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Boards 23' > GI > Flashcards

GI Flashcards

1
Q

The digestive tube is derived from what embryonic structure?

A

the yolk sac (later endoderm)

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2
Q

the lining of the GI tract and visceral organs is derived from which primary germ layer?

A

endoderm; GI epithelium, glands; many organs bud off: liver, pancreas and trachea

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3
Q

The stroma (CT) and muscles of the GI tract are derived from which primary germ layer?

A

mesoderm; stroma, muscles, peritoneum and spleen

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4
Q

The IMA is derived from which embryonic structure?

A

hindgut; transverse colon to rectum

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5
Q

The transverse colon to the rectum is supplied by which artery and is derived from what embryonic structure?

A

the IMA and the hindgut

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6
Q

The SMA is derived from which embryonic structure?

A

midgut; ampulla of vater to the transverse colon

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7
Q

the ampulla of vater to the transverse colon is supplied by which artery and is derived from what embryonic structure?

A

the SMA and the midgut

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8
Q

The celiac trunk is derived from which embryonic structure?

A

the foregut; mouth (oral cavity) to the ampulla of vater

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9
Q

The mouth (oral cavity) to the ampulla of vater is supplied by which artery and is derived from what embryonic structure?

A

the foregut and the celiac trunk

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10
Q

Mesentery is derived from which germ layer?

A

mesoderm

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11
Q

Dorsal mesentery

A

greater omentum; gut moves away from posterior wall in development and covers most abdominal structures

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12
Q

Structures that the ventral mesentery cover?

A

the lesser omentum and falciform ligament; bottom of the esophagus, stomach and upper duodenum; liver grows into it; derived from the septum transversum

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13
Q

ventral mesentery are what structures in an adult?

A

lesser omentum and falciform ligament; derived from the septum transversum

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14
Q

What structure divided the foregut structures (respiratory diverticulum which forms the lung buds and the esophagus)?

A

tracheoesophageal septum; abnormal septum development leads to esophageal atresia (closed esophagus) when the septum deviates posteriorly

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15
Q

Characteristic findings in a neonate with esophageal atresia

A

esophagus does not connect to stomach, fetus will not be about to swallow fluids leading to polyhydramnios; when born baby will present with drooling, choking and vomiting (unable to swallow secretions building up in oral cavity); diagnosis with NG tube unable to go into stomach because of closed cavity

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16
Q

Physiology herniation of the midgut

A

6th week of development, abdomen becomes too small so intestines herniate through umbilical cord; visible on fetal ultrasound; reduction of herniation by 12th week

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17
Q

Omphalocele vs Gastroschisis

A

both are pediatric abdominal wall defects

  1. omphalocele - abnormal rotation of the midgut; contents will be covered by peritoneum (membrane) and will be midline
  2. gastroschisis - full thickness abdominal wall defect; contents will NOT be covered by membrane, elevated maternal AFP because it leaks out, and will be paraumbilical (typically to the R) - note that insertion site is usually normal and separate from the defect
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18
Q

omphalocele

A

pediatric abdominal wall defects; abnormal rotation of the midgut; contents will be covered by peritoneum (membrane) and will be midline

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19
Q

associated congenital abnormalities to omphalocele

A

trisomy 21 (few associated abnormalities with gastroschisis)

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20
Q

gastroschisis

A

full thickness abdominal wall defect; contents will NOT be covered by membrane, elevated maternal AFP because it leaks out, and will be paraumbilical (typically to the R) - note that insertion site is usually normal and separate from the defect; pt will later have poor GI function after repair

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21
Q

the midgut rotates around what structure in development?

A

the SMA

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22
Q

Where should the cecum be located after midgut rotation has taken place?

A

cecum should be in right lower quadrant where it is normally located

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23
Q

malrotation of the midgut can lead to what defect?

A

volvulus - small bowel twist around SMA, there is vascular compromise leading to ischemia; presents with vomiting, sepsis, distended abdomen and blood in stool; tx w urgent surgery

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24
Q

L sided colon (cecum) can develop from which malformation?

A

malrotation of the midgut during development

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25
Q

persistence of the vitelline duct results in what abnormality?

A

Meckel’s diverticulum - outpouching or “bulging” that occurs at the ileum

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26
Q

Meckel’s diverticulum

A

outpouching or “bulging” that occurs at the ileum; formed due to the persistence of the vitelline duct (disappears by week 9); known as a TRUE diverticulum because contains ALL layers of the bowel (mucosa, submucosa and muscular); contain ectopic gastric tissue - can be diagnostic using a technetium scan

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27
Q

Rule of 2’s

A

Meckel’s diverticulum; occurs in 2% of the population, male to female ratio is 2:1, located within 2 feet from the ileocecal valve and usually 2 inches in size

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28
Q

duodenal atresia

A

most common type of GI atresia; results in failed “recanalization”; associated with Down syndrome; can see the Double Bubble Sign on imaging - dilation of duodenum and stomach with a tight pylorus in the middle

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29
Q

jejunal-ileal-colonic atresia

A

causes due to vascular disruption leading to ischemic necrosis that is reabsorbed and a blind end of the bowel is left; “apple peel atresia” - bowel distal to blind end may be curled

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30
Q

pyloric stenosis

A

hypertrophy of the pyloric leading to stenosis; projectile “non-bilious” vomiting; olive mass felt on palpation; usually in first born children

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31
Q

spleen embryology

A

arises from dorsal mesodermal tissue; NOT from endoderm!!; blood supply is the celiac trunk; gastrosplenic ligaments carries the short gastric arteries and the left gastric epiploic vessels

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32
Q

If there is a IVC or abdominal aorta rupture where would blood pool?

A

in the back of the abdomen - retroperitoneal bleeding; they are retroperitoneal strcutres along with the kidneys, 2nd/3rd parts of duodenum, ascending/descending colon, part of the rectum and head and body of the pancreas

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33
Q

Pectinate line

A

part of the anal canal

above the line - derived from the hindgut; columnar epithelium simulator to stomach; supplied by superior rectal artery (branch of IMA); venous drainage is superior rectal veins (IMV to portal system); can swell in portal HTN and lead to internal hemorrhoids; lymph drainage of internal iliac nodes

below the pectinate line - derived from proctoduem (ectoderm); stratified squamous epithelium similar to skin; supplied by inferior rectal artery (to internal pudenal to internal iliac to IVC); lymph drainage is superficial inguinal nodes; painful external hemorrhoids

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34
Q

above the pectinate line

A

derived from the hindgut; columnar epithelium simulator to stomach; supplied by superior rectal artery (branch of IMA); venous drainage is superior rectal veins (IMV to portal system); can swell in portal HTN and lead to internal hemorrhoids; lymph drainage of internal iliac nodes

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35
Q

portal HTN affects what part of the pectinate line?

A

above the pectinate line; venous drainage is superior rectal veins (IMV to portal system); can swell in portal HTN and lead to internal hemorrhoids

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36
Q

below the pectinate line

A

derived from proctoduem (ectoderm); stratified squamous epithelium similar to skin; supplied by inferior rectal artery (to internal pudenal to internal iliac to IVC); lymph drainage is superficial inguinal nodes; painful external hemorrhoids

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37
Q

lymph drainage above the pectinate line

A

nternal iliac nodes

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38
Q

Imperforate anus

A

handout and ectoderm meet to form anus but there is an absence of an anal opening; commonly associated with GU malformations (renal agencies and bladder exstrophy); baby will fail to pass meconium; can be a urethra or vagina fistula present

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39
Q

3 main branches of the celiac trunk

A

common hepatic, left gastric and splenic

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40
Q

the right gastric arteries originates from which artery?

A

the proper hepatic artery, which comes from the common hepatic artery which is one of the 3 branches off of the celiac trunk

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41
Q

The 2 most common perforated ulcers and their bleeding source

A

gastric ulcers at the lesser curvature of the stomach - bleeding from left gastric artery (celiac trunk)

posterior duodenal ulcers - bleeding from gastroduodenal artery ( branch off common hepatic artery - celiac trunk)

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42
Q

Short gastric arteries

A

branches of the splenic artery (celiac trunk); supply funds and upper cardiac portions of the stomach; vulnerable to ischemia if splenic artery is occluded; no dual blood supply

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43
Q

Pringle’s maneuver

A

clamping of the hepatoduodenal ligament in the OR to find the source of bleeding in a pt with internal hemorrhaging; used to control liver bleeding (via portal vein or proper hepatic artery), if bleeding continue then most likely IVC or hepatic veins

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44
Q

the 3 structures contained within the hepatoduodenal ligament?

