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USMLE: step 1 > GI > Flashcards

GI Flashcards

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USMLE® Step 1 flashcards
1
Q

What do rostral and caudal mean?

A

Rostral: head
Caudal: tail

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2
Q

What does failure of caudal wall lead to?

A

Bladder exstrophy

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3
Q

What does failure of caudal wall =?

A

Sternal defects

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4
Q

What does failure of lateral wall =?

A

Gastroschisis

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5
Q

3 arterial supplies to gut and what do they supply?

A

Celiac: foregut
SMA: Midgut
IMA: hindgut

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6
Q

What does the foregut become and what supplies it?

A
  1. Pharynx -> duodenum
  2. Liver
  3. Gallbladder
  4. Distal stomach
  5. Pancreas
    - Supplied by celiac
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7
Q

Organ supplied by celiac that is not derived from foregut?

A

Spleen: derived from mesoderm, NOT endoderm

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8
Q

What layer makes most GI tract?

A

Endoderm

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9
Q

What does the hindgut become?

A

Distal 1/3 gut -> internal anus

- supplied by IMA

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10
Q

What does the midgut become? What supplies it?

A
  1. Jejunum -> proximal 2/3 colon

- Supplied by SMA

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11
Q

How does midgut develop?

A

Needs more space so from week 6 - 10 develops outside of abdomen
- Must rotate 270 degrees around SMA before can move back in

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12
Q

What is omphalocele?

A
  • Failure of gut to rotate around SMA and reduce into abdomen at week 10
  • Left stuck outside body with peritoneal covering
  • Associated with trisomies
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13
Q

Difference between gastroschisis and omphalocele?

A

Gastroschisis does not have peritoneal covering and is adjacent to belly button

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14
Q

Presentation of esophageal atresia with TE fistula?

A
  • Polyhydramnios as fetus cannot swallow
  • Vomit / regurg on first feeding
  • Drooling choking
  • Gastric air bubbles on CXR
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15
Q

What is associated with duodenal atresia?

A

Down syndrome

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16
Q

What does double bubble sign mean?

A

Duodenal atresia

- Air is stuck in stomach and again in duodenum below pyloric sphincter

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17
Q

What does triple bubble sign mean?

A

Jejunal or ileal atresia

- Ligament of treitz is separating air into third bubble

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18
Q

Signs of duodenal atresia?

A
  1. Polyhydramnios

2. Bilious emesis (green)

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19
Q

How to tell duodenal from esophageal atresia?

A

There is not bilious emesis seen in in esophageal as atretic lumen is before bile is secreted in SI

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20
Q

What is sphincter of Oddi?

A

Where bile enters duodenum from common bile duct

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21
Q

What is hypertrophic pyloric spincter?

A
  • Slow hypertrophy of sphincter AFTER birth
  • Presents 1 month AFTER birth in contrast to atresias
    1. Palpable olive shaped mass
    2. Projectile vomiting
    3. Non bilious vomit
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22
Q

What are the retroperitoneal structures?

A

“SAD PUCKER”
Suprarenal glands
Aorta / IVC
Duodenum 2 - 4th parts

Pancreas - except tail 
Ureters
Colon (ascending and descending)
Kidneys
Esophagus 
Rectum
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23
Q

Which ligament does the portal triad travel through? What makes up the triad?

A

Hepatoduodenal ligament

  1. Common bile duct
  2. Hepatic artery
  3. Portal vein
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24
Q

What is the pringle maneuver?

A

Getting the liver to stop bleeding by compressing the hepatoduodenal ligament: the hepatic artery is found in here as well as rest of portal triad

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25
Q

First branch of aorta and where does it branch?

A

Common iliac arteries at L4

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26
Q

Where is IVC relative to aorta?

A
  • To the right
  • Anterior to renal / adrenal A
  • Posterior to right gonadal A.
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27
Q

Left abdominal venous drainage to IVC?

A
  • Renal vein is only vein that makes it to IVC

- Both gonadal and adrenal vein merge with renal then ride over

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28
Q

What is SMA syndrome?

A
  • Normally, SMA travels in mesentery of fat over curvature of duodenum which give it cushion
  • In malnourished folks, mesentery is lost and duodenum compressed between SMA and aorta = obstruction
    1. Postprandial pain
    2. Nausea / vomiting
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29
Q

Innervation of celiac / SMA area?

A

Greater and lesser splanchnic nerves T5-T12

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30
Q

Innervation of IMA area?

A

Lumbar splanchnic nerves L1 - L2

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31
Q

What does celiac arterial branch into?

A
  1. Left gastric: lesser curvature of stomach
  2. Common hepatic
  3. Splenic
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32
Q

What does left gastric artery do?

A
  1. Small branch to esophagus

2. Anastomosis on lesser curvature of stomach

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33
Q

What does splenic artery do?

A
  1. Body and tail pancreas
  2. Spleen
    * **Short gastric artery: supplies fundus
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34
Q

What does hepatic artery do?

A
  1. Gastroduodenal:
  2. Proper hepatic: part of portal triad to liver
    * *Also branches into Right gastric which anastomoses with left
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35
Q

Main blood supply to liver?

A

Portal vein: 80% volume, 50% oxygen

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36
Q

Venous blood to liver?

A

Portal to liver, hepatic veins to IVC

- Splanchnic, IMV, SMV feed liver

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37
Q

What is the ligamentum teres?

A

Used to be umbilical vein: if pressure in portal vein too high, recanalized and blood flows through it to umbilical area where cutaneous veins head back to VCs
**Caput medusae in portal HTN

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38
Q

Left gastric anastomoses from portal vein?

A

Left gastric -> esophageal veins -> Azygos vein - > SVC

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39
Q

IMV anastomosis from portal?

A

Rectal veins -> IVC - > heart

***This is why rectal absorption of drugs is better than liver as it bypasses liver

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40
Q

What does TIPS connect?

A

Hepatic vein to portal vein to bypass increased pressure

- However, the liver is no longer filtering

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41
Q

What is pectinate line?

A

Where the endoderm and ectoderm met at the anus

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42
Q

Venous drainage above pectinate line? Lymph? Cell type? Nervous?

A
  1. Superior rectal
  2. IMV
  3. Portal vein
    Lymph: internal iliac
    Histo: simple columnar
    Nerves: Visceral pelvic splanchnic
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43
Q

Venous drainage below pectinate line? Lymph? Nervous?

A 
Bypasses liver:
1. Middle / inferior rectal veins 
2. Internal pudendal 
3. Internal iliac 
4. IVC 
Lymph: superficial inguinal 
Histo: Stratified squamous 
Nerves Pudendal
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44
Q

Which hemmorhoids are painful?

A
  • External

- Internal = visceral innervation = non specific and dull `

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45
Q

Presentation of anal fissures?

A

Caused by constipation

  1. Painful defecation
  2. Blood on TP
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46
Q

What is central vein?

A

Found at center of hepatic lobules: drains blood from hepatic a. and portal vein to carry blood to hepatic veins and IVC

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47
Q

What are Kupffer cells? What are the important in?

A

Macrophages that line hepatic sinusoids

  • Break down RBCs to make heme which makes bilirubin
  • Hepatocytes accept the bilirubin to conjugate and excrete it
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48
Q

Where are Zone 1/3?

A

Zone 1: closest to triad, metabolizes and does O2 intensive tasks
Zone 3: Closest to central vein: CYP450 metabolism

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49
Q

Which zone of liver most susceptible to ischemia?

