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GI/Liver > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

does esophagus have serosa?

A

upper esophagus = no serosa

lower esophagus = serosa (intraperitoneal)

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2
Q

oral mucosa histological characteristics/layers

A
  1. stratefied squamous unkeratinized/lightly keratinized epithelium
  2. underlying CT - lamina propria with BVs
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3
Q

saliva contents (4)

A
  1. secretory IgAs
  2. beta defensins from epithelial cells (antibacterial)
  3. amylases
  4. lysosyme
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4
Q

tongue histology features (5)

A
  1. strategied squamous unkeratinized/slightly keratinized
  2. papillae (mostly filiform, some fungiform, few circumvallate papillae at root of tongue with taste puds, foliate papillae on lateral surface with taste buds and serous glands)
  3. lots of skeletal muscle (intrinsic and extrinsic)
  4. minor salivary glands (mixed or either or, associated with folate and circumvalate)
  5. lingual lymph nodes (GALT)
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5
Q

difference between the nuclei of supportive and sensory cells in taste buds

A

sensory have rounder, lighter stained nuclei,

supportive have darker and more elongated nuclei

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6
Q

what tastes can you detect

A 
sugar
salt
bitter
sour
umami
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7
Q

are sensory cells attached to myelnated or unmyelinated nerve fibers

A

myelinated

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8
Q

minor salivary glands are where

A

all over oral cavity

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9
Q

what are major salivary glands (what are they made of)

A
  1. parotid (mostly serous - amylase, proteinaceous)
  2. submandibular (mix of serous and mucous)
  3. sublingual (mostly mucous acini)
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10
Q

mucous vs serous characteristics

A

mucous is lighter than serous

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11
Q

ducts

A

intercalated to striated to interlobular and main excretory

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12
Q

what makes enamel

A

ameloblasts

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13
Q

what is deep to enamel

A

dentil, which is vital, innervated, and bone-like

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14
Q

what secretes dentin

A

odontoblasts. odontoblasts processes radiate throughout dentin in dentinal tubules, like osteocyte processes in canaliculi of bone

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15
Q

how many teeth to children have

A

20 primary teeth

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16
Q

which teeth are lost first to last

A
  1. central incisors
  2. lateral incisors
  3. first molar
  4. canine
  5. second molars
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17
Q

how many teeth do adult have

A

32

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18
Q

tooth development stages

A
  1. ectoderm thickens as dental lamina

2. invaginates due to inducement of NCC mesenchyme called dental pipilla

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19
Q

what do NCC develop in teeth

A

odontoblasts (dentin) and pulp of tooth

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20
Q

what does ectoderm form in teeth

A

ameloblasts (enamel)

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21
Q

oropharynx histologic characteristics (4)

A
  1. SS uK epithelium
  2. lamina propria
  3. submucosa with lymphoid follicles
  4. skeletal muscle in walls
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22
Q

how long is the human GI tract

A

30 feet

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23
Q

myenteric is associated with what layer

A

muscular

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24
Q

auerbach is associated iwth what layer

A

muscular - myenteric = auerbach

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25
Q

meissner’s plexus is associated iwith what layer

A

submucosal

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26
Q

myenteric stimulation causes (4)

A

motility:
1. increases tone,
2. contraction intensity,
3. contraction rate,
4. speed of conduction)

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27
Q

submucosal stimulation causes (3)

A

secretion and absorption:

  1. integration of signals
  2. local contraction
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28
Q

what does NOT count as research (2)

A
  1. undisciplined or systematic

2. doesn’t seek to add to body of knowledge

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29
Q

tenants of nurenburg code (3)

A
  1. voluntary consent
  2. benefits outweigh risk
  3. participates can terminate at any time
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30
Q

declaration of Helsinki

A

international standard for biomedical research ethics - interest of subject must prevail over the interest of science

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31
Q

belmont principles (3)

A
  1. respect for persons
  2. beneficience
  3. justice
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32
Q

respect for persons

A

individual autonomy, protection of individuals with reduced autonomy)

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33
Q

beneficence

A

maximize benefits and minimize harms

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34
Q

justice

A

equitable distribution of research costs and benefits

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35
Q

C.A.G.E. interview

A

for alcohol dependence

  1. ever had to cut down
  2. annoyed when people tell you to quit?
  3. guilt
  4. need eye opener

for women - does it take more and more alcohol to get you drunk

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36
Q

mesolimbic circuit

A

goes from ventral tegmental to nucleus accumbens – reward circuit, mediated by dopamine and endorphins

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37
Q

alcohol’s affect on arousal and sleep circuit

A

alcohol suppresses brainstem mechanisms for rapid heart rate etc. and withdrawal can cause seizures etc - over-excitation

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38
Q

aeclaspian authority

A

tell your patients the health adverse effects

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39
Q

naltrexone

A

blocks endorphin mediated sensation of reward- reduces craving

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40
Q

topiramate

A

reduces appetitive behavior - food or drink

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41
Q

most of vagus is afferent or efferent?

A

afferent - receiving signals

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42
Q

short reflex pathway

A

entirely within enteric system causing stimulus and response (change in motility or secretion)

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43
Q

long reflex pathway

A

involve sympathetic ganglia and transmit signals to other parts - including vago-vasal pathway

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44
Q

the enteric nervous system produces most of the bodies ____ neurotransmistter

A

seratonin -95%

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45
Q

what does Ach do in GI tract (3)

A
  1. contracts SM
  2. relax sphincters
  3. increase secretion (salivary, gastric and pancreatic)
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46
Q

what does NE do in the GI tract (3)

A
  1. relax SM
  2. contract sphincter
  3. enhance salivary secretion
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47
Q

what does VIP do in the GI tract

A

relax SM

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48
Q

what does NO do in the GI tract

A

relax SM

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49
Q

What does GRP do in the GI tract

A

increase gastric secretion

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50
Q

cephalic phase of digestion

A
  1. Sight, smell, thought of food relays info to dorsal vagal complex
  2. vagovagal reflex triggers secretory and motor behavior in stomach – releases GRP (triggers G cells to release of gastrin which activates parietal and chief cells) and ACh (to inhibit somatostatin)
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51
Q

what is the stimulation for salivation (hormonal, paracrine etc.)

A

neurocrine

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52
Q

is saliva acidic or basic?

A

alkaline

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53
Q

why is bicarb secretion necessary in saliva

A

to protect from gastric acid reflux

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54
Q

what does amylase do

A

initiates startch digestion

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55
Q

what does lingual lipase do

A

picks up slack from pancreas in triglyceride digestion

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56
Q

stages of salivary secretion (2)

A
  1. acinar cells secrete isotonic primary saliva (amylase +/- mucin)
  2. ductal cells make saliva alkaline (sodium and chloride reabsorb, potassium and bicarb secrete) - low perm to water – makes saliva hypotonic
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57
Q

things that stimulate saliva secretion (4)

A
  1. conditioning (pavlov)
  2. food
  3. nausea
  4. smell
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58
Q

things that inhibit saliva secretion (4)

A
  1. dehydration
  2. fear
  3. sleep
  4. anticholinergic drugs (atropine)
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59
Q

what happens to saliva glands if you cut the vagus

A

decreased secretion (Same with cut sympathetic) but ALSO get glandular atrophy

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60
Q

what can you measure clinically in saliva? (5)

A
  1. biomarkers
  2. steroid levels (free not bound)
  3. viral infections (HIV, hepC, EBV)
  4. bacterial (H. pylori)
  5. drug levels
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61
Q

phases of swallowing

A
  1. voluntary
  2. pharyngeal (controlled by swallowing center in medulla)
  3. esophageal
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62
Q

when breathing, is UES open or closed?

