypogonadism
Arthropathy
HCC is common cause of death
168
Q

How is hemochromatosis treated?

A

Repeated phlebotomy

Chelation with deferasirox (deferoxamine) oral deferipone

169
Q

What is path, epi, of scleorising cholanitis?

A

Unknown cause, has strictures and dilatation of bilary duct
Usually middle age men with IBD

Associated with p-ANCA And IGM

Can lead to cholangiocarcinoma or gallbladder cancer

Diagnosis with ERCP or MRCP

170
Q

What is path, epi, of primary biliary cirrhosis?

A

Autoimmune reaction
Usually middle aged women
Anti-michrondrial
Associated with Sjogren, CREST, hasimotot

171
Q

What is secondary biliary cirrhosis?

A

Extrahepatic biliary obstrcution
Increased pressure in hepatic ducts
Injury/ fibrosis to bile ducts

Patients often are known for gallstones, bilary structres, or pancreatic carciunoma

Can be complicated by ascending cholangitis

172
Q

How are gallstones caused?

A

Increased cholesterol
Increased bilirubin
Decreased bile salts

173
Q

What are the risk factors for gallstones?

A

Female
Fat
Fertile
Forty

174
Q

what are the two types of gallstones?

A

Cholesterol (radiolucent in 10-20%)
Pigment (black biliary colic)
Associated with cirrhosis, advanced age,

175
Q

How does gallstones manifest?

A 
Biliary colic (neurohormonal activation with CCK)
or a fatty meal

Triggers contraction of the gallbladder, forcing the stone into the cystic duct

176
Q

What is the treatment of cholecystitis?

A

Diagnose with U/S, treat with Cholecystectomy

177
Q

What are the symptoms of Charcot cholangitis?

A

Jaunedice
Fever
Right upper quadrant pain

178
Q

How can a fistula be caused between the gallbladder and the gastrointestinal tract?

A

Pneumobilia leads to passage of gallstones into the intestinal tract, leads to ileocecal valve (gallstone ileus)

179
Q

What are signs of cholecystitis?

A

Acute or chronic inflammation of the gallbladder
Leads to infection (rarely acalculous due to ischemia and stasis)

Murphy’s sign (inspiratory arrest on RUQ palpation due to pain)

180
Q

How to diagnose a cholecystitis?

A

With U/S
Cholescintigraphy
HIDA scan

181
Q

What is a procelain gallbladder?

A

Calcified gallbladder due to chronic cholecystitis found on imaging

Treatment: prophylactic cholecystectomy due to high rates of carcinoma

182
Q

What are causes of acute pancreatitis?

A 
Idiopathic
Gallstones
ETOH
Trauma
Steroids
Mumps
Autoimmune
Scorpion 
Hypercalcemia
ERCP
Drugs
183
Q

What are the characteristics of pancreatitis?

A

acute epigastric pain, radiating to the back
increase in amylase or lipase (3X upper limit of normal)
Imaging that is characteristic of pancreatitis

184
Q

What are the complications of pancreatitis?

A 
1)Pseudocyst
Necrosis
hemorrage
infection
organ failure
hypocalcemia
185
Q

What are the causes of chronic pancreatitis?

A

ETOH
cystic fibrosis
Chronic pancreatic insufficiency
DM

186
Q

What happens to the amylase and lipase within chronic pancreatitis?

A

Can sometimes stay normal

187
Q

What are the characteristics of pancreatic adenocarcinoma?

A

Tumor arising from the pancreatic ducts
Often mets upon presentation
More common at the pancreatic head which can cause obstructive jaunedice
High CA 19-9

188
Q

What are the risk factors for pancreatic adenocarcinoma?

A 
Tobacco use
Chronic pancreatitis (especially more 20 yers)
DM
Age more 50 
Jewish and African American
189
Q

How does pancreatitis present itself?

A 
Abdominal pain radiating to the back 
weight loss
Migratory thrombophlebitis
Trousseau syndroms
Obstructive jaundice
190
Q

what is the treatment for pancreatic cancer?

A

Whipple procedure
Chemotherapy
Radiation Therapy

191
Q

what are the mechanism, use, effects of H2 blocker?

A

Cimentidine, ranitidine
Mechanism: Blocks H2 receptors and leads to decreased H2 secretion
Adverse effects: inhibits cytochrome P-450 (multiple drug interactions)

Can cause prolactin release, gynecomastia,impotence, decrease in libido

192
Q

What is the mechanism, clinical use, adverse of proton pump inhibitors?

