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CABS III > Gastrointestinal System > Flashcards

Gastrointestinal System Flashcards

1
Q

function of abdominal muscles

A

support the viscera by compressing the abdominal cavity, stabilize the vertebral column, and help in respiration, urination, defecation, and childbirth

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2
Q

abdominal muscles include

A

external oblique, internal oblique, transverse abdominis, and rectus abdominis

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3
Q

Linea alba

A

runs in between the rectus abdominis muscles in the abdomen

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4
Q

layers of the GI tract

A

beginning externally - serosa, muscularis, submucosa, and the mucosa

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5
Q

mucosa contains

A

epithelium, glands that secrete GLP-1 and cholecystokinin (CCK), the lamina propria which contains blood vessels and lymphoid tissue (mucosa-associated lymphoid tissue - MALT), and smooth muscle

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6
Q

submucosa contains

A

connective tissue, Meissner’s plexus with autonomic neurons, and Peyer’s patches

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7
Q

muscularis contains

A

skeletal/voluntary muscle within the mouth, pharynx, superior esophagus, and external anal sphincter and smooth muscle everywhere else with an inner circular layer and an outer longitudinal layer, also contains myenteric plexus of autonomic innervation

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8
Q

serosa

A

connective tissue that lines the surface of the organ

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9
Q

peritoneum

A

the serous membrane that encases the bowel which carries vasculature, nerves, and lymphatics and consists of 2 layers, the visceral and parietal layers, with a small space (peritoneal cavity) between them that is filled with fluid (the visceral layer lines the organs and the parietal layer attaches to the abdominal wall providing support and protection of visceral organs)

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10
Q

retroperitoneal organs

A

pancreas, kidneys, and aorta

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11
Q

omentum

A

composed of two parts, the greater and lesser omentum, where the lesser omentum arises from the lesser curvature of the stomach and extends to the liver and the greater omentum arises from the greater curvature of the stomach and forms a large sheet that lies over the intestines and converges into the parietal peritoneum

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12
Q

GI tract overall functions

A

mechanical breakdown of nutrients, further chemical breakdown, absorption, and excretion of unneeded elements/wastes, and immune protection

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13
Q

phases of swallowing

A

oral phase = voluntary, pharyngeal phase = voluntary, and esophageal phase = involuntary

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14
Q

mastication

A

voluntary process of chewing causing the mechanical breakdown of food with teeth using the temporalis and masseter facial muscles, salivary amylase begins the breakdown of complex carbohydrates and lingual lipase begins the breakdown of fats

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15
Q

function of incisor teeth

A

to cut food

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16
Q

function of premolars

A

to crush and tear food

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16
Q

function of canine teeth

A

to tear and grasp food

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17
Q

function of molars

A

chew and grind food

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18
Q

dental caries (cavities)

A

tooth decay caused by bacteria (mainly strep mutans) in dental plaque which begins as a soft film of bacteria, dead cells, and food debris

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19
Q

number of taste buds on the tongue

A

3,000 - 10,000 taste buds on average (each contain 100 taste cells), number decreases with age

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20
Q

sense of taste

A

the chemical binds to a taste hair receptor causing depolarization of the cell, generating an action potential

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21
Q

posterior aspect of tongue innervation

A

glossopharyngeal nerve and vagus nerve (at the base/pharynx)

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22
Q

gustatory cortex

A

the area within the brain (anterior insula-frontal operculum) where taste signals are processed following synapse within the hypothalamus

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23
Q

salivary gland function

A

stimulated by parasympathetic nervous system and secrete 1 liter of saliva per day which mostly consists of water but also contains sodium, mucus, bicarbonate, chloride, potassium, and salivary amylase

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24
Q

pH of saliva

A

7.4

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25
Q

superior constrictor muscle of the pharynx function

A

prevents movement of food bolus into the nasal cavity along with uvula

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26
Q

pharyngeal phase of swallowing

A

occurs when the food bolus reaches the oropharynx sending sensory signals from CN IX (glossopharyngeal) to the swallowing center in the medulla which responds by sending efferent signals to the pharynx to initiate the swallowing reflex which involves blockage of the airway by the epiglottis and relaxation of the UES

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27
Q

esophageal phase of swallowing

A

the involuntary portion of swallowing that takes 5-10 seconds and stimulates peristalsis through the esophagus, UES (cricopharyngeal muscle) closes and LES (gastroesophageal sphincter) opens resulting in bolus reaching the stomach, the epiglottis then reopens and the LES closes to prevent backflow of stomach contents

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28
Q

esophagus

A

measures 25 cm in length from the oropharynx to the stomach, contains UES and LES, lower esophagus innervated by the vagus nerve and upper esophagus has mixed innervation, peristalsis of inner circular and outer longitudinal musculature is initiated by stretch receptors