A

closed

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63
Q

when swallowing, is UES open or closed?

A

open, and glottis is closed

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64
Q

4 layers of GI tract histology

A
  1. mucosa (epithelium, lamina propria, muscularis mucosae)
  2. submucosa (BVs, folds)
  3. muscularis externa (inner circular, outer longitudinal)
  4. adventitia (if retroperitoneal) serosa (if introperitoneal)
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65
Q

what in GI is derived from spanchnic mesoderm (4)

A
  1. lamina propria
  2. submucosal CT
  3. muscularis externa
  4. adventitia
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66
Q

what in gI is derived from regular mesoderm

A

lymphoid tissue - from bone marrow - GALT

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67
Q

what is the derivation for liver/pancreas parenchymal cells

A

endoderm

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68
Q

foregut is from where to where

A

buccopharyngeal membrane (stomodial) to anterior intestinal portal

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69
Q

midgut is from where to where

A

from anterior to posterior intestinal portal

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70
Q

hindgut is from where to where

A

from posterior intestinal portal to coacal memrane

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71
Q

lower foregut is supplied by what

A

celiac trunk

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72
Q

midgut is supplied by what

A

superior mesenteric artery

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73
Q

hindgut is supplied by what

A

inferior mesenteric artery

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74
Q

cranial foregut derivatives (6)

A
  1. epithelium in posterior oral cavity
  2. respiratory diverticulum
  3. auditory tube epithelium
  4. palatine tonsilar crypt epithelium
  5. parathyroid epithelium
  6. thymus epithelium
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75
Q

caudal foregut derivatives (4)

A
  1. oropharynx and esophagus epithelium
  2. stomach epithelium
  3. first part of duodenum epithelium
  4. liver, pancreas, gall bladder and duct epithelium
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76
Q

midgut derivatives (5)

A
  1. second part of duodenum
  2. ileum and jejunum
  3. cecum and vermiform appendix
  4. ascending colon
  5. transverse colon to approximate middle
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77
Q

hindgut derivatives (5)

A
  1. second half of transverse colon
  2. descending colon
  3. sigmoid colon
  4. rectum
  5. anal canal to anal valves (pectinate line)
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78
Q

gastric rotations

A
  1. first, rotates dorsal to ventral and elongates over to form greater omentum
  2. second rotation brings cardiac portion inferiorly to the left, and pyloric superiorly and to the right
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79
Q

septum transversum and liver

A

liver diverticulum grows into septum transversum mesoderm and branches, but remains connected

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80
Q

what is the rotation of the midgut and what’s the axis of rotation

A

270 degrees counter clockwise

axis of rotation is formed by vitelline duct and superior mesenteric artery

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81
Q

secondarily retroperitoneal

A

becomes plastered to body wall

  1. pancreas
  2. part of duodenum
  3. ascending colon
  4. descending colon
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82
Q

do you have sensation above pectinate line?

A

no

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83
Q

where would a carcinoma above the pectinate line drain into

A

inferior mesenteric nodes

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84
Q

where would a carcinoma below the pectinate line drain into

A

superficial inguinal nodes

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85
Q

epithelial changes at pectinate line

A

simple columnar to stratefied squamous unkeratinized

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86
Q

pyloric stenosis cause (2)

A

congenital defect - due to hypertrophy of pyloric sphincter

also early exposure to erythromycin

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87
Q

clinical finding of pyloric stenosis

A

projectile vomiting in newborns - curdled milk (no bile)

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88
Q

pyloric stenosis treatment (2)

A

reducing muscular layers and with atropine

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89
Q

ileal diverticulum incidence

A

most common congenintal GI defect 2%

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90
Q

ileal diverticulum description

A

remnant of vitelline duct, finger like projection toward end of midgut - ileum

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91
Q

clinical presentation of ileal diverticulum

A

often astymptomatic, but if it contains atopic gastric or pancreatic tissue, you will get ulceration

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92
Q

omphalocele description

A

defect in anterior abdominal wall covered by peritoneum and amnionic sac - failed retreat of midgut loop

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93
Q

gastrochisis

A

raw exposed bowel loops - can disinguish in utero from omphalocele via sonogram

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94
Q

congenital megacolon

A

neural crest cells don’t populate a certain area of the colon (aganglionic segment), resulting in no myenteric plexus and poor motility

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95
Q

parietal cells secrete

A

hydrochloric acid

gastric intrinsic factor (for B12)

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96
Q

what do chief cells secrete

A

pepsinogen

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97
Q

where do you find villi

A

only small intestine

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98
Q

where do you find crypts

A

in stomach, small and large intestines

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99
Q

histological characteristics of esophagus from epithelium to muscularis externa (5)

A
  1. stratefied sqamous unkeratinized epithelium
  2. submucosal folds
  3. submucosal mucous glands
  4. muscularis mucosae
  5. thick inner circular and outer long (upper third skeletal, middle mixed, lower smooth)
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100
Q

barret esophagus

A

reflux of gastric contents causes changes of esophageal epithelium to look more like small intestinal epithelium - metaplasia. can then undergo malignant hyperplasia

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101
Q

hiatal hernia

A

stomach can project up through the diagraph - end up getting chronic reflux because the sphincter doesn’t work well

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102
Q

esophageal varices

A

alcoholics

vessels get dilated and varicosed by constant irritation. have difficulty swallowing food

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103
Q

general stomach histological layers from in to out (5)

A
  1. pitted - mucosal gastric pits (faveoli) NO VILLI.
  2. epithelium has many cell types
  3. rugae - transient submucusal folds
  4. muscularis externa has 2-3 poorly defined layers
  5. serosa - intraperitoneal
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104
Q

cardiac stomach specific findings (3)

A
  1. gastric pits are short
  2. only mucous cells
  3. absolute thickness is less
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105
Q

fundic/corpic stomach specific findings (5)

A
  1. much thicker
  2. pits have variety of cell types and are deeper
  3. mucous cells on surface and neck
  4. acidophilic parietal cells by neck
  5. deeper basophilic chief cells
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106
Q

pyloric stomach specific characteristics (3)

A
  1. lymphoid tissue
  2. fewer parietal and chief, more mucous cells
  3. still thick
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107
Q

where are stem cells in gastric pit

A

in the neck and isthmus

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108
Q

what makes parietal cells acidophilic?