A

Zone 3, furthest from triad which has higher O2

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50
Q

Which zone most susceptible to toxins?

A

Zone 1: has not yet hit cyp450 which is in liver

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51
Q

What is toxic to zone III?

A

Alcohol and tylenol: both need to be metabolized before they become toxic

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52
Q

Which zone susceptible to hepatitis?

A

Zone 1

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53
Q

What is zone 2 susceptible to?

A

Yellow fever

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54
Q

Flow of bile from liver?

A
  1. Hepatic duct: drains bile from liver to sphincter of oddi to duodenum
  2. As oddi is usually closed, refluxes up cystic duct into gallbladder
  3. Common bile duct is distal to cystic and hepatic duct
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55
Q

What is the ampulla of vater?

A

Where common bile duct and pancreatic ducts meet

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56
Q

What are cholelithialsis?

A

Gallstones

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57
Q

What is cholecystitis?

A

Inflammation of gallbladder resulting from cholelithiasis

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58
Q

What is choledocolythiasis? Presentation?

A

Stone that has migrated down to common bile duct

  1. Jaundice: bile buildup in body
  2. Pale stools: bile colors stools
  3. Liver inflammation
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59
Q

Where would stone need to be to obstruct bile flow completely?

A

Common bile duct “choledocolithiasis”

- If only obstructing cystic duct, liver can still drain some of content town towards oddi

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60
Q

Where does stone need to be to cause inflammation of both bile duct and pancreas?

A

Confluence of pancreatic duct and common bile duct “ampulla of vater”

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61
Q

What else can obstruct the bile duct?

A

Pancreatic cancer

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62
Q

How to tell bile obstruction from stone and cancer?

A

Cancer usually presents with palpable, PAINLESS gallbladder

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63
Q

What hernia is more common in women?

A

Femoral

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64
Q

3 layers of inguinal canal?

A
  1. Transversalis fascia (NOT muscle)
  2. Internal oblique
  3. External oblique
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65
Q

What does the cremaster do?

A

Moves testis up and down to adjust for temperature

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66
Q

What does remnant of distal process vaginalis cause? Proximal?

A

Distal: Hydrocele
Proximal: indirect inguinal hernia, comes through deep inguinal ring to inguinal canal

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67
Q

What do direct and indirect hernias pop through?

A

Indirect: deep inguinal ring
Direct: superficial ring from abdominal wall

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68
Q

Indirect or direct hernal more common in elderly?

A

Direct as it needs to plow through a week abdominal wall

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69
Q

Which hernia covered by all 3 layers of inguinal canal?

A

Indirect

Direct: only covered by external spermatic fascia

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70
Q

Landmark for direct and indirect hernias?

A

Indirect: lateral to inferior epigastric vessels
Direct: Medial to inferior epigastric vessels

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71
Q

What occurs in hesselbach’s triangle?

A

Direct inguinal hernias

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72
Q

Which hernias are almost all male?

A

Indirect

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73
Q

What is sliding hiatal hernia?

A

Stomach pops up through diaphragm

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74
Q

What is paraesophageal hernia?

A

Fundus of stomach passes through diaphragm to side of esophagus

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75
Q

Presentation of diaphragmatic hernia?

A
  1. Asymptomatic

2. Reflux

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76
Q

Risk of congenital diaphragmatic hernia?

A
  1. Deadly lung HYPOplasia as lungs have nowhere to go

2. Causes pulmonary HTN and right HF

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77
Q

Where is gastrin produced and what does it do?

A

G cells of stomach antrum:

  1. Stimulates ECL to secrete histamine (endocrine)
  2. Stimulates parietal HCL
  3. Promotes growth of gastric mucosa
  4. Increases gastric motility
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78
Q

Regulation of gastrin?

A 
Increased:
1. Stomach distension
2. AAs / peptides in stomach
3. Vagal release of GRP 
4. Alkalinization
5. PPIs
6. ZE syndrome
7. Chronic gastritis
Decreased:
1. PH
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79
Q

What is Zollinger ellison syndrome?

A

Gastrinoma

- Pancreatic tumor secreting gastrin

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80
Q

What occurs in chronic gastritis?

A

Parietal cells are destroyed, G cells keep secreted gastrin as not receiving negative feedback

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81
Q

Where is somatostatin made and what does it do?

A

D cells of pancreas:

  1. Stops secretions of pretty much everything
  2. Decreased gallbladder contraction: increased risk gallstones from stasis
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82
Q

What does somatostatin do in brain?

A

Released by hypothalamus to reduce GH secretion

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83
Q

What is octreotide? Side effect?

A

Somatostatin analogue: side effect of gallstones as it stops gallbladder contractions

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84
Q

Stimulation of somatostatin?

A

Increase:
1. Acid
Decrease:
1. Vagas

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85
Q

What does cck do? Where is it made? What increases?

A

“Cholecystokinin” ***Think CHOLE = gall bladder

  • Made by I cells in SI
    1. Increase pancreatic secretions
    2. Contract gallbladder
    3. Increase pyloric emptying
    4. Relax oddi: bile secretion
  • **Increased by fat in duodenum
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86
Q

Main purpose of bile?

A

Help emulsify fats from food

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87
Q

Where is secretin made? What does it do?

A
  • Increases secretions
  • Made by S cells of duodenum
    1. Increased bicarb
    2. Increased bile
    3. Decreased gastric emptying
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88
Q

What is GIP?

A

“Glucose-dependent insulinotropic peptide” aka “gastric inhibitory peptide”

  • Increases insulin when glucose in duodenum
  • Decreases gastric acid secretion: slows food coming down for insulin to take effect
  • ***Much more highly stimulated with oral glucose than IV
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89
Q

Why is more insulin released in oral admin than IV?

A

GIP

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90
Q

What is motilin?

A
  • Produced by M cells in SI
  • Responsible for migratory motor complexes
  • More prevalent in fasted state as we want to slow food down in fed for absorption
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91
Q

What drug is a motilin agonist?

A

Erythromycin

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92
Q

What does VIP do?

A
  1. Smooth muscle relaxation of sphincters
  2. Increased water / electrolyte secretion
    * Increased by vagal stimulation
    * Decreased by adrenergic NE
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93
Q

Presentation of VIPoma?

A
  • Watery diarrhea from excess water / electrolyte secretion
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94
Q

NO roll in stomach?

A
  1. LES relaxation
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95
Q

What is loss of NO implicated in?

A

Achalasia

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96
Q

What is ghrelin?

A
  • Produced by stomach in fasting state to remind you to eat
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97
Q

Disease in which ghrelin is increased?

A
  • Prader willi syndrome from Chromosome 15 anomaly

- Causes overeating

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98
Q

What is IF?

A

“Intrinsic factor”

  • Made my parietal cells in stomach and necessary for B12 absorption
  • Allows for its absorption in terminal ileum
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99
Q

What is pernicious anemia?

A
  • Destruction of parietal cells = decreased IF and macrocytic anemia
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100
Q

How does vagal stimulate parietal cells?

A
  • ACH
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101
Q

3 Stimulators of Parietal cell?

A
  1. ACH: vagal binding M3 receptor
  2. Histamine: ECL cells via gastrin
  3. Gastrin
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102
Q

What does cimetidine do?

A

Block H secretion by blocking histamine receptor

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103
Q

How does H leave parietal cell?