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29
Q

enteric innervation

A

includes plexuses within different layers such as the Meissner submucosal plexus, the Auerbach myenteric plexus, and the subserosal plexus which regulate motility, reflexes, blood flow, and absorption

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30
Q

stomach function

A

acts as a short-term food storage reservoir and is the location where chemical and enzymatic digestion is initiated, secretes intrinsic factor (absorption of B12), pacemaker cells cause rhythmic depolarization going toward the pylorus to mix the food which liquifies it into chyme that is then slowly released into the duodenum for further processing, microbes are killed, proteins are broken down, and bile is triggered to be released, the stomach is impermeable to water but will absorb ETOH and NSAIDs (rate of absorption depends on food ingested)

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31
Q

cephalic phase of gastric acid secretion

A

accounts for 30% of gastric acid secretion and is a response to seeing, smelling, and anticipation of PO intake which stimulates the medulla, vagus nerve, and submucosal plexus to increase HCl secretion, hypoglycemia increases acid response

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32
Q

gastric phase of gastric acid secretion

A

accounts for 60% of gastric acid secretion which is stimulated by food hitting the stomach which increases pH and causes distention triggering stretch receptors and chemoreceptors in the stomach leading to myenteric and vasovagal reflexes causing increase in HCl secretion

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33
Q

intestinal phase of gastric acid secretion

A

accounts for 10% of gastric acid secretion which is triggered by the initial movement of food into the small intestines causing distention and stimulating more HCl secretion, cholecystokinin (CCK) will decrease motility and emptying and somatostatin will slow the release of gastric acid

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34
Q

primary area of gastric acid secretion

A

gastric pits

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35
Q

types of cells within the stomach

A

goblet cells, parietal cells, chief cells, D cells, and G cells

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36
Q

gastric goblet cells produce

A

mucous which protects stomach lining

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37
Q

gastric parietal cells produce

A

hydrochloric/gastric acid and intrinsic factor

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38
Q

gastric chief cells produce

A

pepsinogen which is a pepsin (protease) precursor

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39
Q

gastric D cells produce

A

somatostatin which inhibits gastric acid secretion

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40
Q

gastric G cells produce

A

gastrin which stimulates gastric acid secretion

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41
Q

pH of pepsin

A

2

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42
Q

chyme

A

a mixture of gastric acid and mechanically broken down food

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43
Q

hydrochloric acid (HCl) function

A

breaks down proteins into amino acids and establishes an acidic environment that is inhospitable to bacteria, parietal cells secrete ~ 3-4 liters/day

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44
Q

gastric emptying

A

takes around 3 hours on average but will vary depending on the type of food ingested, mechanical and chemical breakdown of food will decrease food to 1 mm size particles, the stomach can hold about 1.5 liters of food/fluid

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45
Q

stimulation of bile and pancreatic enzyme secretion

A

stimulated by secretin which is released by the duodenum causing bile release from the liver/gallbladder combined with pancreatic enzymes through the sphincter of Oddi

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46
Q

small intestine

A

includes duodenum, jejunum, and ileum which is about 20 feet long and is the primary site of chemical digestion and nutrient absorption (90% nutritional absorption), contains a vast absorptive surface (brush border with microvilli) where each section differs functionally

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47
Q

duodenum function

A

separated from the jejunum at the Treitz ligament, accepts chyme from the stomach and readily absorbs water, thiamine (B1), and iron (via intestinal transferrin in proximal duodenum) which enter the portal venous system

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48
Q

ileum function

A

has the largest lumen, is the longest, and most distal section of the small intestine, and functions to absorb water, nutrients, magnesium, phosphate, vitamin B12 (in the distal ileum), and bile salts (terminal ileum)

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49
Q

jejunum function

A

the section between the duodenum and the ileum which functions to absorb water, thiamine (B1), magnesium, phosphate, amino acids, sodium, potassium, ETOH, and fats

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50
Q

cells within the small intestine

A

enterocytes are the most abundant and contain microvilli for absorption, scattered goblet cells that secrete mucus, and occasional enteroendocrine cells

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51
Q

movement through the small intestine

A

food causes distention which stimulates sensory autonomic neurons and mechanical digestion via segmentations created by contractions of circular inner musculature (occur more frequently in 1-4 cm segments to mix chyme and enzymes), peristalsis pushes chyme forward and is created by contractions of the longitudinal outer layer of musculature (occurs more slowly in 10 cm sections)