A

mitochondria

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109
Q

what stimulates parietal cells

A

gastrin - get more boarder with proton pump

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110
Q

what starts being broken down in stomach

A

proteins and lipids

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111
Q

duodenum histological layers (5)

A
  1. villi
  2. crypts of libercuhn
  3. submucosal brunner glands (bicarb and mucous for protection)
  4. inner circular outer long muscularis external
  5. some parts secondarily retroperitoneal with adventitia, some intraperitoneal with serosa
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112
Q

what are submucosal folds in small intestine called

A

plicae ciruclaris, they all have villi on them, and the folds are permanent

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113
Q

where are lacteals and what do they do

A

in lamina propria absorb lipids

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114
Q

what do paneth cells do and where are they

A

at bases of crypts

secrete antimicrobial protesins like lysosome, defensins and immunoglobulins

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115
Q

what do paneth cells look like

A

acidophilic - bright red granules

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116
Q

what are M cells

A

epithelial cell type that are antigen presenting (like macrophages) present to lymphocytes - overlie peyer’s patches in Ileum

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117
Q

enteroendocrine cells - what do they do, what basic 2 kinds are there

A

secrete regulatory hormones - can be open (access to lumen) or closed

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118
Q

G cells - where are they

A

stomach mostly

nerve fibers reselase Ach with distension, Ach stimulates G cells to secrete gastrin (which then activates HCl secretion from parietal cells)

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119
Q

What do D cells do

A

secrete somatostatin (which is inhibitory to secretion)

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120
Q

Zollinger Ellison Syndrome presentation

A

abdominal pain, diarrhea and fatty stool, duodenal ulcers

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121
Q

what causes Zollinger Ellison

A

tumor causing too many G cells – too much gastrin - -too much acid – mucosal ulceration in stomach

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122
Q

what to do for Zollinger Ellison

A

resection and proton pump inhibitors (omeprazole)

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123
Q

brain-gut axis and eating disorders

A

ingested tryptophan becomes serotonin

psychotropic drugs modify seratonin, which benefits binge eating, not anorexia

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124
Q

DSM5 criteria for anorexia nervosa

A
  1. significantly low body weight
  2. persistent behavior that interferes with gaining weight
  3. persistent lack of recognition of the seriousness/disturbance in one’s body image
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125
Q

examples of compensatory behavior in bulimia nervosa (4)

A
  1. fasting
  2. vomiting
  3. laxatives
  4. exercise
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126
Q

DSM5 criteria for bulemia nervosa

A
  1. recurrent episodes of binge eating - lack of control
  2. compensatory behavior
  3. binge-purge cycle at least once a week for 3 months
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127
Q

DSM5 criteria for binge eating

A
  1. large amounts over short time (2 hours)

2. 1x/week

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128
Q

SCOFF screenint

A
  1. do you make yourself Sick because you’re so full
  2. do you worry you have lost Control
  3. have you lost more than One stone (14lbs) in past 3 months
  4. do you believe yourself to be Fat when others believe you are thin
  5. would you say Food dominates your life
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129
Q

demographic for avoidant

restrictive food intake disorder

A

children mostly

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130
Q

approved medication for bulemia nervosa

A

fluoxetine (prozac)

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131
Q

intestinal feedback with stomach (3)

A
  1. positive feedback via gastrin released by duodenal mucosa
  2. negative feedback of acid secretion via vagally mediated secretin release from S cells
  3. negative feedback of gastrin release via paracrine mediated somatostatin release from D cells
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132
Q

how fast is duodenal pacemaker

A

12 slow waves per minute

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133
Q

how fast is ileal pacemaker

A

8 slow wakes per minute

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134
Q

orad vs aborad

A

orad is closer to mouth

aborad is further from mouth

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135
Q

NO, Ach and VIP - what causes contraction and relaxation of LES

A

Ach = contraction

VIP and NO = relaxation

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136
Q

Achalasia

A

inability of LES to relax - issue with enteric nervous system

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137
Q

examples of drugs that cause relaxation of LES tone (3)

A
  1. nitroglycerine
  2. beta blockers
  3. calcium channel blockers
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138
Q

what sets BER

A

pacemaker cells in stomach - interstitial cells of Cajal

waves of membrane potential propagated by Na/K movement

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139
Q

action potentials in gut motility driven by what ion

A

calcium influx (somewhat sodium too)

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140
Q

motility during fasting

A

MMC (migrating motor complex)

- housekeeping function - cleans out gut

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141
Q

phases of MMC

A
  1. quiescent
  2. intermittent motor activity
  3. repetitive contractions (lasts 5 min)
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142
Q

what hormone dictates MMC

A

motilin

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143
Q

where is the majority of fluid absorbed in GI tract

A

small intestine

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144
Q

is mucus acidic or basic

A

basic

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145
Q

cephalic phase accounts for what percent of gastric secretion with meal

A

30%

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146
Q

which part of stomach grinds food

A

antrum

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147
Q

what does acid environment of stomach do enzymatically

A

enables activation of pepsinogen to pepsin, which in turn begins protein digestion and co-secretes lipase

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148
Q

what happens when food enters duodenum (2)

A
  1. stretch receptors send local feedback to fundus to further relax via NO and VIP
  2. CCK feeds back to dorsal vagal center to further relax proximal stomach
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149
Q

when does pyloric sphincter open, and how much does it open

A

opens with secondary contractions in stomach, and allows for particles smaller than 1mm to exit stomach

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150
Q

where in stomach are G cells located

A

antrum

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151
Q

where in stomach are parietal cells located

A

fundus

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152
Q

where in stomach are chief cells lcoated

A

fundus

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153
Q

where in stomach are D cells located

A

antrum

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154
Q

where in stomach are ECL cells located

A

fundus

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155
Q

where are oxyntic glands

A

body/fundus

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156
Q

what triggers gastrin release (3)

A
  1. stretch
  2. vagus
  3. products of digestion - peptides amino acids
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157
Q

what triggers somatostatin release

A
  1. H+
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158
Q

at what pH is pepsinogen cleaved

A

less than 3.5

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159
Q

GRP

A

releases gastrin into bloodstream in atrum in G cell, which acts back on parietal cell

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160
Q

what does ECL cell produce

A

histamine

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161
Q

what does Ach bind to in stomach (2)

A
  1. parietal cells

2. ECL cells

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162
Q

what substances are involved in relaxation of stomach

A

Ach
NO
VIP
CCK

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163
Q

what substances trigger parietal cells to be activated

A

Ach
Histamine
Gastrin

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164
Q

alkaline tide

A

every proton pumped into lumen means a bicarb into bloodstream

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165
Q

which empties faster, carbs or fat

A

carbs

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166
Q

ileal brake

A

fat in ileum causes relaxation in stomach - slows down

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167
Q

gastrocolic reflex

A

induces need to defecate shortly after meal

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168
Q

gastroileal reflex

A

allows ileocecal valve to relax in response to gastric distention

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169
Q

what stimulates pancreatic secretion

A

Ach
CCK (stim by prot/fat)
Secretin (stim by acid)

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170
Q

what substances regulate ileal brake? (2)

A

peptide YY

GLP-1

171
Q

what is the jejunum responsible for *2)

A

net absorption of bicarb and water

172
Q

what is the ileum responsible for (3)

A

net absorption of NaCl, vitamin B12 and bile salts

173
Q

what stimulates secretin secretion

A
  • H+ in duodenum

- fatty acids

174
Q

what does secretin do (4)