A

H/K ATPase which is stimulated via ACH on M3 Gq via I# Ca cascade

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104
Q

How does histamine signal on parietal?

A

Via H2 receptor increasing cAMP which stimulates H/K ATPase

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105
Q

How do somatostatin and PGs signal on parietal cell?

A

Decreased cAMP decreasing H secretion

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106
Q

What do chief cells do?

A

Secrete pepsin: enzyme that aids in protein digestion

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107
Q

What do brunner glands secrete?

A

Bicarb into SI

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108
Q

Effects of PGs on GI?

A

Protect mucosa via increased bicarb and decreased H

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109
Q

What triggers CCK secretion?

A

Fats entering SI: think CCK increases bile and bile helps emulsify fats so this makes sense

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110
Q

What stimulates secretin?

A

Acid

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111
Q

What do D cells secrete?

A

Somatostatin

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112
Q

What releases GIP?

A

K cells

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113
Q

How is pancreatic bicarb secreted?

A
  • Via pancreatic Cl / bicarb exchanger in pancreatic ducats cells
  • Secretin increases this action
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114
Q

Flow dependency of pancreatic secretions?

A

Low flow: Cl high

High flow: bicarb high

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115
Q

What does alpha amylase do?

A

Starch digestion from pancreas

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116
Q

Why is trypsinogen?

A

Enzyme that activates all the zymogens secreted by pancreas

***Needs to first be activated by brush border enzyme enterokinase

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117
Q

What is enterokinase?

A

Brush border enzyme of SI that activates trypsinogen

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118
Q

Does stomach secrete anything for starch digestion?

A

No, only proteins and fats

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119
Q

What are the 3 major monosaccharides?

A
  1. Glucose
  2. Galactose
  3. Fructose
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120
Q

How are glucose and galactose taken up in stomach?

A

SGLT1 - uses Na gradient

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121
Q

How is fructose taken up on GI?

A

Glut-5

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122
Q

What is D xylose test?

A
  • D xylose does not require pancreatic enzymes to be absorbed
  • If problem with brush border enzymes: will not appear in bloodstream
  • If problem with pancreatic enzymes: will appear in bloodstream
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123
Q

Where are Fe, B12, and folate absorbed?

A

“Iron First Bro”
Iron: duodenum
Folate: Jejunum / ileum
B12: distal ileum, needs IF

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124
Q

Where are bile acids absorbed?

A

Terminal ileum

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125
Q

Where are peyer’s patches found? What are they?

A

Lamina propria of and submucosa of illeum

  • Lymphoid patches that can present antigens from GI tract
  • Patches respond to antigens by secreting secretory IgA
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126
Q

Where are breuners glands found?

A

Duodenum

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127
Q

What can and cannot be absorbed by GLUT2?

A

Cannot: lactose (not a monosaccharide)
Can: Glucose, galactose, fructose

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128
Q

Composition of bile?

A
  1. Bile salts
  2. Phospholipids
  3. Cholesterol
  4. Bilirubin
  5. Water / ions
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129
Q

Rate limiting step in bile synthesis?

A

Cholesterol synthesis via 7-a-hydroxylase

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130
Q

What is a bile salt?

A

Bile acid conjugated with glycine or taurine to make water soluble

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131
Q

What is 7-a-hydroxylase?

A

Rate limiting step in bile synthesis that makes cholesterol

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132
Q

What is only way body can get rid of cholesterol?

A

In the bile

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133
Q

How is bilirubin made?

A
  1. Macs eat RBCs makin heme
  2. Heme oxygenase makes biliverdin -> unconjugated bilirubin
  3. Binds albumin to make blood soluble
  4. UDP-glucuronyltransferase conjugates in liver
  5. Excreted as bile in duodenum
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134
Q

Another name for unconjugated bilirubin?

A

Indirect

*** Both are water insoluble

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135
Q

Important train in unconjugated bilirubin?

A

Water insoluble

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136
Q

What happens to bile in gut?

A
  1. Gut bacteria convert to urobilinogen
  2. 80% excreted in stool as stercobilin = brown color
  3. 20% urobilinogen reabsorbed at terminal ileum
    3a. 10% leaves urine as urobilin = yellow color
    3b. 90% returned to liver
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137
Q

What does heme oxygenase do?

A

Makes indirect bilirubin

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138
Q

Cause of cleft lip and palate?

A

Failure of facial prominences to fuse

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139
Q

What is an aphthous ulcer?

A

Painful superficial ulcer on oral mucosa

  • Arises from stress and spontaneously resolves
  • Gray base surrounded by erythema
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140
Q

What is behcet syndrome?

A
  1. Aphthous ulcers
  2. Genital ulcers
  3. Uveitis
    * from small vessel IC vasculitis
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141
Q

Cause of oral herpes?

A

HSV1

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142
Q

Where is HSV1 latent?

A

Ganglia of trigeminal nerve

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143
Q

What causes hairy leukoplakia?

A

EBV

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144
Q

What is bilateral inflamed parotids indicative of?

A

Mumps

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145
Q

What causes elevated amylase in mumps?

A
  1. Parotitis

2. Pancreatitis

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146
Q

What is a fistula?

A

Abnormal connection between 2 tubes

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147
Q

4 signs of TE fistula?

A
  1. Vomit
  2. Polyhydramnios
  3. Air in GI - distension
  4. Aspiration
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148
Q

What is an esophageal web?

A
  • Protrusion of upper esophageal mucosa into lumen = obstruction
    1. Presents with dysphagia for poorly chewed food
    2. Risk of SCC
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149
Q

What is plummer vinson syndrome?

A
  1. Severe Fe anemia “Iron pipes / plumber”
  2. Esophageal web “Web / vines / vinson”
  3. Beefy red tongue “Jake plummer is a beefy guy”
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150
Q

What is zenker diverticulum?

A
  • Outpouching of pharyngeal mucosa through muscle
  • Occurs above UES at junction of esophagus and pharynx
  • Caused by increased swallowing pressure in pharynx
    1. Dysphagia
    2. Obstruction
    3. Halitosis
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151
Q

Is zenker true of false diverticulum?

A

False

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152
Q

What is mallory weiss?

A
  1. LONGITUDINAL laceration of mucosa at GE junctions
  2. Seen in severe vomit
  3. PAINFUL hematemesis vs. varices which is no pain
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153
Q

What is boerhaave syndrome?

A
  • Rupture of esophagus = air in mediastinum
  • Creates air bubbles in skin that make crackling noise
  • Can be caused by mallory weiss tear
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154
Q

2 drainages of esophagus?

A
  1. Azygous to SVC

2. Esophageal veins -> Left gastric -> portal vein: risk of varices is here

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155
Q

What is achalasia?

A

“Without relaxation”

  • Disordered esophageal motility / cannot relax LES
  • Caused by damaged ganglion cells in myenteric plexus
    1. Dysphagia for both solids and liquids
    2. Esophageal dilation with bird beak on CXR
    3. High LES pressure
    4. Bad breath
  • Seen in chagas
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156
Q

What is bird beak on CXR indicative of?

A

Achalasia

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157
Q

What cells line esophagus?

A

Non keratinizing, squamous epithelium

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158
Q

When is hourglass appearance of stomach seen?

A

Sliding hiatal hernia

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159
Q

GERD presentation?

A
  1. Adult onset asthma
  2. Cough
  3. Heartburn
  4. Damage teeth enamel
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160
Q

What happens in barrett’s esophagus?