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52
Q

amount of water absorbed in small intestine

A

92% of the water that is ingested and secreted by the GI tract

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53
Q

amount of water absorbed in large intestine

A

6-7% of the water that is ingested and secreted by GI tract

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54
Q

Brunner’s glands

A

mucus-secreting glands within the duodenal submucosa which have excretory ducts that drain into the crypts of Lieberkuhn

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55
Q

Peyer’s patches

A

part of the gut-associated lymphoid tissue (GALT) that contains lymph nodes and forms large follicles that extend through the lamina propria and submucosa mostly within the ileum, create antimicrobial peptides and IgA which help maintain a happy relationship with the gut microbiome and have primarily B cells (also macrophages, T cells, and mast cells)

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56
Q

differences in microvilli throughout small intestine

A

the villi are leaflike and wide in the duodenum, have a fingerlike shape and are long in the jejunum, and are fingerlike but shorter in the ileum

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57
Q

ileocecal valve

A

sphincter between the end of the ileum and the cecum of the large intestine which opens with pressure within the ileum and shuts with pressure or contents within the cecum

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58
Q

cecum

A

a pouch at the beginning of the ascending large intestine

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59
Q

large intestine

A

1.5 meters long where it begins at the cecum and leads to the ascending colon, the hepatic flexure, the transverse colon, the splenic flexure, the descending colon, the sigmoid colon, the rectum, and the anus

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60
Q

liver

A

largest solid organ which weighs about 2% of total body weight and typically measures 10-12.5 cm in height and 20-23 cm wide, protected by ribs 7-11 and crosses midline into LUQ and epigastric region, broken into 4 lobes - right (largest) and left lobes which are separated by the falciform ligament (which is attached to the anterior abdominal wall) and caudate and quadrate lobes posteriorly which are part of the right lobe, covered by visceral peritoneum with a bare area posteriorly

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60
Q

Couinaud classification

A

functionally divides the liver into 9 sections which contain branches of portal vein, hepatic artery, and bile duct that separate them, these sections can be removed surgically without causing problems for the remaining parenchyma

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61
Q

porta hepatis

A

where the hepatic artery, portal vein, and left/right hepatic duct enter

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62
Q

Glisson capsule

A

encases the liver and contains neurovascular supply for the liver - irritation to this capsule can cause pain

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63
Q

ligamentum teres (round ligament)

A

remnant of umbilical vein which extends inferiorly off of the falciform ligament and attaches to the umbilicus

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64
Q

coronary ligament

A

extends superiorly off the falciform ligament to support superior to the diaphragm

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65
Q

blood supply to liver

A

the common hepatic artery which comes off the celiac axis/trunk and leads to the proper hepatic artery dividing into right and left hepatic arteries

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66
Q

amount of blood filtered by the liver

A

400-500 mL/minute from the arterial system and 1000-1200 mL/minute from the venous system

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67
Q

liver lobule

A

the functional unit of the liver which are made up of hepatocytes that are the functional unit for protein production (able to regenerate) and sinusoids

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68
Q

sinusoids

A

capillaries between hepatocytes within the liver lobule that receive both arterial and venous blood and are very permeable to nutrients and chemicals metabolized in hepatocytes, they drain into the central vein followed by the hepatic vein and then the IVC

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69
Q

Kupffer cells

A

specialized macrophages that line the walls of sinusoids in the liver and perform many key functions including blood monitoring, liver defense against invaders, and secrete anti-inflammatory cytokines

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70
Q

liver functions

A
  • forms and secretes 700-1200 mL of bile per day which is made in hepatocytes and drained by the bile canaliculi
  • produces plasma proteins including albumin, transferrin, ferritin, cholesterol, and lipoproteins
  • converts excess glucose into glycogen to be stored and vice versa
  • produces glucose through gluconeogenesis
  • regulates blood levels of amino acids
  • stores iron (ferritin) and breaks down hemoglobin
  • converts poisonous ammonia (from protein breakdown) to urea by adding CO2 which is excreted in the kidneys
  • clears the blood of drugs and toxic substances
  • produces most blood clotting and clot breakdown factors and regulates clotting
  • helps to create platelets by release of thrombopoietin - TPO
  • removes or metabolizes hormones into inactive or active forms (which can accumulate in liver dysfunction)
  • produces immune factors (complement proteins and C-reactive peptide) and removes bacteria from the bloodstream
  • produces angiotensinogen which participates in the RAAS
  • clears bilirubin from the body through bile and intestinal excretion
  • activates vitamin D
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71
Q

bile function

A

composed of bile salts (acids), phospholipids, cholesterol, bilirubin, electrolytes, IgA antibodies and H2O which helps small intestine to emulsify and absorb fats, bile is alkaline