A

part of the lesser omentum; contains the common bile duct, the portal vein and proper hepatic artery

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45
Q

SMA syndrome

A

rare cause of bowel obstruction; SMA can press downward and obstruct the duodenum leading to obstruction; classic pt - recent massive weight loss (fat pad shrinks)

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46
Q

dual blood supplies (abdominal collaterals) of the celiac trunk and the SMA

A

protects against ischemia if one is occluded; via superior and inferior pancreaticoduodenal arteries - supplies the duodenum and pancreas

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47
Q

dual blood supplies (abdominal collaterals) of the SMA and the IMA

A

protects against ischemia if one is occluded; via marginal artery of Drummond

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48
Q

dual blood supplies (abdominal collaterals) of the IMA and the iliac artery

A

protects against ischemia if one is occluded; via superior rectal and middle rectal arteries; rectal ischemia occlusion is RARE

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49
Q

pt with belly pain from ischemic colitis, where should you look next?

A

check the heart for A Fib - mostly caused by emboli from cardiac origin - typically affect jejunum the most due to traveling to the SMA; don’t look for somewhere in the abdomen; pt will have “pain out of proportion to exam” and occult blood in stool

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50
Q

Watershed areas of the colon

A
  1. splenic flexure - marginal artery of Drummond - vulnerable to under perfusion
  2. Rectosigmoid junction - narrow branches of IMA
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51
Q

Chronic mesenteric ischemia

A

intestinal angina; usually older pt with vascular dz; they have recurrent abdominal pain after eating so develops a fear of eating that results in weight loss; they will have sudden worsening on top of history of recurrent pain and may suggest acute thrombosis

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52
Q

Submucosa of the GI

A

CT that contains the meissner’s plexus - clinical correlation to Hirschsprung’s disease (missing this layer - aganglionic)

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53
Q

Auerbach’s plexus is found in which layer of the GI tract?

A

controls GI motility; in the muscular layer between the inner and outer muscular layers; controls peristalsis; abnormality can lead to achalasia (esophagus) and also absent in kids with Hirschsprung’s dz

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54
Q

epithelium of esophagus

A

non-keratinized stratified squamous epithelium; esophagus is the collapse structure filled with air behind the trachea on the CAT scan

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55
Q

epithelium of stomach

A

simple columnar epithelium; you will see gastric pits and gastric glands

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56
Q
A

histology of the small intestine; simple columnar epithelium; villi - MUCOSA extensions (finger-like) into the lumen - increase SA for absorption; crypts of Lieberkuhn - contain goblet cells; microvilli - microscopic extensions- epithelial cell membrane

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57
Q

the villi of the small intestines are extensions of what layer?

A

extensions of the mucosa layer into the lumen; increases surface area for absorption

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58
Q

Plicae circulares

A

folds of mucosa and submucosa found throughout the small intestines (most abundant in jejunum); increases surface are for absorption

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59
Q

Brunner’s Glands

A

only found in duodenum in the submucosa; produces alkaline fluid to protect from acidic stomach fluid; will be increased thickness in PUD

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60
Q

Peyer’s patches

A

lymph cell aggregates found in ileum; contain M cells collect antigens and presents the to initiate an immune response

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61
Q

Slow waves of the GI tract

A

maximum # of contractions per time

Stomach 3/min
Duodenum 12/min
ileum 8/min

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62
Q

Sphincter of Oddi dysfunction

A

narrowing that can occur after pancreatic or gallstone disease, contents (pancreatic enzymes and bile) are unable to be released via the Ampulla of Vater; presents with episodic RUQ pain and can see recurrent pancreatitis due to buildup of pancreatic enzymes

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62
Q

Sphincter of Oddi dysfunction

A

narrowing that can occur after pancreatic or gallstone disease, contents (pancreatic enzymes and bile) are unable to be released via the Ampulla of Vater; presents with episodic RUQ pain and can see recurrent pancreatitis due to buildup of pancreatic enzymes

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63
Q

Sphincter of Oddi Spasm

A

smooth muscle contractions caused by opioids (morphine); drug of choice in patients with pancreatitis is Meperidine (Demerol) because believed to not cause muscle spasms

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64
Q

the portal triad consists of what 3 vessels?

A

portal vein, hepatic artery and bile duct

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65
Q

Which hepatic zone is affected by viral hepatitis first?

A

zone 1 - right next to the portal blood coming from the intestines

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66
Q

Which hepatic zone is affected by ischemia first?

A

zone 3 furthest away from the hepatic artery

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67
Q

Pancreas embryology

A

two buds from foregut - ventral and dorsal - retroperitoneal organ (secondarily)

ventral - main pancreatic duct, part of head and uncinate process

dorsal - body, tail, accessory duct and the rest of the head

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68
Q

Annular pancreas

A

ventral bud fuse around the duodenum (ring of pancreatic tissue) and causes bowel obstruction; presents distention and abdominal pain

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69
Q

pancreas Divisum

A

dorsal and ventral ducts to not fuse leading to 2 senate ducts; often asymptomatic but can cause pancreatitis

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70
Q

Ampulla of Vater

A

where biliary and pancreatic ducts merge; empties into major duodenal papilla; anatomical transition from foregut to midgut; celiac trunk transitions to SMA

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71
Q

the 3 main salivary glands

A

submandibular glands
sublingual gland
parotid gland

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72
Q

submandibular glands

A

AKA Wharton’s duct; located at floor of the mouth;

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73
Q

sublingual gland

A

located at floor of the mouth

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74
Q

parotid gland

A

located behind angle of the jaw below and in front of ears;

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75
Q

saliva contains a large amount of which antibodies

A

IgA antibodies; also lysozymes - disrupt bacterial cell walls and lactoferrin - prevent bacterial growth

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75
Q

saliva contains a large amount of which antibodies

A

IgA antibodies; also lysozymes - disrupt bacterial cell walls and lactoferrin - prevent bacterial growth also found in breastmilk)

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76
Q

Sjogren’s disease

A

autoimmune dz resulting in loss of saliva leading to infections and dental carries (cavities)

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77
Q

Saliva electrolytes

A

becomes hypotonic as it travels passed the ductal cells (secreted as isotonic by acinar cells) due to the removal of Na and Cl and addition of K+ and HCO3

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78
Q

regulation of saliva

A

increased by both sympathetic (smaller effect) and parasympathetic (major effect) - M1 and M3 receptors; also activated by food smell and sight

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79
Q

muscarinic antagonist on saliva

A

causes dry mouth; atropine, scopolamine - motion sickness

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80
Q

muscarinic agonists on saliva

A

increase saliva production; pilocarpine (use in Sjögren’s syndrome - causes excessive sweating) and organophosphate poisoning - nerve gas or famers exposed to pesticides

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81
Q

Sialadentitis

A

inflame of salivary gland usually secondary to an obstructing stone (sialolithiasis) most often to Staph aureus or anaerobes; treatment is Nafcillin (stop coverage) or Metronidazole or Clindamycin (anaerobes)

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82
Q

Mumps

A

caused by RNA mumps virus; largely prevented by MMR vaccination; key feature is parotitis - often b/l leading to facial swelling

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83
Q

Pleomorphic adenoma

A

most common salivary tumor mainly affecting the parotid gland; benign mixed tumor (BUZZWORD: epithelial and storm tissue cells) with rare malignant transformation; painless mobile mass at the angle of the jaw

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84
Q

Warthin’s Tumor

A

2nd most common salivary tumor mainly affecting the parotid gland; AKA papillary cyst adenoma lymphomatosum; key risk factor is SMOKING 8x); key findings - presence of cyst filled fluid that are surrounded by dense lymphoid infiltrates and this lymph tissue can aggregate into germinal centers