A

stimulates pancreatic secretion of bicarb

increases intestinal secretion of mucus and bicarb

increases hepatic secretion of bicarb and bile

inhibits gastric sercretion of acid

175
Q

what stimulates CKK (2)

A
  • fatty acids

- amino acids

176
Q

what does CKK do (4)

A

increase pancreatic secretions

stims gallbladder to contract, relaxes sphincter of Oddi

inhibits gastric emptying

can potentiate the effect of secretin

177
Q

Ach relationship with CKK and secretin

A

augments effects

178
Q

when is GIP secreted

A

in response to all three types of nutrients

179
Q

what cells secrete GIP

A

K cells in duodenum and jejunum

180
Q

what does GIP cause (2)

A

stimulates insulin secretion from beta cells of pancreas

inhibits gastric hydrogen ion secretion

181
Q

Hirschsprung’s disease

A

congenital absence of myenteric plexus in distal portion of colon leading to functional obstruction and toxic megacolon

182
Q

ghrelin secreted in response to what (2)

A

starvation

weight loss

183
Q

leptin is secreted from where

A

adipose tissue

184
Q

what does leptin do

A

inhibits ghrelin

185
Q

peptide YY and CCK do what from where

A

in intestines, decrease appetite in response to nutrients

186
Q

where are carbs absorbed

A

proximal - duodenum and jejunum

187
Q

where are fats and proteins absorbed

A

all small intestine

188
Q

where are bile salts and vit B12 absorbed

A

terminal ileum

189
Q

where are iron and calcium absorbed

A

duodenum

190
Q

what cells secrete CCK

A

I cells

191
Q

what cells secrete secretin

A

S cells

192
Q

what part of the pancreas does CCK work on

A

acinar cells to secrete enzymes (colipase, lipase etc.)

193
Q

what part of the pancreas does secetin work on

A

ductal cells to secrete acqueous secretions like sodiumand bicarb

194
Q

what kind of saccharides (poly, di, mono) are absorbed

A

mono only (glucose, galactose and fructose)

195
Q

what parts of GI tract are resonsible for starch digestion

A

salivary glands (10-20%)

pancreas (80-90%)

small intestinal brush border (can break up di and trisaccharides)

196
Q

sucrose is broken down by what into what

A

sucrase breaks sucrose down into glucose and fructose

197
Q

lactose is broken down by what into what

A

lactase breaks lactose down into glucose and galactose

198
Q

what transporter does fructose use to get from lumen to intestinal cell

A

GLUT5

199
Q

what transporter does glucose, galactose and fructose all use to get from intestinal cell to blood

A

GLUT2

200
Q

what transporter does glucose and galactose use to get from lumen into intestinal cell

A

SGLT1

201
Q

what kinds of peptides can we absorb (amino acides, dipeptides, tripeptides, macromolecules etc.)

A

can absorb di, tri and amino acids (nothing larger)

HOWEVER, once inside the intestinal cell, di and tri peptides have to be broken down into amino acids in order to get into the blood

202
Q

what protein cleaving enzymes exist in small intestine (4)

A

trypsin
chymotrypsin
carboxypepdidases (A and B)
elastase

203
Q

what enzyme cleaves trypsinogen into trypsin

A

enterokinase

204
Q

what does trypsin do

A

activates all the other enzymes (chymotrypsin, elastase, carboxypepditases A and B)

205
Q

what kind of transporters do di and tri peptides use to get into intestinal cells

A

hydrogen ion dependent co transporters

206
Q

what kind of transporters do amino acides use to get into intestinal cells

A

sodium dependent co transporters

207
Q

CCK and gall bladder relationship

A

as a hormone CCK is stimulus for gallbladder to release bile

as a neurotransmitter, CCK feeds up to dorsal vagal complex to release Ach on gall bladder to also cause smooth muscle contraction

208
Q

what kind of transporter is used to reabsorb bile salts from ileum back to liver

A

bile salt/ sodium cotransporter

209
Q

What are the primary bile acids (2)

A

cholic acid

chenodeoxycholic acid

210
Q

what is the rate limiting step in bile acid formation

A

the 7-alpha-hydroxylation of cholesterol

211
Q

what happens to primary bile acids in colon

A

get dehydroxylated into secondary bile acids - deoxycholic acid and lithocholic acid

212
Q

what happens to bile acids in liver

A

get conjugated to amino acids - glycine or taurine

213
Q

what does colipase do

A

associates with micelle on fat droplet and attracts lipase so it can do its job (Without colipase the lipase would get kicked off fat droplet)

214
Q

once in liver cell, what do these lipid components do

A

form chylomicron which then goes into lymph

215
Q

cimetidine mechanism

A

H2 histamine receptor antagonists - directly block histamine-stimulated gastric acid secretion on parietal cells

specific and reversible

216
Q

cimetidine adverse effects

A

least potent
renal elimination
can develop tolerance
crosses placenta

DRUG DRUG RXNS - inhibits a whole lot of p450 (warfarin too high etc.)

HORMONAL effects at high doses - increases prolactin, inhibits estradiol metabolism inhibits dihydrotestosterone receptor binding – causes gynecomastia and impotence in lames and female galactorrhea

217
Q

famotidine mechanism

A

(pepcid)
most potent
DECREASES % of ulcers in NSAID use

H2 histamine receptor antagonists - directly block histamine-stimulated gastric acid secretion on parietal cells

specific and reversible

218
Q

famotidine adverse effects

A

renal elimination

can develop tolerance

219
Q

sucralfate mechanism

A

mucosal protective agent - forms a paste at low pH that adhere to charged proteins of epithelial cells and ULCERS

take BEFORE meal

220
Q

sucralfate adverse effects

A

can adsorb other drugs

don’t coadmin with antaacids

221
Q

bismuth subsalicylate mechanism

A

mucosal protective agent - active ingredient in pepto-bismol

forms bismuth oxychloride and salicylic acid in acid, binds selectively to ULCERS

is ANTIMICROBIAL

222
Q

bismuth subsalicylate adverse effects

A

blackens stool and tongue

causes Reyes syndrome in chidlren

223
Q

misoprostol mechanism

A

mucosal protective agent - prostaglandin analog (PGE1)

inhibits acid secretion from ECL and pareital cell

augments MUCUS and bicab secretion

224
Q

misoprostol adverse effects

A

causes uterine contractions - CONTRA IN PREG

225
Q

metoclopramide mechanism

A

anti-emetic
CENTRAL dopamine receptor antagonist

PERIPHERAL seratonin receptor agonist

can enhance ACh release in myenteric plexus, improves SM response to Ach

works against cytotoxic drug induced emesis

226
Q

metoclopramide adverse effects

A

can cause parkinsonian like muscle spasms

227
Q

ondansetron mechanism

A

selective seratonin receptor antagonist

works against cytotoxic drug induced emesis

228
Q

ondanetron adverse effects

A

constipation

229
Q

omeprazole mechanism

A

irreversible parietal cell proton pump inhibitor

is a prodrug - doesn’t work unti lit gets to stomach

gets stuck in canaliculus in parietal cell

230
Q

omeprazole adverse effects

A

crosses placenta
liver metabolized

slight risk of fractures and decreased B12 absorption

231
Q

what is the first choice drug for zollinger ellison

A

proton pump inhibitors

232
Q

antacin mechanism

A

weak base, neutralize stomach acid

233
Q

Mg(OH2) adverse

A

diarrhea

234
Q

Al(OH2) adverse

A

constipation

235
Q

antacid drug interactions

A

many drug interactions because drugs depend on pH

alters urinary pH - traps acidic drugs

236
Q

lubiprostone mechanism

A

chloride channel activator - increases intestinal fluid seretion via chloride mobilization