A

Metaplasia from non keratinizing squamous epithelium to non ciliated columnar epithelium with goblet cells

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161
Q

Facts for esophageal adenocarcinoma?

A
  • Most common esophageal carcinoma
  • Lower 1/3 esophagus
  • Usually from barrett’s
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162
Q

Squamous cell carcinoma of esophagus facts?

A
  1. Middle to upper 1/3 esophagus

2. Most common worldwide

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163
Q

Where does cancer from esophagus spread?

A

Upper 1/3: cervical nodes
Middle 1/3: tracheobronchial or mediastinal nodes
Lower 1/3: Celiac / gastric nodes

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164
Q

What is gastroschisis?

A

Congenital exposure of abdominal wall usually on right side and not covered with peritoneum
- From lateral wall

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165
Q

Causes of acute and chronic gastritis?

A 
Acute: burning of stomach by acid 
1. Increased acid production 
2. Decreased protection 
Chronic:
1. Autoimmune 
2. H Pylori
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166
Q

Risks for acute gastritis?

A
  1. NSAIDs - GPs were protective
  2. Severe burn (curling ulcer) - decreased blood flow
  3. Booze
  4. Chemo
  5. Increased ICP - Cushing ulcer
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167
Q

How are prostaglandins protective to stomach?

A
  1. Decreased Acid
  2. Increased mucus
  3. Increased bicarb
  4. Increased ICP - Cushing ulcer
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168
Q

What is a cushing ulcer?

A
  • Increased ICP = acute gastritis
  • Increased vagal stimulation = increased ACH
  • ACH = more acid from parietal cell
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169
Q

Difference between ulcer and erosion?

A

Erosion: loss of epithelium
Ulcer: loss of mucosa

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170
Q

What happens in autoimmune gastritis?

A
  1. Autoimmune destruction of parietal cells in body fundus
  2. Achlorhydria - decreased acid
  3. Increased Gastrin / G cell hyperplasia
  4. Megaloblastic anemia
  5. Intestinal metaplasia
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171
Q

Where are parietal cells found?

A

Fundus and body of stomach

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172
Q

What is intestinal metaplasia?

A
  • Chronic gastritis leads to increased inflammatory cells in gastric lining which are not normally seen here but are seen in peyer’s patches of intestine
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173
Q

How does H. pylori cause gastritis? Where does it impact?

A
  • Create ureases and proteases that damage defenses

- Antrum is most common site

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174
Q

Location breakout of peptic ulcer?

A

Proximal duodenum: 90%

Distal stomach: 10%

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175
Q

Causes of duodenal ulcer?

A
  1. H. Pylori, almost always

2. ZE syndrome

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176
Q

Which ulcer improves with meals?

A

Duodenum, this is because it is preparing itself for the meal and extra acid to arrive so it gets better

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177
Q

What happens on anterior and posterior duodenal wall rupture?

A 
Anterior wall: 
- More common 
Posterior wall: 
1. Rupture form gastroduodenal artery 
2. Acute pancreatitis
178
Q

Main cause of gastric ulcer?

A
  1. H Pylori 70%
  2. NSAIDs 20%
  3. Bile reflux
179
Q

What ulcer worsens with meals and why?

A

Gastric: stomach secretes more acid to prepare for meal

180
Q

Where is gastric ulcer usually found and what is risk?

A
  • Found on lesser curvature of antrum

- Can lead to left gastric artery bleeding

181
Q

Duodenal or gastric ulcer more likely malignant?

A

Gastric

182
Q

2 types gastric carcinoma?

A
  1. Intestinal type: large irregular ulcer with heaped margins in antrum
  2. Diffuse type
183
Q

What do nitrosamines in smoked foods give risk for?

A
  • Intestinal type gastric carcinoma
184
Q

Characteristics of diffuse gastric carcinoma?

A
  1. Signet rings cells infiltrate wall resulting in:

2. Desmoplasia causing thickening and linitis plastica

185
Q

When are signet ring cells seen?

A

Diffuse type gastric carcinoma

186
Q

What is linitis plastica indicative of?

A

Diffuse type gastric carcinoma

187
Q

When is ulcer see in gastric cancer?

A

Intestinal type

188
Q

Signs of gastric carcinoma?

A
  1. Acanthosis nigricans

2. Leser trelat sign

189
Q

What is lesser trelat sign?

A

Dozens of seborrheic keratosis on skin

- Sign of gastric carcinoma

190
Q

What is virchow node?

A
  • Left supraclavicular node that drains stomach where cancer often spreads
191
Q

Type of cancer causing krukenberg?

A

Diffuse type: signet ring cells seen

192
Q

Type of cancer causing sister mary joseph?

A

Intestinal type

193
Q

Association with duodenal atresia?

A

Down syndrome

194
Q

What is meckels diverticulum?

A
  • True diverticulum (all 3 layers) of bowel wall

- Failure of vitelline duct to involute

195
Q

What does vitelline duct to?

A
  • Nutrients from yolk sac to midgut early in fetus
  • Forms in 4th week, gone by 7th
  • Persistence = diverticulum
196
Q

What does passing meconium through belly button at birth mean?

A

Failure of vitelline duct to close

197
Q

What is being able to feel stool in belly button area indicative of?

A

Meckel’s diverticulum

198
Q

Presentation of meckel’s diverticulum”?

A
  1. Bleeding: from heterotopic gastric mucosa that produces acid
  2. Volvulus
  3. Intussusception
  4. Obstruction
199
Q

What is volvulus?

A
  • Twisting of bowel along mesentery
  • Obstructs blood supply = infarct
  • Usually at sigmoid or cecum
200
Q

Presentation of intussusception?

A
  1. Obstruction

2. Infarction - currant jelly stools

201
Q

Causes of intussusception?

A

Adults: tumor
Kids: lymphoid hyperplasia of peyer’s patches
- Terminal illeum gets dragged into cecum

202
Q

Presentation of small bowel ischemia?

A
  1. Abdominal pain
  2. Bloody diarrhea
  3. Decreased bowel sounds
203
Q

Associations of celiacs?

A

HLA-DQ-2/8

204
Q

Process of gluten?

A
  • Most pathogenic form is gliadin
  • Deamidated by tTG then presented to APCs via MHCII
  • Helper Ts cause tissue damage
205
Q

Celiacs presentation in kids?

A
  1. Abdominal distention
  2. Diarrhea
  3. Failure to thrive
  4. Dermatitis herpetiformis - IgA deposition in dermal papillae
206
Q

Lab findings in celiacs?

A

IgA against:

  1. Endomysium
  2. tTG - (transglutaminase)
  3. Gliadin
207
Q

Histo in celiacs?

A
  1. Flat villi
  2. Crypt hyperplasia
  3. Lymphocytic infiltrate
208
Q

What is tropical sprue? Main characteristics?

A

Damage to small bowel villi by unknown org = malabsorption

  1. In tropical regions
  2. After infectious diarrhea
  3. Responds to antibiotics
    * **Normally seen in jejunum and ileum
209
Q

Main thing absorbed in jejunum?

A

Folic acid

210
Q

What is whipple disease?

A
  • Systemic tissue damage with macs loaded with whipple
  • Partially destroyed orgs found in lysosomes with PAS +
  • Usually in small bowel lamina propria
211
Q

Presentation of whipple disease?

A
  1. Fat malabsorption

2. Steatorrhea

212
Q

What are lacteals?