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72
Q

gallbladder function

A

stores and concentrates bile which is released when triggered by cholecystokinin (CCK) from the duodenum into the bloodstream (begins 30 minutes after eating), the smooth muscle layer of the gallbladder contracts causing bile to flow through the cystic duct to the common bile duct, through the ampulla of Vater and sphincter of Oddi, and into the duodenum

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73
Q

portal triad includes

A

a branch of the bile duct, branch of the hepatic portal vein, and branch of the hepatic artery

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74
Q

process of bilirubin formation

A

old/damaged RBCs (120 days) are broken down in the liver/spleen by macrophages (Kupffer cells) leading to hemoglobin breakdown where heme is separated from iron and converted first into biliverdin and then bilirubin to be sent into plasma, iron is stored in ferritin in the liver to be utilized during erythropoiesis

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75
Q

unconjugated (indirect) bilirubin

A

a waste product formed when RBCs are broken down by the spleen and heme is metabolized in the bloodstream to biliverdin through enzymatic reactions which then forms unconjugated bilirubin which is lipid-soluble and must be bound to albumin to be transported to the liver

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76
Q

conjugated (direct) bilirubin

A

upon reaching the liver, an enzyme combines unconjugated bilirubin with glucuronic acid which then becomes conjugated bilirubin which is water-soluble, conjugated bilirubin is converted by bacterial proteases to urobilinogen which is then excreted in feces as bile or in urine through the kidneys

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77
Q

process of bile formation

A

in the liver, hepatocytes break down cholesterol to create primary bile acids and amino acids conjugate with bile acids to form bile salts (bile), while some bile is stored in the gallbladder for release with a fatty meal, bile salts in the duodenum and jejunum break down fats and allow fat transport - 15-30% of bile salts are excreted in stool and 65-85% enter circulation with protein binding for re-transport to the liver

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78
Q

effect of insulin on the liver

A

in the fed state, insulin is released as an unbound protein into the bloodstream and enters the liver where it inhibits glycogenolysis and stimulates glycogenesis by increasing the activity of glycogen synthase, it also stimulates lipogenesis (fat storage), when glucose levels drop insulin levels fall and glycogenesis and glucose uptake is inhibited, enzymatic phosphorylation will cause glycogen to be broken down into glucose to keep glucose levels normal

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79
Q

effect of insulin on skeletal muscle and adipose tissue

A

in muscle, insulin increases amino acid influx, protein synthesis, and glycogenesis whereas in adipose tissue it stimulates lipogenesis and inhibits lipolysis (fat breakdown)

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80
Q

effect of glucagon on the liver

A

in the fasting state, glucagon is released from the pancreas into the bloodstream and enters the liver where it stimulates glycogenolysis to raise blood glucose levels and can also stimulate gluconeogenesis to form glucose from other molecules such as amino acids (produces ammonia), lactic acid, and fatty acids

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81
Q

systemic effects of glucagon

A

increases cardiac contraction, increases renal blood flow, increases bile excretion, inhibits gastric acid secretion, and rises during exercise (possibly to prevent hypoglycemia)

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82
Q

crystalloid solution

A

fluid made of small molecules including salts and electrolytes

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83
Q

colloid solution

A

fluid made of macromolecules including proteins (albumin), starches, gelatins, and dextrans

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84
Q

albumin function

A

makes up 50% of all plasma proteins and is required for the transport of hormones, fats, nutrients, and medications, and helps maintain intravascular volume (osmotic/oncotic pressure)

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85
Q

clotting factors made by the liver

A

all clotting factors of the intrinsic and extrinsic pathways besides factor VIII (although some is made in the liver in sinusoidal endothelial cells) including factor I (fibrinogen - precursor to fibrin), vitamin K-dependent clotting factors - II (thrombin), VII, IX, and X, and protein C & S, clotting factors are formed as the inactive form in the liver, the liver also produces factors that break down clots including plasminogen and antithrombin

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86
Q

important proteins within blood

A

albumins (osmotic pressure), fibrinogen (clotting), ferritin (iron storage), transferrin (iron transfer), enzymes, antibodies, and hormones

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87
Q

importance of Ca2+ within blood

A

assists with clot formation and multiple other processes including cardiac and muscle contraction, nervous system excitability, and bone density

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88
Q

pancreas

A

composed of head, neck, body, and tail where the head is attached to the duodenum and opens into it via the ampulla of Vater allowing the release of exocrine contents into GI tract, pancreatic duct begins in the tail and runs the length of the organ, the neck lies next to the stomach pylorus and the tail lies anterior to the kidney

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89
Q

blood supply to head of pancreas

A

superior mesenteric artery (SMA)