237
Q

lubiprostone adverse effects

A

diarrhea, nausea

238
Q

laxative vs carthartic effect

A

laxative - evacuation of soft stool from rectum

cathartic - increased intestinal activy and watery stool - ie for colonoscopy prep

239
Q

linaclotide mechanism

A

chlroide channel activator - cystic fibrosis channel - increases fuild secretion

240
Q

linaclotide adverse

A

diarrhea

contra in children

241
Q

Mg(OH)2 mechasnism as laxative

A

osmotic laxative - osmotic presure leads to accumultion of fluids in gI tract and stimulation of perstalsis - works within 3 hours for colonoscopy prep

242
Q

Mg(OH)2 laxative adverse

A

can cause hypermagnesemia in patients with renal insufficiency

243
Q

loperamide mechanism

A

opioid - poorly absorbed, slow intestinal transit time – antidiarrheal

244
Q

loperamide adverse

A

constipation

risk of toxic megacolon in patients with UC or dysentery

245
Q

IBS description

A

functional disease - no underlying structural abnormalities, no drug targets

246
Q

alosteron use/mechanism

A

for women with diarrheal IBS you can use ALOSETRON which is a seratonin receptor antagonist

247
Q

alosteron side effect

A

ischemic colitis

248
Q

treatments for IBD

A

prednisone - anti-inflammatory, not useful for long term therapy

immunosupprssives - azathioprine, adverse is bone marrow suppression

249
Q

azathioprine mechanism and enzymes that are present

A

anti-metabolite - gets incorporated into DNA/RNA

HGPRT needs to work to convert to active

TPMT can make it toxic to liver

XO makes it inactive

250
Q

first line treatment for UC

A

mesalamines - sulfasalazine

251
Q

sulfasalazine mechanism

A

obscure, but needs to be topical not systemic

252
Q

sulfasalazine adverse

A

40% can’t tolerate because of headaches, hypersensitivity, diarrhea, nausea, bone marrow suppression

253
Q

infliximab mechanism and use

A

remicade
anti TNF-alpha
IV administered

254
Q

adalimumab mechanism and use

A

humera
anti TNF-alpha
subcutaneous administration
100% humanized

255
Q

infectious sialadenitis

A

infectious salivary gland disease caused by staph strep viridans and mumps

256
Q

autoimmune sialadenitis

A

sjogrens - lymphocytic infiltrates destroy secretory cells - get dry mouth and dry eyes

don’t see acinar structures, just glands - ducts

257
Q

what is the most common benign salivary gland neoplasm

A

pleomorphic adenoma - frequencly recurs - more common than malignant

258
Q

what is the most common malignant salivary gland neoplasm

A

mucoepidermoid carcinoma

259
Q

major vs minor salivary neoplasms

A

major is more common and more commonly benign

minor is less common and more commonly malignant

260
Q

pleomorphic adenoma characteristics (gross and histo)

A

encapsulated, freely movable, adpiose - white/tan
NO ULCERATION of skin

in histo - gross pattern is pleomorphic - very variable in appearance (have epithelial and myoepithelial cells, as well as stromal component)

261
Q

mucoepidermoid carcinoma characteristics (gross and histo)

A

low grade and high grade (pain and speed of growth)

gross: unencapsulated, infiltrating, solid white pink, not well delineated

histo:
3 cell types - not a lot of stroma. epidermoid, intermediate and mucous cells - more mucous means lower grade

262
Q

atresia

A

no functional lumen - developmental disorder between trachea and esophagus

263
Q

achalasia

A

spasm of lES with esophageal dilation - commonly idiopathic but also can be due to Chagas disease

264
Q

schatzki’s ring/ web

A

LES ring = circumfrential

web = partial circumference in the upper esophagus

associated iwth iron deficiency (Plummer-Vinson syndrome)

265
Q

Zenker’s diverticula

A

upper - pulsion through weakened muscle

266
Q

traction diverticula

A

adhesed to outside tissue - lower/middle of esophagus

267
Q

esophageal varices

A

caused by cirrhosis or portal htn - most common cause of upper GI bleeding

268
Q

Mallory Weiss syndrome

A

longitudinal linear laceration of small vessels at gastroesophageal junction - history of severe committing, most commonly seen in alcoholics

269
Q

esophagitis causes (3)

A

infection - viral: herpes, CMV, fungi: candida, bacterial superinfection

chemical - drugs, lye

reflux of gastric juice - peptic esophagitis leading to ulceration and epithelial metaplasia

270
Q

Barrett Esophagus

A

metaplasia to columnar epthelial will GOBLET CELLS (looks intestinal) that replaces squamous epithelium

271
Q

esophageal cancer types

A

adenocarcinoma (most common in US) - from Barret’s, at GE junction - histo has glands and goblet

squamous cell (most common world-wide) - mid-low esophagus. histo looks like swirls

272
Q

what is in oxyntic mucosa and where is it

A

fundus and body - has cheif cells and pareital cells

273
Q

causes of pyloric stenosis

A

congenital and aquired (complication of PUD)

274
Q

Menetrier’s disease

A

hypertrophic gastropathy - ideopathic incrased TGFalpha induced hypertrophy of mucous cells and rugae - atrophy of parietal cells

275
Q

gastritis - causes

A

H. Pylori, NSAIDS, Cig, alcohol, gastric hyperaciditiy, duodenal-gastric reflux

ischemia, shock, delayed gastric epmtying

276
Q

what inflammatory cell type do you see in acute gastritis

A

neotrphils in lamina propria

277
Q

erosion vs ulceration

A

erosion is mucosa only, ulceration extends through submucosa

278
Q

what inflammatory cell types do you see in chronic gastritis

A

lymphocytic infiltrate - and plasma cells etc.

undergoes metaplasia

279
Q

autoimmune metplastic atrophic gastritis - location and associated disorders

A

in body-fundus
attacks parietal cells - diecreased acid production

associated with pernicious anemia

and neorendocrine tumor

280
Q

H pylori gastritis - location and associated disorders

A

in antrum - swims in mucous layer and secretes urease - increases acidity

association with peptic ulcers

and lymphoma (MALToma)

281
Q

levels of gastric ulcers (4)

A
  1. superficial necroinflammatory debris with necrosis and neutrophils
  2. acute inflammation - polys (neutrophis)
  3. chronic inflmmation (lymphocytes) and granulation tissue
  4. fibrosis scarring
282
Q

gastric polyp types

A

epithelial cell growth - benign

  1. inflammatory - most common
  2. adenomatous - low grade dysplasia - associated iwth chronic gastritis
  3. hamartomatous
283
Q

benign UGI tumors (2)