A
  • Areas for absorption of chylomicrons found in lamina propria of SI villi
  • Drain to lymphatics
  • Chylomicrons made in enterocytes surrounding LP
213
Q

What is lamina propria of of SI loaded with macs indicative of?

A

Whipple disease

214
Q

What is abetalipoproteinemia?

A
  • AR deficiency of apolipoprotein B48/100
215
Q

What is B 48 required for?

A

Creation of chylomicron

216
Q

What is B100 required for?

A

LDL / VLDL

217
Q

What is positivity for chromogranin indicative of?

A

Carcinoid tumor

218
Q

Most common site of carcinoid tumor?

A

Small bowel: chromogranin positive

219
Q

What does carcinoid tumor usually secrete?

A
  1. Serotonin: only presents in liver because otherwise 5HT is draining to liver which just metabolizes it
220
Q

What breaks down 5HT in liver?

A

MAO: breaks it down into 5-HIAA which is seen in urine

221
Q

What is 5-HIAA in urine indicative of?

A

Carcinoid tumor

222
Q

Presentation of carcinoid syndrome?

A
  1. Bronchospasm
  2. Diarrhea
  3. Flushing of skin
  4. Right sided fibrosis of heart valves: deposition of collagen = pulmonary stenosis and tricuspid regurg
223
Q

Why doesn’t carcinoid tumor cause left sided fibrosis?

A

Lungs have MOA which breaks down MAO so fibrosis is not seen on the left side

224
Q

Cause of appendicitis?

A

Obstruction of appendix by lymphoid hyperplasia or fecalith

225
Q

Wall involvement in IBD?

A

Ulcerative: mucosal/submucosal ulcers

Crohn’s: full thickness with knife like fissures

226
Q

Location in IBD?

A

Ulcerative: Continuous from rectum to colon

Crohn’s: Mouth to anus with skip lesions, ileum most common

227
Q

Symptoms of IBD?

A

Ulcerative: left pain with blood diarrhea

Crohn’s: right pain, non bloody diarrhea

228
Q

Inflammation in IBD?

A

Ulcerative: Crypt abscesses with neuts

Crohn’s: Lymphoid aggregates with granulomas

229
Q

Gross appearance of IBD?

A

Ulcerative: Pseudopolyps, loss of haustra, lead pipe

Crohn’s: Cobblestone mucosa, creeping fat, strictures, string sign

230
Q

What are crypt abscesses with neuts indicative of?

A

Ulcerative colitis

231
Q

IBD complications?

A

Ulcerative: toxic megacolon, carcinoma

Crohn’s: Malabsorption, calcium ox stones

232
Q

What is smoking protective against?

A

Ulcerative colitis

233
Q

When is P-anca seen in stomach?

A
  1. Ulcerative colitis
  2. Churg strauss
  3. Microscopic polyangiitis
234
Q

What is hirschsprung? Association?

A
  • Defective relaxation and peristalsis of rectum and distal sigmoid
  • Congenital failure of ganglion cells to descend
  • Associated with Downs
235
Q

Presentation of Hirschsprung?

A
  1. Failure to pass meconium
  2. Empty rectum on DRE
  3. Bowel dilation
  4. Rectal suction with lack of ganglion cells
236
Q

What are colonic diverticula?

A
  • Outpouching of mucosa and submucosa through muscular layer
  • Caused by increased wall stress usually occurring where vasa recta cross
237
Q

Complications of diverticula?

A
  1. BRBPR
  2. Fistula
  3. Diverticulitis
238
Q

What is angiodysplasia?

A
  • Acquired malformation of mucosal / submucosal capillary beds
  • Usually in right colon and cecum due to high wall tension
  • Presents as hematochezia
239
Q

What do high stress in left and right colon caus?

A

Both present with hematochezia
Left: Diverticula
Right: angiodysplasia

240
Q

What is hereditary hemorrhagic telangiectasia?

A
  • Genetic thin walled vessels in GI and nasopharynx
241
Q

Cause and location of ischemic colitis?

A
  • Splenic flexure due to atherosclerosis of SMA
242
Q

What is a hyperplastic polyp?

A
  • Hyperplastic glands with serrated appearance
  • Left colon
  • Benign with no malignant potential
243
Q

What is serrated appearance indicative of?

A

Hyperplastic polyp - benign left colon

244
Q

What is adenoma carcinoma pathway?

A
  1. APC mutation = polyp (tumor suppressor)
  2. KRAS
  3. a P53 mutation
  4. b increased COX expression
245
Q

What protects against gastric adenocarcinoma?

A

Aspirin - COX is part of pathway and aspirin inhibits this

246
Q

What are sessile and pedunculated polyps and risk?

A

Sessile: flat growth, higher risk
Pedunculated: like mushroom

247
Q

Histology in adenocarcinoma and risk?

A

Villous: high risk (villous = villain)
Tubular: low risk

248
Q

What is FAP?

A

“Familial adenomatous polyposis”

  • Inherited APC mutation on chromosome 5
  • 1000s of colonic polyps
  • Prophylactic colon resection
249
Q

What is gardner syndrome?

A
  1. FAP
  2. Osteomas
  3. Fibromatosis
250
Q

What is turcott syndrome?

A
  1. FAB
  2. Glial tumors
  3. Meduloblastomas
251
Q

What is peutz jeghers syndrome?

A
  1. Hamartomatous GI polyps
  2. Mutocutasenous hyperpigment on lips, oral, genitals
  3. Increased risk for many cancers
252
Q

What is MSI pathway?

A

“Microsatellite instability pathway”

- Instability seen in DNA replication that can lead to cancer

253
Q

What is HNPCC?

A

“Hereditary non polyposis colorectal carcinoma”

  • Inherited mutations in DNA repair
  • Carcinomas arise de novo
254
Q

Presentation of left sided GI carcinoma?

A

“Napkin ring lesion”

  • Decreased tool caliber
  • LLQ pain
  • Blood in stool
  • *Adenoma carcinoma sequence
255
Q

Right sided GI carcinoma presentation?

A

“Raised lesion”

  • Fe deficiency anemia
  • Microsatellite sequence
256
Q

WHat is CEA tumor marker for?

A

Progress / response of colon cancer

257
Q

What is finely granular, large, hepatocytes with pale pink cytoplasm indicative of?

A

HBV

258
Q

What does ventral pancreatic bud become?

A
  1. Main pancreatic duct

2. Uncinate process

259
Q

What is adenosine demainase deficiency seen in?

A

SCID: Both B and T cell deficiency

260
Q

What is deficient in SCID?

A

Adenosine deaminase

261
Q

What cholesterol, bile salt, and phosphatidylcholine levels lead to gallstones?

A

Cholesterol: high
Bile salts: low
Phosphatidylcholine: low

262
Q

Difference in cause of proximal and distal duodenal atresia?

A

Proximal: failure of recanalization
Distal: Vascular occlusion in utero

263
Q

What does IL8 do?

A
  • Attracts neuts and induces phagocytosis
264
Q

What does C3a/C5a do?

A

C3: recruits eos/basos
C5: recruits neuts

265
Q

What does IL3 do?

A

Bone marrow stimulation and growth

266
Q

What does IL10 do?

A

Antiinflammatory from macs and TH2

267
Q

Landmark for appendix?

A

Taenia coli

268
Q

Risk of high triglycerides?

A

Acute pancreatitis

269
Q

2 most common causes of acute pancreatitis?