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85
Q

Mucoepidermoid carcinoma

A

most common malignant salivary tumor; risk factor of prior radiation (child w lymphoma that was treated w radiation); occur in parotids; can cause facial nerve paralysis; look for squamous (epidermoid) cells AND mucus screwing cells

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86
Q

femoral triangle borders

A

superior - inguinal liagment
medial - adductor longus
lateral - sartorius

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87
Q

Femoral vessels

A

lateral to medial - “NAVeL”
nerve, artery (pulse), vein and then lymphatics

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88
Q

Contents of femoral sheath

A

below the inguinal ligaments; contains the femoral vein, artery and ring (opening to femoral canal) NOT the nerve

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89
Q

the 3 fascial layers of the spermatic cord

A

external spermatic fascia, cremasteric fascia and internal spermatic fascia

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90
Q

Inguinal contents in males vs females

A

males - spermatic cord
females - round ligament

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91
Q

Indirect inguinal hernia

A

“indirectly” through abdominal wall; LATERAL to epigastric vessels; covered by all layers of the spermatic fascia; due to congenital defect that causes bowel to protrude through the processes vaginalis (should have closed after the descent of the testes - to become tunica vaginalis testis); defect more common on the R

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92
Q

typically pt that presents with an indirect hernia

A

males are most common; adulthood pt who are heavy lifters (contraction workers) or straining (constipation) and newborns on mechanical ventilation

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93
Q

Key points on indirect inguinal hernias

A
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94
Q

Direct inguinal hernias

A

bowels bulges “directly” through the abdomen wall through Hesselbach’s triangle; MEDIAL to epigastric vessels; through the external ring; only covered by external spermatic fascia only and never bulges into the scrotum; usually older man of years of CT stress

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95
Q

Borders of Hesselbach’s triangle

A

inguinal liagment
inferior epigastric vessels
rectus abdominis
on the floor is the transversals fascia

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96
Q

Borders of Hesselbach’s triangle

A

inguinal liagment
inferior epigastric vessels
rectus abdominis
on the floor is the transversals fascia

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97
Q

Femoral hernias

A

herbal through the femoral ring medial to the femoral vessels; protrudes through the inguinal ligament; more common in women (but indirect is MOST common for both genders); high risk of incarceration - bowel trapped in hernia sac - can lead to strangulated (blood flow cut off and bowel becomes ischemic and necrotic)

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98
Q

Hiatal hernias

A

hernia where stomach herniates into the thorax leading to GERD; major risk factor is obesity; most common is the sliding hiatal hernia (95%); both due to phrenoesophageal membrane - laxity in sliding and defect (hole) in paraesophageal

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99
Q

sliding hiatal hernia

A

most common type of hiatal hernia; displacement of the GE junction above the diaphragm; funds remains below the GE junction; gives “hourglass” appearance on imaging

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100
Q

sliding hiatal hernia

A

most common type of hiatal hernia; displacement of the GE junction above the diaphragm; funds remains below the GE junction; gives “hourglass” appearance on imaging

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101
Q

CDH - Congenital diaphragmatic hernia

A

development defect in diaphragm - pleuroperitoneal membrane; basically a hole in the diaphragm; abdominal organs protrude into chest resulting in pulmonary hypoplasia; often fatal

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102
Q
A

GI barium contract showing and “hour-glass” appearance seen with a sliding hiatal hernia; protrusion of the stomach through the diaphragm into the thoracic cavity

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103
Q

Splenic vein thrombosis

A

splenic vein runs along the posterior surface of the pancreas and develop a clot from pancreatic inflammation (as in pancreatitis); short gastric vein drains fungus of stomach; splenic vein thrombosis can increase pressure in short gastric veins and cause gastric varies ONLY in the fundus; stomach and esophagus are spared

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104
Q
A

Meckel diverticulum; intestinal outpouching shows gastric mucosa due to failure of the vitelline duct to obliterate; various ectopic (heterotopic) tissues can be present - most common is gastric tissue - can secrete HCl and pt will present with lower GI bleeding and anemia

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105
Q

surgical landmark in removal of the appendix

A

pt with appendicitis - during the procedure, the tenure coli can be used as a surgical landmark - following it to its origin at the cecal base

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106
Q

External hemorrhoids

A

below the pectinate line; covered by squamous epithelium and have cutaneous innervation from the inferior recta nerve - branch off the pudendal nerve; sensitive to touch, temperature and pain

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107
Q

Internal hemorrhoids

A

above the pectinate line; covered by columnar epithelium; have autonomic innervation from inferior hypogastric plexus - only sensitive to stretch and NOT pain, temperature or touch

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108
Q

Which part of the GI is ALWAYS involved in Hirschsprung disease?

A

rectum is always involved - neural crest cells migrate caudally; newborn will fail to pass meconium within 48 hours of birth

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109
Q

Stool incontinence

A

internal and external sphincter or more commonly the puborectalis muscle fails to relax resulting in chronic constipation

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110
Q

Retroperitoneal organs

A

SAD PUCKER

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111
Q

Retroperitoneal hematomas

A

commonly associated with blunt abdominal trauma and typically reflect injury to retroperitoneal organs; pancreatic injury a frequent cause - high-riding seat belt; can lead to life-threatening blood loss

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112
Q

Pernicious anemia

A

autoimmune disorder involving cell-mediated destruction of parietal cells predominantly found in the upper glandular layer of the gastric body and fundus

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113
Q

Which two structures are added to cholic acid in conjugation to make it a better surfactant ?

A

taurine - an organic acid - this forms taurocholic acid

glycine - an amino acid - this forms glycocholic acid

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114
Q

what is the rate limiting enzyme in the synthesis of bile acid?

A

7 alpha hydroxylase (classic pathway - P450 enzyme - requires NADPH and O2); converts cholesterol to 7-alpha hydroxycholesterol which later turns into cholic acid - a major form of bile acid

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115
Q

Enterohepatic circulation of bile acids

A

most lipid absorption occurs in the jejunum (conjugated BA not absorbed); bile salts remain behind and are passed to distal small intestine and absorbed by active transporters in the terminal ileum (95%); the rest are secreted in the stool - a way cholesterol is excreted from the body

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116
Q

Main mechanism in which cholesterol is secreted from the body?

A

excreted in stool; cholesterol is NOT water soluble so can’t be passed in the urine; cholesterol drugs such as bile acid resins will encourage more excretion in stool by preventing bile reabsorption (largely replaced by statins)

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117
Q

Antimicoribal effects of bile salts

A

disrupts bacterial cell membranes

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118
Q

Cholestasis

A

disrupted bile flow to the intestines; lab findings - direct hyperbilirubinemia and elevated alkaline phosphatase; symptoms - jaundice, pruritus (itching due to bile salts in skin), dark urine, clay colored stools no stercobilin); can lead to fat malabsorption and decrease fat soluble vitamins

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119
Q

Alkaline phosphatase

A

alk phos - produced by the bile duct epithelial cells; obstruction of bile flow will cause increase all phos synthesis - you will see a more elevated alk phos than AST/ALT in cholestasis because the primary site of dysfunction is the bile ducts

120
Q

patterns of bile/liver damage

A

example 1 - AST/ALT are 2x norm limit but alk phos is about 5x normal limit - cholestatic pattern (gallstone)

example 2 - AST/ALT 10x norm limit and alk phos 2x norm limit - hepatocellular pattern (cirrhosis)

121
Q

magnitude of liver function test

A

rises in AST and ALT; only about 2 causes of 10,000 rise in these enzymes - a shock liver and acetaminophen toxicity

122
Q

best first test in a pt with cholestasis?

A

RUQ ultrasound; differentiates extrahepatic (dilated bile ducts) from intrahepatic (normal bile ducts)

123
Q

Intrahepatic cholestasis of pregnancy ICP

A

sometimes called pruritus gravidarum; reversible form of cholestasis (lack of bile flow) that affects women in 2nd and 3rd trimesters; believed to be caused by elevated estrogen and progesterone levels decreasing bile flow in the liver

124
Q

Heme is converted to biliverdin via which enzyme?

A

heme oxygenase - turns it green color

125
Q

Biliverdin is metabolized by which enzyme into bilirubin?