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90
Q

blood supply to the body/tail of pancreas

A

branches off of the splenic artery

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91
Q

exocrine pancreas function

A

when acidic chyme enters the duodenum, cholecystokinin (CCK) and secretin are released into the bloodstream which stimulates the acinar (exocrine) cells of the pancreas to release pancreatic juice rich in bicarbonate ions and digestive enzymes which assist with breaking down fats, carbohydrates, and proteins and helps to neutralize the sudden acidity from the stomach contents

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92
Q

pH of stomach

A

2

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93
Q

pH of duodenum

A

6

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94
Q

pH of ileum

A

7.4

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95
Q

enzyme released from pancreas that helps with fat breakdown

A

lipase - forms small micelles around fat with a hydrophilic outer layer that allows for diffusion

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96
Q

enzyme released from pancreas that helps with carbohydrate breakdown

A

amylase

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97
Q

enzymes released from pancreas that help with protein breakdown

A

trypsin (activates proteases) and chymotrypsin

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98
Q

large intestine/colon

A

begins at the cecum which contains the ileocecal valve and is the site for remaining undigested food sent from the small intestine, contains haustra which allow for segmental contraction/movement and teniae coli which run longitudinally beginning at the cecum, has rugae internally

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99
Q

internal anal sphincter

A

made of circular involuntary smooth muscle and innervated by the autonomic nervous system where sympathetic stimulation causes contraction and parasympathetic causes relaxation

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100
Q

large intestine function

A

point at which chyme is considered feces, responsible for the absorption of the remaining water from stool which occurs within haustral saccules, absorption of ions including sodium and potassium and acids/bases, storage and elimination of waste, and production of vitamins B and K, contains > 400 bacterial species

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101
Q

external anal sphincter

A

made of striated voluntary skeletal muscle overlapping the internal anal sphincter and is innervated by the pudendal nerve of the somatic nervous system

102
Q

Griffith’s point

A

watershed area of the large intestine that is supplied by both the SMA and IMA and is more prone to ischemic colitis because it does not have its own artery

103
Q

descending and sigmoid colon/rectum venous drainage

A

IMV which drains into hepatic portal vein

104
Q

cecum and ascending colon venous drainage

A

SMV which drains into hepatic portal vein

105
Q

enteric nervous system includes

A

the submucosal plexus (Meissner plexus), the myenteric plexus (Auerbach), and the subserosal plexus

106
Q

enteric nervous system function

A

assists with movement, blood flow, and secretions

107
Q

rectosigmoid sphincter

A

allows stool to move from the sigmoid colon to the rectum where stretch on the rectum signals the need to defecate

108
Q

anal canal length

A

2.5 - 4 cm

109
Q

dentate/pectinate line

A

the area where anal glands open, dividing the anal canal into upper and lower segments, and is the transition zone between the columnar epithelium of the proximal segment and the stratified squamous epithelium of the distal segment

110
Q

ghrelin

A

hunger hormone that is released from the stomach and rises with food limitations, it helps with energy utilization and glucose usage

111
Q

area of intestine with the most microbes

A

the large intestine which is referred to as the microbiome and colonized within a few hours of birth, can change fairly rapidly depending on diet/exposure where aging will decrease the variations in microbes but does not change the number of bacteria

112
Q

microbiome function

A

assists with the metabolism of bile salts, androgens, carbohydrates, nitrogen compounds, medications, and lipids, produces hormones, neurotransmitters, anti-inflammatory products, and vitamins K and B, destroys certain toxins, and prevents bad guys from setting up shop

113
Q

brain-gut axis (GBA)

A

complex bidirectional communication network between the CNS and the GI tract that is made up of nerve cells (vagus nerve), chemicals, and microbes and involves many pathways including the autonomic and enteric nervous systems, the immune system, and the HPA axis

114
Q

ammonia

A

nitrogen waste primarily from protein breakdown which is converted to ammonia via deamination and then to urea via the ornithine or urea cycle in the liver

115
Q

aspartate aminotransferase (AST)

A

found within the mitochondria of hepatocytes and also the heart, kidney, and brain (functions in gluconeogenesis), will accumulate in the bloodstream 8 hours after cellular damage - will elevate 10X in obstruction and 20X in viral hepatitis

116
Q

alanine aminotransferase (ALT)

A

primarily found within the cytosol of hepatocytes (functions in gluconeogenesis), but also in the kidney, heart, skeletal muscle, and pancreas and elevates with damage/necrosis and cellular breakdown of hepatocytes (more specific for liver damage than AST because it is mostly found in liver and has a longer half-life)

117
Q

alkaline phosphatase (alk phos)