A
  1. Booze

2. Gallstones

270
Q

How does staph cause food poisoning?

A

Preformed exotoxin

271
Q

How does C diff toxin work?

A

Toxin A/enterotoxin:
Toxin B/cytotoxin:
* both enter cell and disregulated cytoskeletal stability

272
Q

Strongyloides appearance in stool?

A

Rhabidiform larvae

273
Q

Vein in gastric varices?

A

Short gastric / splenic

274
Q

What bleeds in perforation of posterior duodenum?

A

Gastroduodenal artery

275
Q

What is seen in cholera diarrhea?

A

Flecks of mucus and, sloughed epithelial cells, no leukocytes

276
Q

Most common cancer in liver?

A

Metastasis

277
Q

Chrons hypothesis?

A

TH1 overactivity

278
Q

What acid base abnormality does vomit lead to?

A

Metabolic alkalosis

279
Q

What does exocrine pancreas do?

A

Digestive enzymes

280
Q

Etiology of acute pancreatitis?

A
  • Premature activation of trypsin causing other enzymes to be activated and causing autodigestion of pancreatic parenchyma
281
Q

Appearance of prancreas in acute pancreatitis?

A
  1. Liquefactive necrosis
  2. Extensive hemorrhage
  3. Fat necrosis and saponification
282
Q

2 most common causes acute pancreatitis?

A
  1. Alcohol - contracts spincter of oddi
  2. Gallstones
  3. Trauma
  4. Hypercalcemia
  5. Hyperlipidemia
  6. Drugs
  7. Scorpions
  8. Mumps
  9. Posteriors duodenal ulcer - head of pancreas sits here
283
Q

Presentation of acute pancreatitis?

A
  1. Epigastric abdominal pain radiating to back
  2. Nausea / vomit
  3. HYPOcalcemia
  4. Elevated amylase and lipase
  5. Periumbilical and flank hemorrhage
284
Q

2 things that could cause increased amylase?

A
  1. Pancreatitis

2. Damage to salivary gland

285
Q

Complications of pancreatitis?

A
  1. Shock
  2. Pancreatic pseudocyst
  3. Abscess
  4. DIC - enzymes eat coag factors
  5. ARDS - enzymes eat alveolar lining
286
Q

What is pancreatic pseudocyst?

A
  • Seen in acute pancreatitis
  • Fibrous tissue surrounding areas of necrosis and pancreatic enzymes to wall them off
  • Presents with:
    1. Abdominal mass
    2. Persistence of amylase enzyme
    3. Rupture
287
Q

Causes of acute pancreatitis?

A
  1. CF: kids

2. Booze

288
Q

Signs of pancreatic insufficiency / chronic pancreatitis?

A
  1. Malabsorption
  2. Steatorrhea
  3. Fat soluble vitamin deficiencies
  4. TIIDM
  5. Calcification
    * *Amylase and lipase not elevated as pancreas is destroyed
289
Q

What does pancreatic carcinoma arise from?

A

Ducts

290
Q

Risks for pancreatic carcinoma?

A
  1. Smoking

2. Chronic pancreatitis

291
Q

Signs of pancreatic carcinoma based on location?

A 
Head:
1. Obstructive jaundice
2. Pale stools
3. Palpable gall bladder 
Body / Tail:
1. Secondary diabetes
292
Q

Serum tumor marker for pancreatic cancer?

A

Ca - 199

293
Q

What is ca 199 tumor marker for?

A

Pancreatic carcinoma

294
Q

Cause of biliary atresia?

A

Failure to form extrahepatic bile ducts

295
Q

Presentation of biliary atresia?

A
  1. Biliary obstruction
296
Q

Increase / decrease in what can cause cholelithiasis?

A 
Increased:
1. Bilirubin
2. Cholesterol 
Decreased:
1. Phospholipids (lecithin) (helps solubilize cholesterol)
2. Bile acids
297
Q

2 types of gallstones?

A
  1. Cholesterol stones

2. Bilirubin stones

298
Q

What is cholestyramine?

A
  • Lipid lowering agent that binds bile acids

- Increases risk for gallstones because of this

299
Q

How does stasis cause bili gallstones?

A
  1. Allows bacteria to flourish
  2. Bacterio unconjugated bili
  3. Deconjugated is not soluble = stones
300
Q

Cholesterol stones radiolucent or opaque? Bilirubin?

A

Cholesterol: Lucent
Bilirubin: Opaque

301
Q

Risk for cholesterol stones?

A
  1. Age
  2. Estrogen - Increases HMG CoA reductase
    - Increases cholesterol uptake in hepatocytes via more receptor expression
  3. Cirrhosis
  4. Crohn’s - damages terminal ileum - decreased bile acids
  5. Clofibrate
302
Q

Risk for bili stones?

A
  1. Extravascular hemolysis - increased unconjugated bilirubin
  2. Biliary tract infection: causes deconjugation
303
Q

Breakdown path of hemoglobin

A

Broken down into:

  1. Heme: which is broken into
    a. Iron (recycled)
    b. Protoporphyrin: becomes unconjugated bili (UCB)
  2. Globin
    - Broken into AAs which are recycled
304
Q

Complications of gallstones?

A
  1. Biliary colic
  2. Cholecystitis
  3. Ascending cholangitis
  4. Gallstone ileus
  5. Gallbladder cancer
305
Q

What is biliary colic?

A
  • Waxing / waning RUQ pain from gallbladder contraction against stone in cystic duct
306
Q

Acute cholecystitis presentation?

A
  1. RUQ pain radiating to right shoulder
  2. Fever / elevated WBC
  3. Increased alkaline phosphatase
307
Q

What is porcelain gallbladder complication of?

A

Chronic cholecystitis

308
Q

What is RUQ pain after eating indicative of?

A

Acute cholecystitis: bladder is trying to contract to release bile

309
Q

Cause of jaundice?

A

Serum bili >2.5

310
Q

What is urobilinogen?

A
  • Enteric flora in GI act on conjugated bilirubin when released in bowel
  • Makes poo brown / pee yellow
311
Q

Why does ineffective erythropoiesis cause jaundice?

A

Macs are destroying poorly made RBCs

312
Q

Do hemolysis and ineffective erythropoiesis case elevated conjugated or unconjugated?

A
  • Unconjugated as system is overwhelmed
313
Q

Whats happening in physiologic jaundice of newborn?

A
  • Baby has deficiency conjugating due to low UGT
314
Q

What is kernicterus?

A
  • UCB is fat soluble so can deposit in basal ganglia if too much seen in baby
  • Causes neurologic deficits and death
315
Q

What does phototherapy do?

A

Makes UCB water soluble: ISNOT conjugating

316
Q

What is gilberts?

A
  • Genetically low UGT = increased UCB during stress

- Normally not clinically significant

317
Q

Two spectrums of decreased UGT in adults?

A
  1. Gilberts: mild

2. Crigler: severe

318
Q

What is Crigler Najar?

A
  • Absent UGT
  • High UCB
  • Kernicterus and death
319
Q

What is Dubin Johnson?

A

Dubin “think dubin = dumpin” problem with dumbing bili

  • Deficiency in canalicular bili transport protein
  • Increase in CB as conjugating system is fine
  • Liver is pitch dark
320
Q

What is pitch dark liver indicative of?

A

Dubin Johnson syndrome: think that it’s getting dark from all the bile that is accumulating in there

321
Q

What is rotor syndrome?