A

biliverdin reductase - turns it brown/yellow color

126
Q

unconjugated bilirubin (carried by albumin in the blood) in converted to conjugated bilirubin via which enzyme?

A

UDP glucuronyltransferase (UGT); converts bilirubin from insoluble to soluble

127
Q

bacterial enzyme in the small intestine that converts conjugated bilirubin back into the unconjugated form?

A

bacterial beta-glucuronidase; this unconjugated bilirubin is converted into urobilinogen

128
Q

fate of urobilinogen?

A

fate 1 - excretion in the feces as stercobilin (90%); makes stool dark

fate 2 - reabsorbed by intestines, converted to urobilin and excreted in urine (10%); makes urine yellow

129
Q

fate of bilirubin

A
130
Q

direct and indirect bilirubin

A

Van den Bergh reaction

direct - measurement of conjugated bilirubin

indirect - measurement of unconjugated bilirubin

131
Q

dark urine

A

seen in elevated conjugated bilirubin; also seen in rhabdomyolysis (breakdown of skeletal muscle), hematouria and dehydration (common)

132
Q

the 6 special causes of hyperbilirubinemia?

A
  1. Rifampin/Probenecid
  2. Gilbert’s Syndrome
  3. Crigler-Najjar Syndrome (more severe Gilbert’s)
  4. Dubin-Johnson Syndrome
  5. Rotor’s Syndrome (milder form of Dubin-Johnson)
  6. Neonatal jaundice
133
Q

Rifampin/Probenecid cause of hyperbilirubinemia

A

Rifampin (antibiotic commonly used to treat TB) and Probenecid (used to treat gout); both compete with bilirubin for uptake of the liver; causes an increase with unconjugated bilirubin but all LFTs will be normal - look at the pt meds list

134
Q

pt present with elevated unconjugated bilirubin levels after being successfully treated w gout or TB, but all other LFT are normal.

A

first thing you should do is look at med list; Rifampin (antibiotic commonly used to treat TB) and Probenecid (used to treat gout); both compete with bilirubin for uptake of the liver; causes an increase with unconjugated bilirubin

135
Q

Gilbert’s Syndrome cause of hyperbilirubinemia?

A

there is decrease UGT function (defect in UGT promoter gene); when there is an increased bilirubin production due to stress, menses, illnesses or fasting - pt can present w jaundice; no serious consequences

136
Q

Crigler-Najjar Syndrome cause of hyperbilirubinemia?

A

more severe form of Gilbert’s Syndrome; severely reduced/absent UGT enzyme; pt cannot conjugate bilirubin; type 1 presents in infancy and often fatal due to kernicterus (neurotoxin - basal ganglia and brain stem nuclei); type 2 is less severe - tx with phenobarbital or clofibrate

137
Q

Dubin-Johnson Syndrome cause of hyperbilirubinemia?

A

causes CONJUGATED hyperbilirubinemia; defective liver excretion; abnormal gene that codes for multi drug resistance proteins (MRPs) that is necessary for bilirubin excretion to bile; BLACK LIVER - benign condition and no tx necessary

138
Q

Neonatal Jaundice

A

takes about 14 weeks for UGT to reach adult level of function; results in increased unconjugated bilirubin that can lead to kernictrus; preterm babies are most at risk; tx w phototherapy (converts bilirubin to lumirubin - more water soluble - excretion w/o conjugation)

139
Q

Where are parietal cals found in the stomach?

A

in the gastric glands; more so in the upper layers

140
Q

Gastrin binds to which receptor on parietal cells to activate the secretion of HCl?

A

CCKb; gastrin is released from G cells found in the mucosa of the antrum (distal) in the stomach

141
Q

Why is it that if you block acetylcholine release (w atropine), you will not block the vagus nerve input on the stomach?

A

the vagus nerve at the stomach does NOT secrete Ach, instead secretes gastrin releasing peptide (GRP); activated G cells to secrete gastrin; so tx with vagotomy rather than atropine

142
Q

Why does the bicarbonate levels in serum rise slightly after someone has just eaten a meal?

A

due to the alkaline tide; H+ needed to for HCl production in the stomach releases HCO3 as a by product that is secreted in the serum

143
Q

Why does vomiting produce metabolic alkalosis with low urinary chloride

A

you are losing lots of HCl so Cl will be low; there will be an increased production of HCl by parietal cells (if urinaryl Cl is high then think diuretic use); bicarb will build up in the serum as a byproduct causing a metabolic alkalosis

144
Q

young women with an unexplained metabolic alkalosis, she has low urinary chloride, what should you suspect as her diagnosis?

A

surreptitious vomiting; loss of HCl from stomach so the HCl production will be increased and this will generate lots of bicarb in the serum (alkaline tide) causing metabolic alkalosis

145
Q

Second messengers on parietal cells

A

Ach and Gastrin - Gq with PLC/IP3/Ca2+
Histamine, Somatostatin and PGE’s - Gs with AC/cAMP

146
Q

Which amino acids can stimulate gastric release in the stomach?

A

phenylalanine and tryptophan

147
Q

Gastrinoma

A

Zollinger-Ellison syndrome; gastric secreting tumor that occurs in the duodenum or pancreas (G cells are found in the pancreas in fetus); excessive acid secretion of acid and hypertrophy/hyperplasia of the mucosa; presents w abdominal pain and diarrhea; may see distal duodenal ulcers (far beyond where most ulcers are seen)

148
Q

treatment for a gastrinoma

A

Octreotide (somatostatin) - inhibits gastrin release; high does PPI’s (omeprazole, lansoprazole, pantoprazole) or surgical excision

149
Q

Pernicious anemia

A

autoimmune gastritis; loss of parietal cells; loss of intrinsic factor so cannot absorb B12; high gastrin levels are a typical finding along with G-cell hyperplasia

150
Q

Cholecystokinin (CCK)

A

stimulated by FA’s and monoglycerides (NOT triglycerides) released by I cells in the small intestine; hormone for gallbladder contraction and pancreatic enzyme secretion; makes the sphincter of Oddi to relax

151
Q

HIDA scan

A

Hepatic iminodiscetic acid (HIDA) scan; often done when a pt has RUQ pain and a US is non-diagnostic such as with gallstones; sometimes CCK is administered for gallbladder ejection fraction determination

152
Q

Secretin

A

released by S cells of the duodenum; increases HCO3 in pancreatic duct cells to neutralize gastric acid in the small intestine (increases pH); used as a secretin stimulation test in gastrinoma

153
Q

Why is oral glucose metabolized faster than IV glucose?

A

because of the GIP (glucose-dependent insulinotropic peptide) hormone; stimulated by glucose, FA’s and AA’s (only one stimulated by all 3); stimulates insulin release from pancreas; IV glucose does not stimulate GIP release (does not go through the intestines)

154
Q

VIP

A

Vasoactive Intestinal Peptide; its a neurocine (synthesize by neurons); relaxation of smooth muscles; raises pH and inhibits gastrin; can cause a tumor - VIPoma

155
Q

VIPoma

A

VIP from islet cells in the pancreas; presents with a watery diarrhea, tea-colored odorless diarrhea (resembles cholera sometimes called the pancreatic cholera syndrome); pts will have hypokalemia and achlorhydria (absences of gastric acid)

156
Q

VIPoma

A

VIP from (increases pH) islets cells in pancreas; presents with a watery diarrhea, tea-colored odorless diarrhea (resembles cholera sometimes called the pancreatic cholera syndrome); pts will have hypokalemia and achlorhydria (absences of gastric acid)

157
Q

WDHA syndrome

A

watery diarrhea, hypokalemia and achlorhydria as seen in a VIPoma

158
Q

adults (30-50 yrs) with long-standing diarrhea (no blood or pus), no response to diet changes and endoscopic sampling shows elevated pH in the stomach

A

VIPoma - VIP secreting tumor of islet cells of the pancreas; there will be elevated VIP on serum testing; no response to diet changes eliminates lactose intolerant; tx with Octrotide (somatostatin)

159
Q

Which antibiotic can be used to treat gastroparesis (as seen in diabetes) and why?