A

Omeprazole, lansprazole, esomeprazole
Mechainsm: irreverisble inhibit H+/K+
Treatment of peptic ulcers, GERD and Zollinger-Ellison
Can have increase of C.Difficile infection

193
Q

What are side effects of antacid use?

A

affect absorption, bioavailability or urinary excretion by changing gastric and urinary pH
Can cause hypokalemia

194
Q

Side effects of aluminum hydroxide?

A

Constipation
Hypophospatemia
Muscle weakness
Seizures

195
Q

Side effects of calcium carbonate?

A

Hypercalcemia (milk-alkali syndrome) rebound acid

Can chelate and decrease effectiveness of the other drugs

196
Q

What are side effects of magnesium hydroxide?

A

Diarrhea

Hyporelexia

197
Q

Mechanism/use of bismuth, sucralfate?

A

Binds to ucler and makes a protective coat allowing HCO3 secretion

Can be used to heal ulcers

198
Q

Mechanism for Misoprostol?

A

PGE analog
Increase the production and secretion of gastric mucous barrier

Decrease acid production

Can have diarrhea (don’t give pregnant women)

199
Q

Mechanism/adverse of oceterotide?

A

Long acting somatostatin
Inhibits secretion and splanic horomone
Adverse: nausea, cramps, steatorrhea

200
Q

Mechanism of osmotic laxatives?

A

Include: magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose
Clincal use:constipation
Adverse effects: diarrhea, dehydration

201
Q

Mechanism of sulfasalazine?

A

Combination of sulfapyridine (antibacterial) and 5 aminosalicylic acid (anti-inflammatory)

Clinical uses: Ulcerative colitis, Crohn’s disease,
Adverse effects: Maliase, nausea, sulfonamide toxicity, oligosperimia

202
Q

Mechanism/clinical use/adverse loperamide

A

Agonist of u-opiod
Slows gut motility
Clincial: diarrehea
Adverse: constipation and nausea

203
Q

Mechanism/clinical/adverse Ondansetron?

A

5Ht antagonist
Clinical: postoperative vomiting and chemo
Adverse: headache, constipation, QT interval longer

204
Q

Clincal/adverse Orlistat?

A

Mechanims: inhibits gastric and pancreatic lipase
Clincal use: weight loss
Adverse: steatorrhea, decreased absorption of fat soluable vitamins

205
Q

Clincial/adverse of Ursodiol?

A

Mechanism: increase of nontoxic bile acid (increased bile secretion) decreased cholesterol secretion and reabsoprtion
Clinical: primary biliary cirrohisis (gallstone prevention or dissolution)

206
Q

What are propoerties of erythrocytes?

A

Hvae Cl/HCO3 transporters to bring CO2 to the lungs

Anucleate

207
Q

What is erythrocytosis?

A

Polycythemia (increase in hematocrit)

208
Q

What is anisocytosis?

A

Varying sizes

209
Q

What is poikilocytosis?

A

Varying shapes

210
Q

What are reticulocytes?

A

Immature RBC

211
Q

What is a platelet?

A

Small cytoplasmic fragment
Contains ADP and Ca
Graulues with vWF, firbinogen, and fibronectin

212
Q

What is the lifespan of platelet?

A

8-10 days

213
Q

What percentage of the platelet pool is sequestered in the spleen?

A

1/3

214
Q

what happens when there is thrombocytopenia?

A

Developpe petechiae

215
Q

What percentage of leucocytes are neutrophils, lymphocytes, monocytes, eosinophils?

A

About 50% are neutrophils

25% lymphocytes

216
Q

what is the use of neutrophils?

A

Acute inflammatory cells
Phagnocytic
Contain lyzosymes

217
Q

what is seen in neutrophils if have vitamine B/folate deficiency?

A

Hypersegmented neutrophils

218
Q

What do band cells suggest?

A

Increased myeloid proliferation (bacterial infection of CML)

219
Q

Macrophages are important in what type of diseases?

A

Important component of granuloma formation in TB and sarcoidosis

Lipid A from bacterial LPS binds to CD 14

220
Q

What are the causes of Esinophilia?

A 
Neoplasia
Asthma
Allergic process
Chronic adrenal insufficiency 
Parasites

US (17 decks)

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