A

leiomyoma - more common - SM

schwannoma - peripheral nerve tumor

284
Q

malignant UGI tumors (3)

A

adenocarcinoma - associated iwth chronic gastritis - associated with asians, metastesizes. intestinal and infiltrative types

lymphoma - associated with chronic gastritis H.Pylori

gastrointestinal stromal tumor

285
Q

signet ring seen with what cancer

A

infiltrative adenocarciona type

286
Q

gastrointestinal stromal tumor - identification and tx

A

CD 117 positive
looks like spindle cells in histo with mitoses

tx with gleevec

287
Q

Gastroperesis definition

A

impaired transit of contents from stomach to duodenum

288
Q

types of gastroperesis (2)

A
  1. neuropathic

2. myopathic

289
Q

extrinsic innervatino os stomach

A

vagal (para)

splancnic (symp)

290
Q

intrinsic innervation of stomach

A
  1. interstitial cells of Cajal

2. enteric nervous system

291
Q

pacesetter rate of stomach

A

3 contractions per minute

292
Q

what neurotrasmitters/hormones help with accommodation

A

VIP and NO – via vaso-vagal reflex

293
Q

neuromuscular causes of gastroparesis (4)

A
  1. DM
  2. parkinson’s
  3. scleroderma
  4. duchenne’s muscular dystrophy
294
Q

infiltrative causes of gastroparesis (2)

A
  1. malignancy

2. amyloid

295
Q

infectious causes of gastroperesis (4)

A
  1. herpes zoster
  2. lyme
  3. trypanosoma cruzi
  4. EBV
296
Q

medication causes of gastroparesis (3)

A
  1. anticholinergics
  2. opiates
  3. L-Dopa
297
Q

metabolic causes of gastroparesis (3)

A
  1. hyperglycemia
  2. renal insufficiency
  3. hypo/hyper thyroid and parathyroidism
298
Q

gastric emptying study

A

use technitium sulfur - measure at 1, 2, and 4 hours for delayed emptying

299
Q

gastroparesis diet

A

low fat, low fiber, 6 small meals per day

300
Q

gastroparessis pharmacology tx (4)

A

prokinetics - metoclopramide, erythromycin, domperidone (no BBB)

anti-emetics

antidepressants

pyloric botox injection

301
Q

how do NSAIDS cause PUD (2)

A
  1. direct corrosive damage

2. systemic inhibition of prostaglandins (main driving force of damage)

302
Q

coadmin of what drugs with NSAIDS increase risk of PUD (2)

A
  1. corticosteroids

2. anticoags

303
Q

when do you take PPIs

A

30-40 minutes before a meal

304
Q

first line tx for H. pylori (3)

A
  1. PPI
  2. clarithromycin
  3. amoxicillin or flagyl
305
Q

risk factors for stress ulcers (3)

A
  1. mechanical ventillation
  2. coagulopathy
  3. burns

all cause reduced mesenteric perfusion

306
Q

marginal ulcer cause

A

roux en Y bypass within 6 months after surgery

- ischemia

307
Q

diagnostic tests for H pylori (3)

A
  1. stool antigen test
  2. urea breath test
  3. serum IgG antibody - high false positive (low specificity)
308
Q

when should you retest for H Pylori

A

4 weeks after tx to rule out false pos and false neg

also because resistance is increasing

309
Q

why repeat endoscopy after H pylori tx - and when

A

to see if there’s still an ulcer - indicates cancer - 8 weeks after

310
Q

dimensions of esophagus

A

20cm long, 2cm diameter

311
Q

does esophagus of adventitia or serosa

A

adventitia

312
Q

two types of dysphagia (2)

A

oropharyngeal

esophageal

313
Q

type A ring

A

muscular

314
Q

type B ring

A

diaphragm like (shotzki’s) -

315
Q

corkscrew esophagus

A

esophageal spasm - manometry dx tool

316
Q

tx for esophageal spasm (3)

A

calciumc channel blockers, nitrates

botox

myotomy (last case)

317
Q

achalasia dx requirements (2)

A
  1. incomplete relaxation lf LES

2. abnormal motility on manometry

318
Q

treatment for achalaisa (3)

A
  1. myotomy - disrupt LES
  2. botox
  3. calcium channel blocker
319
Q

angle of HIS

A

prevents reflux of stomach contents into esophagus

320
Q

4 mechanisms of reflux

A
  1. transient lower esophageal sphincter relaxations (tLESR)
  2. swallow induced LES relaxations
  3. hypotesnsive LES pressure
  4. hiatal hernia and the “acid pocket”
321
Q

complications of GERD (4)

A
  1. upper GI bleed
  2. benign peptic stricture
  3. barrett esophagus
  4. esophageal adenocarcinoma
322
Q

surgery for GERD

A

nissen fundoplication - tighten sphinchter - wrap stomach around

323
Q

which is more common, GERD or NERD

A

NERD

324
Q

treatment plan for GERD

A

dietary changes

if persists, then PPI or H2 antagonist

if persists, upper endoscopy

325
Q

specialized lymphocytes in GI tract (2)

A

IEL

MAIT cells

326
Q

what are M cells

A

cells in epithelium of GI tract that uptake antigen and transport to tissue of gut

327
Q

what antibody do plasma cells in gut produce predominately

A

IgA

328
Q

small vs large intestine - whcih has more microbes and mucus

A

large has more of both

329
Q

Th17 and the gut

A

promotes barrier function - tight junctions, defensin production etc.

330
Q

mucous and IgA

A

mucin interactions with glycoproteins in mucous, which stabilizes IgA and reduces turnover (same with IgM too - lesser extent)

331
Q

how does IgA get from plasma cell to lumen

A

gets transcytosed - associated with “Secretory component” from poly-Ig receptor

332
Q

sequence of events to make effector T cell (4)

A
  1. dendritic cell processes antigen, presents it with MCH class 1 or 2
  2. costimulation with T cell in peyers patch - cytokines hat stimulate T cell differentiation and activation
  3. T cells help B cells to make cytokines that isotype switch and differentiation into plasma cell
  4. goes out through lymph and hones back through chemoattraction to go back to GI epithelium
333
Q

when do we get colonized with bacteria

A 
at birth (vaginal canal)
and boost at 3-6 months with food intake
334
Q

c. diff microbiome treatment

A

stool trasnplant

335
Q

childhood pancreatic islet autoimmunity microbiome tx

A

earl yadmin of probiotic supplementation

336
Q

TGF-beta and inflammatory response (2)

A

stimulates differentiation of T-reg cells (through IL-10) decrease proinflammatory responses

TFGb also regulates B cells to switch to produce IgA

337
Q

IL12 and inflammatory response

A

promotes differentiation of T cells into Th1 and Th17 - pro-inflammatory

(also by IL-17, 22, IFN-g and TNF-a)

338
Q

antibiotics and microbiome effects (4)

A
  1. decreases diversity of gut flora
  2. decreases mucous layer
  3. decreased efficacy of PD-1 blockade in tumor suppression
  4. obesity phenotype transplantation - food metabolism
339
Q

microbiome, inflammation and plant-based diet

A

plant-based increases production of short chain fatty acids which increase production of Treg cells and create anti-inflammatory environment