A

Erythromycin - because it binds to motilin receptors in the stomach, intestine and colon; promotes motility in the fasting state

160
Q

GERD

A

decreased lower esophageal sphincter (LES) that allows gastric juice to back flow into the esophagus; causes reflux esophagitis; classic history findings - basal zone hyperplasia, lamina propria papilla elongate and increased eosinophils (do not confused and think it is an allergic rxn)

161
Q

Histamine H2 blockers

A

Famotidine, Ranitidine, Nizatidine, Cimetidine; all block histamine receptors on parietal cells; used in GERD

162
Q

Proton Pump Inhibitors (PPI’s)

A

Omeprazole, Pantoprazole, Lansoprazole, Esomeprazole; inhibit H+/K+ pump on parietal cells; used in GERD

163
Q

Ingestion of Lye

A

alkali substances that contain Na+ or KOH - found In household cleaners; typically invested accidentally by children; rapidly injuries wall of esophagus and causes liquefactive necrosis; child usually recovers but can result in strictures that lead to dysphagia

164
Q

Barrett’s Esophagus

A

METAPLASIA of the esophagus due to long-standing GERD; diagnosed with endoscopy; can lead to esophageal cancer

165
Q

Esophageal Cancer

A

two types - SCC - upper esophagus - **hoarse voice and cough (most common worldwide) and adenocarcinoma - distal esophagus (more common w GERD); both have increased risk with smoking and present with “progressive dysphagia” - solids and then liquids as tumor grows;

166
Q

Lymph nodes with esophageal cancer

A

Upper esophagus (neck) - as seen in SCC esophageal cancer - cervical lymph nodes

Middle esophagus (chest) - mediastinal and tracheobronchial nodes

Lower esophagus (abdomen) as seen in adenocarcinoma of the esophagus - celiac and gastric nodes

167
Q

Esophagitis of infectious causes

A

Candida - white membranes and pseudohyphae on biopsy

HSV-1 - causes oral herpes, can involve esophagus and present with “punched out” ulcers

CMV - AIDS pt (CD4 <50) and linear ulcers

168
Q

pt presents with dysphagia, GERD treatments are not working and predominance of eosinophils on biopsy

A

Eosinophilic esophagitis - allergic rxn of unknown antigen; immune-mediated; MUST EXCLUDE GERD

169
Q

Achalasia

A

inability to relax lower esophageal sphincter (LES); loss of ganglion cells in Auerbach’s plexus (muscular layer); often idiopathic but can be caused by Chana’s Disease - protozoa: Trypanosoma cruzi; pt suffers from bad breath

170
Q

Esophageal varices

A

dilated submucosal veins (usually lower 1/3rd - left gastric veins) typically due to portal HTN; tx w/ emergent endoscopy for banding/ligation

171
Q

Mallory-Weiss Syndrome

A

esophageal mucosa damage at the GE junction; causes PAINFUL hematemesis; caused by severe chronic vomiting - alcoholism or bulimia

172
Q

BoerHaave Syndrome

A

more severe than Mallory-Weiss Syndrome; transmural rupture of the esophagus and air is able to exit the esophagus; can see air in mediastinum on cxr “pneumomediastinum” and air under the skin in the neck ** subcutaneous emphysema! - when you press on the skin you can hear bubbling and cracking from the air underneath the skin

173
Q

Schatzki Ring

A

ring at the squamocolumnar junction in the esophagus; common cause of dysphagia to solids; located usually lower esophagus

174
Q

Triad of Plummer-Vinson Syndrome

A

iron deficiency anemia
beefy red tongue
esophageal web
-common in middle-age white women

175
Q

Zenker’s Diverticulum

A

a false diverticulum (does not contain all layers; not the muscular layer); chronic swallowing that occurs at the esophagus and pharynx junction problem due to **cricopharyngeal muscle failure to relax; classic located at the **Killian’s Triangle; pt presents w/ dysphagia and halitosis

176
Q

Gamma-glutamyl transpeptidase (GGT)

A

liver function test similar to alkaline phosphatase (alk phos) but is not elevated in bone disease unlike alk phos; used to determine the origin of elevated alk phos; if both are elevated then there is a hepatobiliary cause to the elevated alk phos; also elevated after heavy alcohol consumption

177
Q

Alcoholic Fatty Liver Disease

A

accumulation of FA’s in liver; usually asymptomatic, may cause hepatomegaly; abnormal AST>ALT; often reversible w/ cessation of alcohol but increased risk of cirrhosis w/ continued use; zone 3 (centrilobular) most at risk

178
Q

Non-Alcoholic Fatty Liver Disease

A

fatty liver not due to alcohol; NASH - fat and inflammation; ALT>AST (contrast with alcoholic liver dz AST>ALT); associated with obesity; improves w/ weight loss

179
Q

Acute Hepatitis

A

classically after heavy, binge drinking on top of a long hx of alcohol consumption; toxic effects from buildup of **actealdehyde!; there is damage of **intermediate filaments that gives the appearance of **Mallory bodies

180
Q

pt goes out on a big binge drinking of alcohol then presents with fever, jaundice and RUQ pain/tenderness

A

Acute Hepatitis; toxic effects from buildup of **acetaldehyde!; there is damage of **intermediate filaments that gives the appearance of **Mallory bodies

181
Q

Reye’s Syndrome

A

rare cause of liver failure and encephalopathy in children with viral infections (chicken pox - varicella zoster/ influenza B) who take aspirin to tx their infection; they present w/ rapid serve liver failure; aspirin **inhibits beta oxidation; AVOID aspirin in children

182
Q

Staining of the liver in a alpha-1 anti-trypsin (AAT) pt

A
183
Q
A

Liver abscess; walled-off infection of the liver; usually bacteria in the US 80% of cases (Staph aureus - hematogenous route; entamoeba histolytica (protozoa) - ascends through biliary tree - transmitted from contaminated water - bloody diarrhea as well; Echinococcus (helminth) - fecal/oral transmission of eggs - will show massive liver cysts

184
Q

Autoimmune Hepatitis

A

autoimmune inflammation of the liver; most common in women in their 50s/60s; most specific antibody test - Anti-smooth muscle antibodies (ASMA); tx w/ steroids and immunosuppressants

185
Q

Liver cirrhosis

A

shrunken liver that is replaced by fibrosis tissue and nodules; hyperammonemia (elevated ammonium levels can lead to neurotoxicity - asterixis, confusion and coma); can tx w/ Lactulose (laxative); cam present w/ jaundice, hypoglycemia (loss of gluconeogenesis), coagulopathy, and hypoalbuminemia (low oncotic pressure), elevated estrogen (normally removed by the liver)

186
Q

Consequences of elevated estrogen in liver cirrhosis

A

normally removed by the liver; gynecomastica in men, spider angiomata and palmer erythema (remember saying - estrogen can make your skin red)

187
Q

Hemodynamics in liver cirrhosis

A

increased vasodilators (NO), leads to decreased SVR leading to decreased BP and CO (decreased effective circulating volume) - sympathetic activation - increased RAAS and ADH, increased Na+/H20 retention = increased total body water (edema/ascities)

188
Q

Esophageal varices in Portal HTN

A

multiple dilated engorged blood vessels around the esophagus, collaterals between the esophageal veins and left gastric veins; they can rupture

189
Q

Gastric varices in Portal HTN

A

multiple dilated engorged blood vessels around the upper stomach (fundus); collateral between the left gastric veins (branch of the coronary vein - systemic) and short gastric veins (splenic vein - portal)

190
Q

Caput Medusa

A

engorged veins around the umbilicus; collaterals between the paraumbilical vein and the epigastric veins

191
Q

Internal Hemorrhoids in Portal HTN

A

multiple dilated engorged blood vessels above the dentate line; collaterals between the superior rectal vein (portal system) and the middle/inferior rectal veins (to IVC)

192
Q

Mechanism of low platelets in portal HTN

A

due to engorgement of the spleen - Hypersplenism via the splenic vein

193
Q

pt with portal HTN symptoms but the liver biopsy is normal, what should you suspect?