A

found in several tissues including bone (particularly in new bone growth) but in the highest concentration within the biliary tract epithelium and elevates with biliary tree obstruction and cholestatic hepatitis, also found in Kupffer cells and elevates with extrahepatic and intrahepatic obstruction and cirrhosis

118
Q

lactate dehydrogenase (LDH)

A

an enzyme that converts lactate to pyruvate and is found within many cells in the body including hepatocytes, it elevates with hypoxic and primary liver damage (specific isozymes of LDH can be more specific - LDH-5 found in liver and skeletal muscles)

119
Q

AST/ALT ratio seen with hepatitis

A

ALT > AST

120
Q

AST/ALT ration seen with ETOH or advanced cirrhosis

A

AST > ALT (>1)

121
Q

liver function tests indicating hepatocellular injury

A

aminotransferases > alkaline phosphatase

122
Q

liver function tests indicating cholestatic pattern

A

alkaline phosphatase > aminotransferases

123
Q

liver function tests indicating bone problem

A

elevated alkaline phosphatase + normal gamma-glutamyl transferase (GGT)

124
Q

visceral peritoneum innervation

A

autonomic nervous system

125
Q

parietal peritoneum innervation

A

somatic nervous system

126
Q

pain associated with visceral peritoneum

A

diffuse, non-localized, dull, crampy, periodic, not associated with movement - patient may writhe around trying to get rid of the pain

127
Q

pain associated with parietal peritoneum

A

sharp, well-localized, excruciatingly painful, persistent, associated with movement of bowels - patient often lies still to avoid abdominal vibration

128
Q

acute abdomen DDx

A

appendicitis, diverticulitis, acute cholecystitis, acute pancreatitis, perforated ulcer, bowel infarction

129
Q

diverticulosis

A

the presence of diverticula that are not inflamed but are a common cause of acute lower GI bleeds due to blood vessel damage and leaks

130
Q

diverticulitis

A

inflammation of the diverticulum caused by fecalith development within the outpouching leading to edema and swelling which compromises blood supply and results in infection from fecalith bacteria, friability, and possible perforation - can go on to develop large perforation, abscess, and bleeding

131
Q

diverticular disease

A

associated with the Western diet and decreased fiber intake leading to decreased fecal bulk and luminal diameter resulting in firm small stools that require stronger contractions for successful peristalsis which increases luminal pressure and causes herniation of the mucosal and submucosal layers through an area of vascular defect

132
Q

Meckel diverticulum

A

a common and often harmless birth defect that occurs in the small intestine (ileum) and affects 2-3% of babies where it occurs during fetal development and can contain leftover tissue from development that wouldn’t ordinarily be there (from the stomach or pancreas) which can secrete gastric acid into the small intestine

133
Q

ischemic bowel disease

A

decreased blood supply to the bowel through the mesenteric artery (most commonly at Griffith’s point/splenic flexure) which can be due to occlusion associated with atherosclerosis, aortic aneurysm, and/or clot formation or diminished blood flow associated with hypotension, arrhythmia, or sepsis which causes anaerobic metabolism and a buildup of cellular waste products leading to necrosis of the bowel wall, leaky gut, translocation of gut bacteria and bowel gas being trapped within the GI wall sepsis, perforation, and abscess which can be fatal if untreated

134
Q

pneumatosis intestinalis

A

the presence of gas within the wall of the small or large intestine which is commonly recognized as a severe sign of GI disease requiring emergency surgery

135
Q

inflammatory bowel disease (IBD)

A

chronic, relapsing, immunologic diseases hallmarked by GI upset, abdominal pain, weight loss, and fatigue which are known to have a genetic disposition with epigenetic triggers driven by inflammation primarily in response to T helper cells and cytokines resulting in increased free radicals and cellular damage, include ulcerative colitis (UC) and Crohn’s disease (CD) which both have increased 30X increased risk for colon cancer

136
Q

Crohn’s disease

A

transmural patchy inflammation of the GI tract that may involve any section from the mouth to the anus, can be associated with NOD2 (CARD15) genes and most commonly affects the ascending colon and ileum triggered by autoimmune-mediated inflammation of deeper crypts and can spread to lymph nodes and/or form granulomas, presents with prolonged diarrhea, abdominal pain, fatigue, and weight loss where skip lesions or cobblestoning will be seen on colonoscopy - anal fistula, abscesses, fissures, and ulcers are also common

137
Q

ulcerative colitis

A

continuous inflammation limited to the mucosal layer of the colon that involves the rectum and extends proximally forming ulcerations associated with HLA-B27, triggered by an immune response against the GI tract thought to be mediated by cytokine release and neutrophil infiltration (P-ANCA antibodies)