340
Q

why is IgA deficiency often asymptomatic

A

body still makes IgM and is host-protective

341
Q

jejunal gross/histo structures (3)

A
  1. submucosal plicae circularis
  2. long villi with branched and expanded tips and internal lacteals (holes) and crypts of libercuhn
  3. tall columnar absorptive cells with interspersed goblet cells
342
Q

ileum gross/histo structures (2)

A
  1. lots of submucosal lymph nodules

2. villi are blunter, crypts of libercuhn

343
Q

vermiform appendix structure (2)

A
  1. all layers of regular gut tube, but has PITS, no villi

2. lots of lymphoid tissue

344
Q

colon histo/gross structures (4)

A
  1. mucosa is pitted and folded (NO VILLI)
  2. numerous goblet cells, tall columnar absorptive cells
  3. periodic thick external outer long muscle - taenia coli
  4. posterior ascending and descending have adventitia – secondarily retroperitoneal
345
Q

colon function

A
  1. home to microbiome

2. water absorption

346
Q

rectoanal junction structure (4)

A
  1. muscularis mucosae ends abruptly at pectinate line
  2. colonic mucosa to stratified squamous un- to keratenized
  3. venous plexuses - hemoroidal
  4. lymph tissue
347
Q

assmiliation

A

= combo of absorption and digestion

348
Q

how much fluid is absorbed per day in GI tract

A

8-10L

349
Q

ions that drive absorbtion and secretion

A

absorption (of water, nutrients, electrolytes, bile salts) in villi driven by sodium absorption via solvent drag

secretion in crypts driven by Cl secretion (disregulation causes diarrhea)

350
Q

absorption of what happens where along small intestine

A

nutrients in proximal SI

electrolyte transport in distal SI

bile salt absorption in terminal ileum

all coupled with sodium driven by gradient established by Na/L ATPase

351
Q

transporters in different parts of colon

A

in right colon - sodium uptake happens via Na+/H+ exchange

in left colon - sodium uptake occurs via ENaC (aldosterone sensitive) channel and K+ secretion occurs simultaneously

352
Q

jejunum and duodenum - what amount of fluid is absorbed

A

5L - high volume, low efficiency

353
Q

what channels regulate secretion in GI tract

A

3 chloride channels - CIC-2, CFTR, CaCC

354
Q

how does CFTR channel get opened (2)

A
  1. VIP –> Gs protein –> cAMP –> protein kinase C phosphorylates CFTR and opens channel
  2. cGMP –> different protein kinase which phosphorylates CFTR and opens channel
355
Q

cholera mechanism

A
  1. cholera toxin binds to G protein permanently activating, keeping channel open and pumping chloride ion out
  2. cholera toxin also binds Na+/H+ exchanger causing decrease in sodium uptake (decreased absorption ability) – give glucose to oral rehydration therapy which will drag sodium in with it
356
Q

what stimulates calcium activated chloride channel (2)

A

Ach (increases calcium)

ecoli increases intracelluar calcium also

357
Q

volume definition of diarrhea

A

an increase in stool fluid volume of more than 200mL within 24 hours

358
Q

malabsorpbtion causes what kind of diarrhea

A

osmotic diarrhea

359
Q

toxins (like cholera) cause what kind of diarrhea

A

secretory diarrhea

360
Q

diarrhea causes what to potassium and pH levels

A

causes loss of K+ and bicarb - so you get hypokalemia and metabolic acidosis

361
Q

what to give someone with cholera to maintain fluid levels

A
  • give glucose to oral rehydration therapy which will drag sodium in with it
362
Q

where does calcium absorption happen, what’s it stimulated by

A

duodenum - stimulated by calcitriol from vitamin D

363
Q

bacterial enzymes help metabolize what (2)

A

bile acids

fiber

364
Q

dietary fiber digestion

A

amylase can’t break down nonstarch polysaccharides

bacterial fermentation causes breakdown into short-chain fatty acids (which in turn pH keeps bacterial overgrowth in check)

365
Q

rectal distension and anal sphincters

A

rectal distension causes relaxation of internal sphincter and excitation of external sphincter, and then we have voluntary control over relaxing external sphincter

366
Q

Knudson’s 2 hit hyptohesis

A

what is needed to develop cancer - cancer needs to same mutation of tumor suppressor gene on both allele

367
Q

on average how long does it take for adenoma to get to cancer

A

10-15 years

368
Q

familial adenomatous polyposis (FAP)

A

80% inherited autosomal dominant germiline mutation in one allele in APC tumor suppressor gene on chrom 5 - second allele mutation during childhood - ton of polyps by age 16, screen at age 10

369
Q

lynch syndrome

A

mismatchrepair gene autosomal dominant - 2-4% of colon cancers

also presents with endometrial cancer

370
Q

when to resect liver with colon mets

A

at least 20% functional liver needs to remain

ensure at least 1mm margin

371
Q

4 serious sequelae of enteritis

A
  1. hemolytic uremic syndrome (HUS) due to shiga producing E. Coli
  2. Guillain-Barre syndrome (GBS) caused by campylobacter
  3. IBS
  4. chronic malnutrition and increased susceptibility to other diseases (malaria, TB)
372
Q

what kind of bacteria cause infectious enteritis (gram staining, shape etc)

A

gram neg rods

373
Q

major bacterial culprits (8)

A
  1. salmonella
  2. capylobacter
  3. shigella
  4. E coli
  5. clostridium dificile
  6. vibrio
  7. yersinia
  8. listeria (extremes of age)
374
Q

what kind of diarrhea is associated iwth entero vs cytotoxins

A

cytotoxins have bloody diarrhea

375
Q

examples of enterotoxins (2)

A
  1. cholera toxin

2. E coli heat labile and stable toxins

376
Q

examples of cytotoxins (2)

A
  1. shiga toxin (from E. Coli and shigella)

2. c diff toxin B

377
Q

examples of neurotoxins (3)

A

preformed in food - cause immediate vomitting (enterotoxin later causes watery diarrhea)

  1. staph aureus
  2. B cereus
  3. clostridium botulinum
378
Q

what kind of diarrhea do viruses cause

A

secretory - watery

379
Q

vibrio cholera - transmission, clinical, management

A

comma-shaped

  1. foodborne/ waterborne
  2. abrupt onset of massive rice water stool
  3. oral rehydration with glucose, antibiotics
380
Q

ETEC - transmission, clinical, management

A
  1. food and water - uncooked veggies, unpeeled fruit, uncooked meat etc.
  2. main cause of traveller’s watery diarrhea
  3. antibiotics and/or antimotility agents (but immunocompetent will recover okay)
381
Q

what is dysentery

A

bloody diarrhea and fever

382
Q

site of intestinal action for secretory vs inflammatory diarrhea

A

secretory = small intestine

inflammatory = colon

383
Q

shigella - characteristics, transmission, clinical, treatment

A

shigella does NOT have H antigen - no flagella, shigatoxin has AB5 structure

  1. fecal-oral, food and water
  2. fever, cramps, watery to bloody diarrhea, high mortality. can progress to HUS and reactive arthritis
  3. tx with fluoroquinolones
384
Q

capylobacter - characteristics, transmission, clinical, treatment

A
  1. comma shaped gram neg rod
  2. transmission - zoonotic, poultry (jejuni) cattle/sheep (fetus)
  3. jejuni causes enterocolitis, fetu causes sstemic disease. associated with GUILLAIN-BARRE, reactive arthritis, septic abortion
  4. tx fluoroquinolones
385
Q