A

portal vein thrombosis

194
Q

SAAG

A

Serum Ascites Albumin Gradient (SAAG)

SAAG >1.1 g/dL (HIGH) - there is a big difference between the serum and ascites albumin = portal HTN

SAAG <1.1 g/dL (LOW) - there is NO difference between the serum and ascites albumin = malignancy ascites

** perform on ALL pt with ascites to rule out malignancy

195
Q

Drug of choice for Ascites Tx

A

Spironolactone - K+ sparing diuretic that blocks aldosterone at the distal tubule; and large volume paracentesis

196
Q

Infectious complication of ascites

A

Spontaneous Bacterial Peritonitis (SBP) - ascitic fluid infections; usually E. coli and Klebsiella (gram negatives); fever, abdominal pain, and increased PMNs; tx with Cefotaxime (3rd generation cephaloporins)

197
Q

Stellate cells

A

perisinusoidal cells in the liver that are a major contributor to cirrhosis; storage site for Vit A metabolites; secreted TGF B to produce fibrosis tissue;

198
Q

Aspergillus in relation to liver

A

fungus that produces **aflatoxin; contaminate in CORN; high dietary intake is associated with hepatocellular carcinoma (HCC); non-industrialized countries

199
Q

Common metastatic site for hepatocellular carcinoma (HCC)

A

**lung and bone (usually solitary tumor if primary); metastasis TO the liver most commonly come from the GI (colon, stomach, pancreas) and will see multiple nodules

200
Q

Hepatic Adenoma

A

benign; solitary in right liver lobe, common in young women (20s and 40s); associated with **contraceptive use; can be a clinical problem during pregnancy (tumor can rupture)

201
Q

Hepatic Angiosarcoma

A

Rare malignant vascular tumor associated with toxic exposures:

Vinyl chloride - used in plastic - inhalation
Arsenic - rock, soil, water

202
Q

Wilson’s Disease

A

AR disorder (mut in ATP7B - chr 13) with dysfunction in copper metabolism; Excess copper is mostly excreted in bile; incorporated into serum via ceruloplasmin; copper accumulates - increased free radical production, deposits in the brain and cornea (Kayser-Fleischer Rings) - slit lamp exam; diagnostic hallmark: low ceruloplasmin level (defect); usually a young pt (12-23yrs); tx with Penicillamine (copper chelator)

203
Q

Pt with suspected Wilson’s Disease, what test should you order next?

A

**Slit lamp exam - detectable for Kayser-Fleischer Rings in the eye; don’t pick liver function test; also a low ceruloplasmin is a hallmark for Wilson’s Disease; tx with Penicillamine

204
Q

Two special features of Hemochromatosis

A

iron overload (hereditary C282Y mut - pts should avoid (never) alcohol consumption because it accelerated liver disease AND avoid Vitamin C supplements because it increased iron absorption

205
Q

Elderly pts with gallstone symptoms should make you suspect what?

A

cancer; gallstones typically occurs in 40s

206
Q

Crohn’s Disease in relation to Gallstones

A

Crohn’s disease commonly involves inflammation of the ileum which causes abnormal resorption of bile salts

207
Q

Biliary Colic

A

episodic RUQ pain, radiate to ** right shoulder pain, usually occurs after fatty meals and lasts for about 30 mins; CCK stimulates gl

208
Q

Chronic Cholecystitis

A

long-standing untreated cholecystitis; chronic inflammation causes a **porcelain gallbladder (Ca2+ deposition - can be seen on imaging); increased risk for gallbladder carcinoma

209
Q

Acalculous cholecystitis

A

acute cholecystitis NOT due to gallstones; caused by gallbladder ischemia and stasis; pt will have thickened gallbladder wall and a + Murphy’s sign; ** Biliary sludge: thickened bile - slow/incomplete gallbladder emptying (hypomotility); this usually occurs in critically ill pts

210
Q

AIDS Cholangiopathy

A

complication of end-stage HIV infection; result from chronic infection involving biliary tree cause biliary obstruction from *strictures; common bugs - Cryptosporidium (most common) and CMV infection

211
Q

Cryptosporidium seen with biliary obstruction

A

Cryptosporidium is a protozoan - transmitted fecal/oral route usually through contaminated water and causes infectious diarrhea; pts who are healthy experience self-limited watery diarrhea but those who are immunocompromised (HIV) can cause life-threatening diarrhea; diagnosed with modified acid-fast stain showing oocytes

212
Q

Charcot’s triad

A

clinical features of ascending cholangitis - fever, abdominal pain and jaundice (can progress to Reynolds pentad)

213
Q

Reynolds pentad

A

clinical features of a severe ascending cholangitis - fever, abdominal pain, jaundice, confusion and hypotension

214
Q

Microbiology of ascending cholangitis

A

usually caused by gram - organisms: E. coli, Klebsiella, Enterobacter

Watch for Chinese liver fluke, may have just consumed sushi - Clonorchis sinensis - helminth found in infected fish; you will see peripheral eosinophilia

215
Q

Gallstone ileus

A

massive gallstone that erodes the gallbladder wall creating a fistula with the small intestine; will cause bowel obstruction at the ileocecal valve looks for air in biliary tree on imaging (should never be filled with air, but bile)

216
Q

Gallbladder carcinoma

A

adenocarcinoma from chronic inflammation or from chronic salmonella infection (S. typhi)

217
Q

Biliary atresia

A

idiopathic biliary obstruction in neonates; on US *gallbladder is absent or abnormal; jaundice, dark urine, pale stools; tx with surgical procedure - Kasai procedure

218
Q

Primary Biliary Cirrhosis

A

Biliary cirrhosis w/o extra hepatic obstruction; autoimmune disorder where T-cells attack interlobular bile ducts; will see granulomatous inflammation; imaging will show absence of biliary obstruction (WILL BE NORMAL contrast with Primary Sclerosing Cholangitis); more common in women; two common symptoms - fatigue and pruritus - REMEMBER ITCHING; commonly associated with Sjogren’s

219
Q

Why is it important to remember ITHING with Primary Biliary Cirrhosis?

A

itching may be before the development of jaundice and can be misdiagnosed with a skin condition - initial complaint! look for the two most common symptoms of itching and fatigue together, more common in women and itching may be severe and often worse at night

220
Q

pt is a women who presents with severe itching and physician orders alk phos, alk phos is elevated, what should you order to confirm your diagnosis?

A

should suspect Primary Biliary Cirrhosis and order anti-mitochondrial antibodies to confirm diagnosis

221
Q

Treatment for Primary Biliary Cirrhosis?

A

Ursodeoxycholic acid is the only effective tx; it is similar to bile acids (so replaced endogenous bile acids) but less toxic hepatocytes

222
Q

Primary Sclerosing Cholangitis

A

do not confuse with Primary Biliary Cirrhosis; this disorders has fibrosis and strictures that obstructs bile flow; involves intra and extra-hepatic bile ducts; STRONGLY associated with ulcerative colitis; labs: elevated IgM and positive p-ANCA

223
Q
A

Primary Sclerosing Cholangitis - fibrosis and strictures that obstructs bile flow; involves intra and extra-hepatic bile ducts; STRONGLY associated with ulcerative colitis; labs: elevated IgM and positive p-ANCA

224
Q

pt has hx of ulcerative colitis and now presents with jaundice and elevated alk phos levels what should you suspect and what labs do you want?

A

Primary Sclerosing Cholangitis; order a cholangiogram to confirm diagnosis - see biliary stricture and dilations “beading” “beads on a string”

225
Q

Curling’s Ulcer

A

occurs in burn pts; there is loss of skin/fluids resulting in dehydration and hypotension to the stomach; resulting in mucosal damage (decreased mucosal perfusion) leading to acute gastritis and ulcers; place on PPI

226
Q

Cushing’s Ulcer

A

caused by increased intracranial pressure due to a tumor or hemorrhage; increased vagal stimulation leading to increased Ach released on the stomach; excess acid production resulting in gastritis/ulcers; place on PPI

227
Q

Stress Ulver’s

A

common among critical ill pt (shock, sepsis, trauma) leads to decreased mucosal perfusion leading to acute gastritis and ulcers; place on PPI

228
Q

Autoimmune Gastritis

A

pernicious Anemia; chronic inflammation of gastric body/fundus; more common in women; associated with HLA-DR antigens and is also associated with gastric adenocarcinoma

229
Q

Type B chronic gastritis

A

bacterial gastritis due to H. pylori; gram negative rod that is urease positive causes ulcers in acute and chronic gastritis; mostly occurs in antrum

230
Q

MALT Lymphoma

A
231
Q

Tx for H. pylori

A

triple therapy:
PPI
Clarithromycin
Amoxicillin/Metronidazole

232
Q

Brunner’s Gland Hypertrophy

A

seen in pts with PUD; it is only in the duodenum and found in the submucosa; produces alkaline fluids that protects from the acidic stomach fluid; there will be increased thickness in PUD

233
Q

Arterial supply that can erode in a duodenal ulcer?