A

Same as dubin Johnson but lacks black liver

322
Q

Signs of obstructive jaundice?

A
  1. Jaundice
  2. Pruritis: bile acids leak and deposit in skin
  3. Xanthomas / HYPERcholesterolemia: cholesterol is leaking from bile
  4. Pale stool as bile cant get in bowel
  5. Steatorrhea
  6. Deficient fat soluble vitamins
  7. Dark urine: CB is water soluble
323
Q

Break out of bili in hepatitis?

A
  • Both UCB and CB as both hepatocytes and ducts are being damaged
324
Q

3 causes viral hepatic?

A
  1. Hepatitis virus
  2. CMV
  3. EBV
325
Q

Presentation of acute hepatitis?

A
  1. Mixed jaundice
  2. Dark urine
  3. ALT > AST
326
Q

Where is inflammation in Acute / chronic hepatitis?

A 
Acute:
1. Within portal tracts
2. Between hepatocytes 
Chronic:
1. Portal tracts
327
Q

Mechanism of hepatocyte destruction in hepatitis?

A
  • Viral antigens presented in MHCI

- CD8 cells perform killing

328
Q

Routes of HAV, HEV? What is chronic state like?

A

HAV: fecal oral, travelers
HEV: fecal oral, contaminated water
*No chronic state seen

329
Q

HEV in pregnancy?

A

Fulminant hepatitis with liver failure / necrosis

330
Q

Which acute hepatitis has vaccine?

A

HAV

331
Q

First serum marker to rise in acute HBV?

A

HBsAg

  • If > 6 months = chronic
  • Gone if infection is resolved
332
Q

Marker of acute HBV battle?

A

IgM vs. core antigen

*If IgG, chronic

333
Q

How to tell if resolved chronic HBV or immunized?

A

Resolved: IgG vs. core and surface
Vax: only surface IgG

334
Q

What indicates HBV infectivity?

A

Envelop antigen

335
Q

How to tell if HCV infx?

A

Viral RNA

336
Q

HDV?

A

Only can occur if infected with HBV

  • Acquire at later time: coinfection, less sever
  • Acquire at same time: super inx, very severe
337
Q

Histo in cirrhosis?

A
  • Disruption of parenchyma by broad bands of cirrhosis and regenerative nodules of hepatocytes
338
Q

What mediates fibrosis in cirrhosis?

A
  • TGF-beta from stellate cells

- Lies below endothelial cells that line sinusoids

339
Q

Funny things that happens in splenomegaly?

A

Hypersplenism: consumes RBCs and platelets

340
Q

Why does cirrhosis cause hyperestrinism and what are results?

A
  • Liver is normally removing estrogen from blood:
    1. Gynecomastia
    2. Spider angioma
    3. Palmar erythema
341
Q

Protein impacts of cirrhosis?

A
  1. HYPOalbuminemia
  2. Coagulopathy: decreased clotting factors
    - Can no longer activate vitamin K
    * *Increased PT AND PTT
342
Q

Is fatty liver reversible?

A

Yes

343
Q

What mediates damage in alcoholic hepatitis?

A

Acetaldehyde

344
Q

Presentation of alcoholic hepatitis?

A
  1. Swelling / ballooning of hepatocytes
  2. Necrosis and acute inflammation
  3. Mallory bodies: damaged intermediate filaments in hepatocytes
345
Q

What are mallory bodies indicative of?

A

Alcoholic hepatitis: from damaged intermediate filaments in hepatocytes

346
Q

What is AST > ALT in alcoholic hepatitis?

A
  • Acetaldehyde is mitochondrial poison

- AST is located in mitochondria

347
Q

What is hemochromatosis / siderosis?

A

Hemochromatosis: excess Fe in body
Siderosis: deposition in tissues
*Damage is being caused by free radical deposition

348
Q

Gi handling of Fe?

A
  • Enterocytes take up and store Fe

- Only passes to blood if body says its needed

349
Q

What happens in primary hemochromatosis?

A
  • No regulation of Fe moving from enterocytes to blood

- Excess Fe now is deposited in tissues

350
Q

Mutation in primary hemochromatosis?

A

HFE gene / C282Y

351
Q

Cuase of secondary hemochromatosis?

A

Transfusions: body has no way to get rid of Fe

352
Q

Presentation of hemochromatosis?

A
  1. Bronze skin
  2. Cirrhosis
  3. Secondary diabetes
  4. Arrhythmia
  5. Gonadal dysfunction
353
Q

Lab values in hemochromatosis?

A

Ferritin: increased
TIBC: decreased
Serum Fe: increased
% Saturation: increased

354
Q

Diagnosis of hemochromatosis?

A
  • Liver biopsy showing brown pigment turning blue on prussian stain
  • If does not turn blue, it is lipofuscin from normal damage
355
Q

Defect in wilson’s? What does it cause?

A
  • ATP7B gene involved in ATP mediated hepatocyte copper transport
    1. Decrease Cu secretion in bile
    2. Decreased Cu incorporation in ceruloplasmin
356
Q

What is ceruloplasmin?

A
  • Molecule that carries copper in blood

- Cannot integrate copper in wilson’s disease

357
Q

Presentation of wilson’s?

A

Presents in childhood:

  1. Variety of neurologic symptoms
  2. Kayser fleischer rings in cornea
  3. Hepatocellular carcinoma
358
Q

What are kayser fleischer rings seen in?

A

Wilsons

359
Q

Treatment of wilson’s disease?

A

D-penicillamine: copper chelator

360
Q

What is decreased serum ceruloplasmin seen in?

A

Wilson’s

361
Q

What is primary biliary cirrhosis?

A
  • Autoimmune, granulomatous destruction of intrahepatic bile ducts
  • Antimitochondrial Ig is diagnostic
362
Q

What is autoimmune, granulomatous destruction of intrahepatic bile ducts?

A
  • Primary biliary cirrhosis
363
Q

What is antimitochondrial Ig diagnostic of?

A

Primary biliary cirrhosis

364
Q

Presentation of primary biliary cirrhosis?

A
  1. Obstructive jaundice

2. Liver cirrhosis

365
Q

What is primary sclerosing cholangitis?

A

“Periductal fibrosis with onion skinning”

  • Inflammation / fibrosis of intra/extrahepatic bile ducts
  • Uninvolved areas are dilated = beaded appearance on imaging
  • P-ANCA positive
  • Causes conjugated jaundice
  • Seen in ulcerative colitis
366
Q

What is the following indicative of:

“Periductal fibrosis with onion skinning”

A

Primary sclerosing cholangitis

367
Q

Associations of Primary sclerosing cholangitis

A

Ulcerative colitis

- p-ANCA

368
Q

What is Reye syndrome?

A
  • Fulminant hepatitis in child who takes aspirin with viral illness
  • Likely due to mitochondrial damage
369
Q

Reye presentation?

A
  1. Nausea / vomit
  2. Elevated liver enzymes
  3. HYPOglycemia
  4. Coma / death
370
Q

Causation of hepatic adenoma?

A
  • Oral contraceptive use: resolves on cessation `

- Risk of rupture in pregnancy which E2 is high

371
Q

What is aflatoxin risk for?

A

Hepatocellular carcinoma

- Induces P 53 mutations

372
Q

What is budd chiari?

A
  • Thrombosis of hepatic vein often from tumor invasion

- Ascites and painful hepatomegaly seen

373
Q

Tumor marker for hepatocellular carcinoma?