STEC - characteristics, transmission, clinical, tx

A
  1. E coli O157:H7 - hamburger disease
  2. food borne (meat, soy butter), water borne, swimming pools
  3. non-bloody within hours, bloody within 1-2 days, HUS concern - renal involvement
  4. supportive management - NO ANTIBIOTICS - will increase chances of HUS
386
Q

non-typhoid salmonella - characteristics, clinical, tx

A
  1. different serovars
  2. foodborne - eggs, poultry etc and contact wit REPTILES
  3. bloody diarrhea, extra-intestinal seeding in bones/joints (esp sickle cell) and endovascular
  4. might have to remove gall bladder (CHRONIC CARRIAGE)
    tx for immunosuppresssesd or heart valves - fluoroquinolones
387
Q

typhoid salmonella - symptoms, dx, tx

A

AKA enteric fever - don’t focus on GI symptoms

gets into blood stream - prolonged fever and bacteremia. see ROSE SPOTS salmon maculopapular rash and HEPATOSPLENOMEGALY
high mortality if untreated - intestinal perforation, endocarditis

blood culture, bone marrow, tx with fluoroquinolones, can have chronic carriage - source of secondary infections (typhoid mary)

388
Q

what pathogens cause chronic diarrhea

A

PROTOZOA - not virus or bacteria

389
Q

giardia - transmission, symptoms, diagnosis

A

water transmission - camping

foul-smelling stool, fat malabsorption, no blood in stool

dx by seeing cysts on smear and fecal antigen test PCR

390
Q

cryptosporidium - smptoms and dx

A

acid fast smear

watery chronic diarrhea in HIV pos, need to get CD4 up

391
Q

cyclospora - symptoms dx

A

acidd fast staining of feces

lots of gas, explosive diarrhea, fatiue

foodborne outbreaks

392
Q

amoebiasis clinical, dx

A

two phases - dysenery (with flask ulceration) and liver abscess

stool PCR and antigen testing but can have negative stool microscopy if only in liver

393
Q

when to do diagnostic test with diarrhea

A

dysentery, sepsis, suspected outbreak, food-handler, c. diff

394
Q

when do you give antimotility agents like loperamide/imodium

A

only when there’s watery diarrhea - don’t give with bloody diarrhea, don’t want to prolong the organisms’ s stay in the gut

395
Q

when to give antibiotics for diarrhea (5)

A
  1. severe/persistant diarrhea
  2. enteric fever
  3. traveler’s diarreah
  4. c. diff (metro, oral vanc)
  5. giardia, E. histolytica (metronidazole)

NOT STEC - WILL GIVE YOU HUS

396
Q

secretory diarrhea definition

A

continues despite fasting, more than a liter

397
Q

osmotic diarrhea definition

A

ceases with fasting, less volume than secretory

398
Q

formula for stool osmotic gap and criteria for high and low

A

290 - 2(stool Na + stool K)

greater than 125 mOsm/kg suggests osmotic diarrhea - large quant of unmeasured non-electrolytes magnesium, phosphate, lactose intolerance

less than 50 is secretory - incomplete absorption of electorlytes - cholera

399
Q

what do lactoferrin and calprotectin indicate

A

inflammatory diarhea

400
Q

choleretic diarrhea cause and tx

A

ileal resection LESS THAN 100cm, malabsoprtion of bile acids, bile acids stimulate choride and fluid secretion in colon causing choleretic diarrhea

tx with cholestyramimne, a ibile acid binding resin

401
Q

fatty acid diarrhea cause and tx

A

ileal ressection MORE THAN 100cm, bile acid malabsorption results in delivery to colon, hepatic synth can’t catch up, bile acid pool is depleted

WORSENS with cholestyramine

402
Q

oxalate kidney stones and malabsorption

A

fat malabsorption (short bowel for example) oxalate gets into colon and gets sent to kidneys where they form stones

403
Q

how to test for lactose intolerance

A

bacteria produce H2 when it hits malabsoprtbed carbohydrate

404
Q

how to test for SIBO

A

give lactulose, measure peak of H2 breath hydrogen testing

405
Q

direct vs indirect inguinal hernia

A

indirect follows path of scrotom through inguinal ring.

direct is through weakening of abdominal wall

406
Q

pathological findings in abetalipoproteinemia

A

inherited autosomal recessive absense of apoprotein fails to mobilize Lipids into circulation - see LIPID VACULOES in enterocytes, RBC “BURR CELLS” and demyelination in the CNS

407
Q

what do you see in pathology of section of dermatatis herpetiformis, and what is it associated iwth

A

celiac

see subepidermal vesicles filled iwth neutrophils

408
Q

whipples disease - cause, symptoms, histo

A

caused by tropheryma whipplei bacteria

affects middle aged men, get fever, migratory arthritis and diarrhea

in histo see foamy macrophages with PAS+ rod like bacteria, and flattening of villi

409
Q

peutz-Jegher polylps - associations

A

hamartomatous - inherited autosomal dominant, associated iwth mucosal pigmentation and non-GI cancer

410
Q

Juvenile popylposis - associations

A

autosomal D, large polyps, associated iwth GI cancer

411
Q

do hyperplastic polyps have stalks?

A

usually no

412
Q

do tubular adenomas have a stalk?

A

usually yes

413
Q

do villous adenomas have a stalk

A

no - they’re sessile

414
Q

do tubulovillous adenomas have a stalk?

A

usually yes

415
Q

what do hyperplastic polyps look lik eon histo

A

frilly serrated appearance that stop HALF WAY down crpt. crypt base is narrow

416
Q

sessile serrated polyp look like on histo

A

serrated epithelium extends all the way down, usually in right colon, base of crypts are dilated, higher risk of BRAF microstellite cancer

417
Q

carcinoid syndrome

A

caused by neuroendocrine tumor - causes excess serotonin production leading to sporadic hypertension, asthma, diarrhea and flushing – due to liver mets

418
Q

IBD specific serology (3)

A

ASCA - cerevisiae - higher in crohns disease

DNase sensitive pANCA - histone H1 - higher in UC

OmpC - E coli - higher in CD

419
Q

central arthritis associated with IBD

A

ankylosing spondylitis (independent of disease process) associated with UC

420
Q

peripheral arhtritis associated iwth IBD

A

runs parallel to disease course of UC - monoarticular, migrating, joint pain

421
Q

skin associations iwth UC

A
  1. erythema nodosum

2. pyoderma gangrenosum

422
Q

what do you use 5-ASA drugs for

A

UC

423
Q

Ogilvie’s

A

pseudoobstruction and mild pain - caused by drugs, surgery, neurological problem

GI/Liver (2 decks)

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