A

gastroduodenal artery

234
Q
A

air under the diaphragm on CXR; occurs with gastric or duodenal ulcers; causes pneumoperitoneum

235
Q

Arterial supply that can erode in a gastric ulcer?

A

left gastric artery; courses the lesser curvature of the stomach

236
Q

Risk factors for intestinal type gastric carcinoma

A

adenocarcinoma (95% of all gastric carcinomas); older men and smoking (no proven association with alcohol); nitrosamines (smoked meats) and Type A blood (mechanism unclear)

237
Q
A

signet ring that is characteristic for diffuse type gastric carcinoma; will also see a diffusely thickened stomach (like a leather) - linitis plastica

238
Q

Special clinical findings in Gastric carcinoma?

A

Acanthosis Nigricans

Leser-Trelat sign (explosive onset of multiple itchy seborrheic keratoses)

Virchows node (enlarged left supraclavicular node - drains stomach)

Sister Mary Joseph nodule (metastasis to periumbilical region - palpable on exam)

Krukenverg tumor (ovarian tumor secondary to another site)

239
Q

Menetrier’s Disease

A

a hypertrophic gastropathy; more common in men, **hyperplasia of mucous cells leading to excessive gastric mucous secretions; there will be a loss of acid (achlorhydria); albuminemia because of a loss of protein

look for pt with edema, facial swelling with abdominal pain - labs will show low serum albumin and a cat scan will show a very large stomach - increased risk for gastric adenomcarinoma

240
Q

Fat malabsorption clinical manifestations

A

steatorrhea
pale if bile absent (no bilirubin)
voluminous stools
stools that float
greasy, foul smelling
loss of fat soluble vitamins (ADEK)

241
Q

Give examples of what causes which type of diarrhea.

A

steatorrhea - malabsorption of high fat content; can occur in gallbladder issues and short bowlel syndrome w/ resection of the terminal ileum

inflammatory - WBC/RBC present on microscopy; happens in infection

water secretory - infection with cholera

watery osmotic - lactose intollerant

242
Q

Carbohydrate malabsorption clinical manifestations

A

watery diarrhea
osmotic effect of sugar molecules

243
Q

Proteins malabsorption clinical manifestations

A

edema (loss of albumin)

244
Q

Celiac Sprue

A

AKA Celiac disease; destruction if the small intestine triggered by gluten (Gliadin) exposure; tissue transglutaminase (tTG) auto T-cell antibodies (anti-tTG) - type IV hypersensitivity; associated w/ HLA-DQ2 and HLA-DQ8

245
Q

Three Key Histological features in Celiac Sprue

A

Blunting of Villi - much smaller
Crypt hyperplasia
Lymphocytes in lamina propria

246
Q
A

Celiac Sprue; Three Key Histological features:

Blunting of Villi - much smaller villi in right photo
Crypt hyperplasia
Lymphocytes in lamina propria

247
Q

Celiac Sprue Clinical manifestations

A

duodenum commonly affected (contrast w/ tropical sprue that affects the entire small bowel); flatulence, bloating and steatorrhea; children - failure to thrive w/ iron deficiency anemia (iron is primarily absorbed in duodenum); can present with Dermatitis Herpetiformis - herpes-like lesions on skin (IgA deposition in dermal papillae)

pts are at risk for T-cell lymphoma; pt who has been adherent to celiac diet and now symptoms are getting worse

248
Q

pt develops chronic diarrhea after recent travel to the Caribbean, all celiacs test will be negative (anti-tTG), there is blunting of the villi in all segments of the small intestine. What condition do you suspect and supplementation you should give?

A

Tropical sprue; tx w/ antibiotics (usually tetracycline) and give **folate supplementation

249
Q

Whipple’s Disease

A

infection w/ Tropheryma whipplei (gram + rod related to actinomycetes); systemic infection involving the small intestine, joints, brain and heart; **HALLMARK: PAS + foamy macrophages seen in the lamina propria of the small intestine

250
Q
A

PAS + foamy macrophages seen in the lamina propria of the small caused by an infection w/ Tropheryma whipplei (gram + rod related to actinomycetes) as seen in Whipple’s Disease

251
Q

D-xylose Test

A

test carbs absorption in the small intestine; D-xylose is a monosaccharide that is absorbed directly w/o an enzyme there only needs to be an intact mucosa; abnormal results are seen in bacterial overgrowth and Whipple’s disease

252
Q

Drugs that can trigger acute pancreatitis

A

GLP-1 agonists (diabetics) - Exenatide and Liraglutide

Sulfa drugs

6-Mercaptopurine (6-MP)

253
Q
A

Pancreatic pseudocyst; a complication of pancreatitis; walled-off collection of edema/fluid with granulation/fibrous tissue that surrounds the fluid; found usually OUTSIDE of the pancreas (most common in the lesser sac); required 4 weeks to mature after pancreatitis (can always develop in people w/ chronic pancreatitis) diagnosed by CT or MRI

254
Q

Chronic Pancreatitis

A

fibrosis/calcification of the pancreas; chronic abdominal pain that can result in a fear of eating; two main complications -
1. Splenic vein thrombosis resulting in gastric varices (left gastric vain and left gastric vein)
2. Pancreatic insufficiency leading to fat malabsorption and steatorrhea, fat-soluble vitamin deficiencies and diabetes (loss of insulin)

255
Q

Pancreatic cancer

A

most common in the head (near the duodenum where bile drains); vague abdominal pain and weight loss “painless jaundice” tumor grows slowly; Courvoisier’s sign - PE finding of an enlarged, non-tender gallbladder plus jaundice

256
Q

Pancreatic Cancer genetics

A

K-RAS gene (chr 12) - 90%
SMAD4 gene (chr 18) - 60%

257
Q

Pancreatic Cancer genetics

A

K-RAS gene (chr 12) - 90%
SMAD4 gene (chr 18) - 60%

258
Q

Pathogensis of appendicitis

A

opening ig the cecum becomes **obstructed; due to fecaliths (hard fecal masses) - more common in adults OR lymphoid hyperplasia - more common in children

259
Q

The “Acute Abdomen”

A

acute onset of abdominal pain with rebound tenderness; reflects peritoneal inflammation; requires urgent surgical intervention; need to avoid life-threatneing complications of perforation

260
Q

Diverticular Disease

A

blind pouch extending out from the GI tract due to breakdown of the muscular layer (occur where vasa recta penetrate muscularis of colon); it is a false diverticulum (does NOT contain all layers); usually occurs in sigmoid colon; caused by straining to pass stool; lower GI bleeding; if gets infected - Diverticulitis

261
Q

Diverticulitis

A

inflammation of the diverticulum; presents with fever and increased WBCs, LLQ pain (sigmoid colon); occult blood in stool; complications of an abscess, bowel obstruction, fistula, and perforation

262
Q

Adhesions

A

bands of scar tissue in peritoneal cavity commonly formed after surgery (C-section in women, appendicitis or bowel obstruction); most common cause of short bowel obstruction; tx would be to surgically lysis the adhesions (risk for more adhesions)

263
Q

Intussusception

A

telescoping of the intestine; intestine folds into lumen; can compromise blood supply and lead to ischemia; GI bleeding with “currant jelly” appearance; medical emergency; common in children <1 yrs; most causes are idiopathic but the most common pathological cause is Meckel’s diverticulum (incomplete obliteration of the vitelline duct) - look for ectopic gastric mucosa in intestines; also strong association with adenovirus

264
Q

Hirschsprung’s disease

A

failure of neural crest cells to migrate leading to an absence of ganglion cells in the nerve plexuses; child will have failure to pass meconium; barium imaging has characteristic finding go “transition zone”; diagnosis is made by biopsy rectal “suction” biopsy; RECTUM is ALWAYS involved