138
Q

extraintestinal manifestations of IBD

A

oral ulcers, arthritis, spondylitis or sacroiliitis, episcleritis or uveitis, erythema nodosum, pyoderma gangrenosum, hepatitis, sclerosing cholangitis, and thromboembolic events

139
Q

toxic megacolon

A

excessive dilation of the colon > 6 cm in diameter due to smooth musculature inhibition which is a rare complication of UC, is associated with infection with C. diff, E. coli, and Salmonella, or caused by medications such as opioids, increases risk of perforation and can also cause leaky gut and translocation of bacteria

140
Q

bowel obstruction

A

small intestinal obstruction is most common but can occur in the large intestine where a mechanical obstruction is a physical blockage and a pseudo-obstruction is an adynamic ileus, obstruction leads to the cessation of flow where chyme, gas, and secretions become built up resulting in proximal luminal distention, emesis, swelling/edema, malabsorption, volume depletion, ischemia, necrosis, and electrolyte abnormalities

141
Q

common causes of small intestine obstruction

A

adhesions or scar tissue from inflammation (from previous surgery and/or infections), hernias, intussusception, tumors, Crohn’s, lymphoma, stricture, stenosis, foreign body, superior mesenteric artery syndrome

142
Q

common causes of large intestine obstruction

A

carcinoma, fecal impaction, ulcerative colitis, volvulus, diverticulitis, intussusception, and pseudo-obstruction

143
Q

ileus

A

a functional small bowel obstruction where there is a lack of peristalsis which is associated with postoperative ileus, opioid use, sepsis or inflammation, bleeding, and neurologic issues - the exact cause unknown

144
Q

volvulus

A

malrotation of the intestine and twisting of the mesentery leading to obstruction most commonly affecting the cecum and sigmoid colon leading to edema, swelling, impaired vascular flow, and necrosis which can be associated with surgeries, congenital risk factors, and shape of GI tract

145
Q

constipation

A

decreased frequency or difficulty with BM from baseline BM habits, it can be primary or secondary with normal transit time, slow transit time, or pelvic floor dysfunction

146
Q

normal transit constipation

A

difficulty with the passage of stool that is able to make it down the sigmoid colon associated with a low fiber diet or low water intake

147
Q

slow transit constipation

A

decreased colonic motor activity that can be idiopathic or secondary to other conditions including DM, autonomic dysfunction, MS, Parkinson’s, medications, hypothyroidism, anorexia nervosa, and systemic sclerosis (may be able to palpate stool)

148
Q

pelvic floor dysfunction

A

when the anal sphincter does not relax and the pelvic floor unable to tighten appropriately which may be associated with hemorrhoids or other anal pathology

149
Q

puborectalis muscle

A

part of the levator ani which stabilizes abdominal and pelvic organs and arises laterally from the symphysis on both sides and encircles the rectum causing a ventral bend between the rectum and anal canal, remains contracted while standing and relaxes when squatting to straighten the rectum and allow defecation

150
Q

appendicitis

A

inflammation of the vermiform appendix which is attached to the cecum near the ileocecal valve causing increased pressure and can lead to necrosis and perforation, most commonly caused by obstruction of the lumen by a fecalith which leads to increased intraluminal pressure and trapped mucus and bacteria (E. coli) which proliferates causing inflammation, tissue ischemia, and rupture followed by the release of bacteria and pus into the peritoneal cavity (can form an abscess, phlegmon, or generalized peritonitis)

151
Q

causes of appendicitis

A

most common is fecalith, calculi, lymphoid hyperplasia, infection, and benign or malignant tumors

152
Q

McBurney’s point

A

1/3 of the distance from the ASIS to the umbilicus

153
Q

anal fistula

A

associated with blockage and/or inflammation of the anal canal and extends to the skin or other contiguous structure/organ with an epithelial lined tract

154
Q

anal abscess

A

associated with infection and inflammation such as an anal gland infection which blocks the anal crypt and prevents drainage

155
Q

anal fissure

A

a tear of the anoderm most commonly in the distal 1/3 of the rectum which can expose the internal anal sphincter causing spasms and pain with decreased blood flow due to tension, associated with trauma, constipation, diarrhea, vaginal delivery, Crohn’s disease, and infectious disease

156
Q

hemorrhoids

A

dilated venous structures classified as internal or external based on whether they originate above or below the dentate line, external hemorrhoids will be more sensitive due to more innervation by the pudendal nerve

157
Q

esophageal diverticula

A

occur at areas of weakness in the musculature of the esophagus and are associated with changes in the UES and difficulty with passage of food bolus, factors that weaken or change esophageal structure such as GERD can increase risk, will not be symptomatic until > 1 cm in diameter