A

AFP

374
Q

What is AFP tumor marker for?

A

Hepatocellular carcinoma

375
Q

What CN moves through parotid gland?

A

VII: as such tumor in parotid can = facial pain, paralysis

376
Q

Another name for achalasia?

A

Megaesophagus: from chagas

377
Q

2 instances in which eosinophils are seen?

A
  1. Allergies

2. Parasitic infections

378
Q

When is trachealization of esophagus seen?

A

Eosinophilic esophagitis

379
Q

Medication causing esophagitis?

A

Bisphosphonates

380
Q

Difference in HSV and CMV esophageal ulcers?

A

CMV: linear
HSV: punched out

381
Q

Cancer risk in H pylori?

A

MALT lymphoma

382
Q

What is menetrier disease?

A

Gastric hypertrophy associated with:

  1. Increased mucus cells
  2. Parietal atrophy
  3. Protein loss
    * *Rugae are so hypertrophic they look like rain
383
Q

What to suspect if ulcers seen further down SI than in duodenum?

A

ZE syndrome

384
Q

When is hypertrophy of brunner’s glands seen?

A

Duodenal ulcers

385
Q

Blood supply to lesser curvature of stomach?

A

Left gastric

386
Q

Blood supply to greater curvature of stomach?

A

Gastroepiploic artery

387
Q

Blood supply to duodenum?

A

Gastroduodenal artery: rungs along posterior

388
Q

What does sudan B stain test for?

A

Fat in stool

389
Q

D xylose test in celiacs?

A

Decreased as BB enzymes are destroyed so can’t absorb as much

390
Q

What does lactose break into?

A

Glucose and galactose

391
Q

Hydrogen breath test relevance in lactose intolerance?

A

Large rise in these patients post lactose as they colonic bacteria ferment lactose making H and they cannot break it down

392
Q

Folate or B12 show neuro symptoms?

A

B12

393
Q

When is string sign seen?

A

Crohn’s

394
Q

When is cobblestone mucosa seen?

A

Crohn’s

395
Q

What are the extra intestinal manifestations of IBD?

A
  1. Pyoderma gangrenosum: rash
  2. Uveitis
  3. Erythema nodosum
  4. Oral ulcers
  5. Arthritis
  6. Ca / ox stones: Crohns
396
Q

Where is mcburneys point?

A

1/3 way between anterior superior iliac spine and umbilicus

- Appendicitis pain often presents here

397
Q

Tissue often found in meckel diverticulum?

A
  1. Gastric

2. Pancreatic

398
Q

Diagnosis of Meckel’s

A

Pertechnetate study

- Molecules are taken up by the ectopic parietal cells in the diverticulum

399
Q

What does pertechnetate study diagnose?

A

Meckel’s

- Molecules are taken up by the ectopic parietal cells in diverticulum

400
Q

Hirschsprung presentation?

A
  1. No stools
  2. Bilious vomit
  3. Distended abdomen
    * *Often seen in down’s syndrome
401
Q

What is ileus? Causes?

A

HYPOmotility of bowel

  1. Opiates
  2. HYPOkalemia
  3. Post opp
402
Q

When is meconium ileus seen?

A

CF

403
Q

“CLAX TPAG” mnemonic?

A 
Syndrome:
Cockayne
Lynch 
Ataxia Telangiectasia
Xeroderma Pigmentosum
Mutation:
Transcription coupled nucleotide excision repair
Post replicative repair 
ATM gene defect 
Genome wide repair
404
Q

What is lynch syndrome?

A

aka “HNPCC”

  • Defect in Post replicative mismatch repair
  • Due to methylation of MHS1, 2, or 6
  • Leads to colorectal carcinoma of right colon
405
Q

Other cancers seen in lynch?

A
  1. Endometrial
  2. Skin
  3. Ovarian
406
Q

Colorectal polyp that does not have risk for cancer?

A

Hyperplastic

407
Q

2 disease processes with increased alkaline phosphatase?

A
  1. Biliary obstruction
  2. Bone disease
    * ***Use GGT to distinguish as is specific to alcoholic liver
408
Q

Which zone at risk for alcoholic liver?

A

Zone III

409
Q

What is a non smoker with panacinar emphysema and PAS+ liver lobules indicative of?

A

A1-antitrypsin deficiency

410
Q

Type I or II crigler more serious?

A

Type I

411
Q

Why is liver black in Dubin Johnson?

A

Buildup of epinephrine metabolites

412
Q

Risks for cholesterol stones?

A
  1. Obesity
  2. Crohns
  3. Weight loss
  4. 4 Fs: fat, female, fertile, forty `
413
Q

What is courvoisier sign?

A
  1. Palpable non tender gallbladder
  2. Obstructive jaundice
  3. Cancer of pancreatic head
414
Q

What does prazole ending indicate?

A

PPIs

415
Q

What kills cells with decreased or absent MHC I?

A

Natural killers

416
Q

What makes up walls of pancreatic pseudocyst?

A

Fibrous tissue, granulation tissue, ABSENCE of epithelial cells

417
Q

What can’t liver to with ammonia in cirrhosis?

A

Convert it to urea

418
Q

Where are fats digest and absorbed?

A

Digested: duodenum
Absorbed: jejunum

419
Q

Where do most anal fissures occur?

A

Posterior, distal to dentate

420
Q

Another name for B12?

A

Cobalamin

421
Q

What could cancer in 3rd part of duodenum compress?

A

SMA

422
Q

Where in duodenum is ampulla and odi?

A

2nd part

423
Q

Where would air be seen in gallstone ileus?

A
  1. Biliary tree

2. SI

424
Q

Presentation of VIPoma?

A
  1. Secretory / watery diarrhea
  2. Achlorhydria
  3. HYPOkalemia
425
Q

Lymphatic drainage proximal and distal to dentate?

A

Proximal: internal iliac and IMA
Distal: inguinal nodes

426
Q

How does HBV replicate?

A
  1. DSDNA
  2. SSRNA
  3. DSDNA
427
Q

What is CREST?

A 
Calcinosis 
Raynauds
Esophageal dysmotility 
Sclerodactyly 
Telangiectasias
428
Q

What is IV bioavailability?

A

100% normally

429
Q

Equation for oral bioavailability?

A

AUC oral dose / AUC IV dose

430
Q

What vitamins do enteric bacteria make?

A
  1. K

2. Folate

431
Q

Where is stomach attached in GI bypass?

A

Jejunum

432
Q

What is SI intestine with large PAS foamy macs indicative of?

A

Whipple

433
Q

Bodies protection form Giardia?

A

Iga and CD4+ helpers

434
Q

Where can splenic pain refer to?

A

Shoulder

435
Q

What can cause hiccups?

A

Phrenic nerve irritation leading to spasm of diaphragm

436
Q

What causes secretin to be released?

A

Duodenal H

437
Q

What is CA 125 marker for? 199?

A

125: ovarian
199: pancreatic

438
Q

Signs of carcinoid syndrome?

A
  1. Watery diarrhea
  2. Flushing
  3. Bronchospasm
  4. Right sided valvular plaques
439
Q

Treatment for carcinoid?

A

Octreotide: somatostatin analog

**Also works in VIPomas

440
Q

How is secretin used diagnostically?

A

Normal: decrease gastrin and increases bicarb
ZE: Increases gastrin

USMLE: step 1 (15 decks)

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