265
Q

Ogilvie Syndrome

A

acute “pseudo-obstruction” of intestines; dilated colon in absence of a lesion; usually in hospitalized or nursing home pts after an illness or surgery. Often associated w/ narcotics

266
Q

Irritable Bowel Syndrome

A

FUNCTIONAL bowel syndrome (problem w/ the function not the structure); normal intestine structure (biopsy is normal); recurrent abdominal pain for 3 days per month for 3 months; relief w/ defeaction

267
Q
A

Necrotizing enterocolitis; occurs in preterm infants due to GI and immune immaturity; bacterial in bowel causes inflammation and ischemic necrosis; bowel becomes congested and gangrenous with formation of intramural gas collections; pneumatosis intestinal can be seen on abdominal x ray (air in bowel wall); tx w/ bowel rest

268
Q

Necrotizing enterocolitis

A

occurs in preterm infants due to GI and immune immaturity; bacterial in bowel causes inflammation and ischemic necrosis; bowel becomes congested and gangrenous with formation of intramural gas collections; pneumatosis intestinal can be seen on abdominal x ray (air in bowel wall)tx w/ bowel rest

269
Q

Angiodysplasia

A

aberrant blood vessels in GI tract; commonly in cecum and right sided colon; caused by high wall stress; can present w/ lower GI bleeding

270
Q

Crohn’s disease

A

one of the IBDs; relapsing, remitting course “flares”; noncaseating granulomatous inflammation; affect entire wall (transmural); any portion of the GI can be affects (mouth to anus); terminal ileum is affects (B12 deficiency and loss of bile salts); RLQ pain (terminal ileum); often skips the rectum; can see cobblestone mucosa and transmural inflammation can lead to fistulas; creeping fat and strictures “string sign”

271
Q

Ulcerative colitis

A

one of the IBDs; relapsing, remitting course “flares”; ulcers of the intestinal tract specifically in the colon; inflammation of the mucosa and submucosal (not full thickness); ALWAYS starts in the rectum and works it way upward; does NOT involve the small intestine; presence of pseudopolyps, loss of haustra “lead pipe appearance” and crypt abscesses (PMNs); p-ANCA

272
Q
A

Pseudopolyps - healing of ulcers as seen in Ulcerative colitis

273
Q
A

seen in Ulcerative colitis

274
Q

Extra-intestinal features of ulcerative colitis

A

Pyoderma gangrenous - deep necrotic skin ulceration (causes ulcers of the colon, can also cause ulcers of the skin)

Primary sclerosing cholangitis
Ankylosing spondylitis - inflamed spine
Uveitis - inflamed eye

275
Q

Feared complication of ulcerative colitis

A

Toxic megacolon - colon stop contracting (increased NO) leading to intestinal dilation (rapid distention occurs) the wall thins and it is prone to rupture and perforation; pt can go into shock and die; obtain a flat plate x ray of the abdomen

276
Q

noncaseating granulomas in the small intestine

A

Crohn’s disease

277
Q
A

Crohn’s disease

278
Q

Extra-intestinal features of Crohn’s disease

A

Migratory poly arthritis - most common - arthritis of the large joints

Kidney stones - calcium oxalate stones; high oxalate levels, so oxalate Is free to be absorbed in the gut

279
Q

Immunology of the inflammatory bowel disorders

A

Ulcerative colitis - Th2 mediated = no granulomas

Crohn’s disease - Th1 mediated = granulomatous disease

280
Q

Immunology of the inflammatory bowel disorders

A

Ulcerative colitis - Th2 mediated = no granulomas

Crohn’s disease - Th1 mediated = granulomatous disease

281
Q

Tx of UC w/ Sulfasalazine with side effects

A

GI upset
Sulfa hypersensitivity
Oligospermia in men - problem w/ men trying to conceive (is reversible)

282
Q

Hyperplastic Polyp

A

most common

283
Q

Hyperplastic Polyp

A

most common type of colon poly; it is benign; often found in the rectosigmoid colon; classically has a “sawtooth” or serrated pattern; no special screening required after biopsy

284
Q

pt has a colonoscopy and a polyp is identified and removed, analysis comes back and it is a hyperplastic poly, what are next steps?

A

no special screening required after biopsy

285
Q

Colon Polys that are high risk for development into colon cancer

A

adenomatous villous polyps (tubular polyps are less common)

286
Q

Peutz-Jeghers Syndrome

A

AD disorder of juveniles; multiple hamartomas are found throughout the GI tract; will present with pigmented spots on lips and buckle mucosa; increased risk for gastric, small intestinal and colon cancer

287
Q

adolescent is brought in due to multiple pigmented spots on lips and buccal mucosa

A

Peutz-Jeghers Syndrome; multiple hamartomas are found throughout the GI tract; increased risk for gastric, small intestinal and colon cancer

288
Q

Genetics of colon cancer (3 things)

A
  1. two well-defined pathways
    - chromosomal instability pathway - APC mut 1st and then KRAS mut and finally a p53 mut = tumor cell growth (FAP and FAP variants)
  • micro satellite instability - de novo w/o polyp (less common mechanism) (HNPCC/Lynch Syndrome)
  1. Cyclooxygenase-2 (COX-2) expression is increased*** (tx w/ aspirin)
  2. Deleted in Colorectal Cancer (DCC) gene mutated in advanced colorectal cancers
289
Q

Familial Adenomatous Polyposis (FAP)

A

AD disorder involving a germline mut of APC gene; ALWAYS 100% progresses to colon cancer; tx; colon removal (colectomy)

290
Q

Gardner’s Syndrome

A

FAP variant - remember is forms bumps all over the body; benign bone growth (osteomas) - esp mandible; skin cysts (epidermal, fibromas, lipomas); CT growths and hypertrophy of the retinal pigment (children are born with flat dark spot in retina)

291
Q

Turcot Syndrome

A

FAP variant - polyposis of the colon plus brain tumors (mostly medulloblastomas and gliomas)

292
Q

Hereditary Non-Polyposis Colorectal Cancer (HNPCC)/Lynch Syndrome

A

inherited mut in DNA mismatch repair enzymes leading to colon cancer via micro satellite instability; 80% lifetime risk; usually R sided tumor

293
Q

pt w/ R sides colon cancer with multiple 1st family members also w/ cancer that person may have what?

A

inherited mut in DNA mismatch repair enzymes leading to colon cancer via micro satellite instability as seen in Hereditary Non-Polyposis Colorectal Cancer (HNPCC)/Lynch Syndrome

294
Q

Step Bovis

A

normal colonic bacteria; gram + cocci and gamma hemolytic; Lancefield group D; cases bacteremia and **endocarditis; STRONGLY associated w/ colon cancer

295
Q

pt w/ Step Bovis organism identified (endocarditis), what test should you do next?

A

Colonoscopy; STRONGLY associated w/ colon cancer

296
Q

Carcinoid Tumors

A

neuroendocrine tumor that secrete the NTM serotonin (5-HT); caused diarrhea and flushing (these pts are miserable!!); may also develop valvular heart disease (fibrous deposits on tricuspid and pulmonic valves); when symptoms present they now have the carcinoid syndrome; liver and lung metabolize (inactive) serotonin (left sided lesions are rare); altered **tryptophan metabolism (deficiency) needed for Niacin (B3) = pellagra; measure 5-HIAA in the urine and elevated levels is diagnostic; tx w/ octreotide

297
Q

HCV tx

A

chronic HCV infection is tx w direct-acting antivirals (DAAs) meds such as ledipasvir and sofosbuvir; these meds target specific HCV enzymes which inhibits viral replication and and assembly; results in cute in >97% pts

298
Q

Hepatitis A infection

A

transmission of HAV occurs through fecal-oral route and is common in areas w overcrowding and poor sanitation; outbreaks frequently result from contaminated water or food, and *raw/steamed shellfish

299
Q

pancreatic cancer

A

pancreatic ductal adenocarcinoma is almost always due to an early activating mut in the KRAS oncogene (KRAS = pan CRE ASS); this leads to constitutively active proteins that allows for uncontrolled proliferation of tumor cells

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