158
Q

Zenker’s diverticula

A

a weakness or outpouching of the esophageal mucosa through Killian’s triangle

159
Q

major esophageal venous drainage

A

esophageal veins (plexus) which drain into the hemiazygos vein which dumps into the left subclavian or azygos vein which dumps into the SVC

160
Q

esophageal varices

A

esophageal venous dilation caused by the backflow of blood into esophageal veins due to increased portal vein pressures > 5mmHg, if > 12 mmHg risk for bleeding or significant varices

161
Q

presinusoidal causes of increased portal vein pressure

A

can be prehepatic (portal vein thrombosis due to sepsis, procoagulopathy, abdominal trauma or surgery, or secondary to cirrhosis) or intrahepatic (schistosomiasis, congenital hepatic fibrosis, drugs, vinyl chloride, or sarcoidosis)

162
Q

sinusoidal causes of increased portal vein pressure

A

hepatic only caused by cirrhosis, polycystic liver disease, nodular regenerative hyperplasia, or metastatic malignant disease

163
Q

post-sinusoidal causes of increased portal vein pressure

A

can be intrahepatic (veno-occlusive disease) or post-hepatic (IVC obstruction, heart failure, Budd-Chiari syndrome)

164
Q

bleeding esophageal varices

A

most commonly occur in the distal esophagus where the risk of bleeding increases with the size of varices because they become more superficial, pressure for the patient, continued drinking, and excess strain on the veins

165
Q

upper GI bleed (UGIB)

A

blood from above the ligament of Treitz

166
Q

lower GI bleed (LGIB)

A

blood from below the ligament of Treitz

167
Q

causes of UGIB

A

esophageal varices, peptic ulcer that erodes into blood vessels, and Mallory-Weiss Tear caused by excessive vomiting (tear in esophageal mucosa near GE junction)

168
Q

UGIB presentation

A

melena (black, tarry, foul-smelling stool due to oxidation by HCl), “coffee-ground” emesis, hematemesis

169
Q

cause of mortality in UGIB

A

metabolic acidosis due to volume loss compensatory failure

170
Q

GERD

A

incompetent lower esophageal sphincter (LES) or decreased tone causing HCl, pepsin, bile, and stomach contents to flow backward into the esophagus causing inflammation, irritation, and breakdown of the esophageal lining, increased vascular permeability and blood flow, edema, friability, erosions, and ulcerations leading to mucosal injury, can lead to fibrosis or precancerous lesions

171
Q

GERD risk factors

A

increased HCl production or exogenous exposure including consumption of ETOH, caffeine, citrus, spicy foods, and soda, impaired gastric emptying, esophageal dysmotility, increased abdominal pressure (obesity and pregnancy), and hiatal hernia

172
Q

Barrett’s esophagus risk factors

A

male, Caucasian, increased age, GERD or reflux, obesity, and smoking

173
Q

complications of GERD

A

strictures, Barrett’s, adenocarcinoma, aspiration, ulceration and bleeding, chronic cough, asthma, sinusitis, chronic laryngitis, and laryngeal and tracheal stenosis

174
Q

H. pylori bacteria

A

a gram-negative curved rod that is transmitted via the fecal-oral route, where most people become infected as a child, and can live in the gastric environment, it has flagella enabling it to burrow into gastric mucus and an outer membrane that protects it from host defenses, when symptomatic it causes a significant inflammatory response through cytokines and releases toxins (ammonia) that cause host epithelial damage resulting in gastritis, peptic ulcers, and suppression of p53 tumor suppressor gene leading to adenocarcinoma, it also causes decreased antral somatostatin

175
Q

esophageal strictures

A

occur most commonly at the GE junction caused by scar tissue formation during the healing process of other primary diseases including GERD, frequent emesis, ETOH use, caustic ingestions, and Crohn’s disease

176
Q

Schatzki’s ring

A

ring of dense membranous tissue that causes a sudden stricture or reduction in the diameter of the esophageal lumen most commonly affecting the distal esophagus, a patient will become symptomatic when the diameter is < 13 mm

177
Q

Barrett’s esophagus

A

a downstream effect of chronic GERD which results from exposure and damage from acidic contents and causes a change from stratified squamous epithelium that typically lines the distal esophageal to metaplastic columnar epithelium or expansion of stomach lining into the esophagus which is a pre-malignant change

178
Q

Mallory-Weiss tear

A

longitudinal tear through the mucosal layer of the esophagus associated with repeated emesis which causes the vascular plexus between the layers to bleed most commonly occurring in the lower portion at the GE junction, does not go through all the esophageal layers

179
Q

esophageal dysmotility

A

umbrella term for lack of coordination or weakness of the expected movements of the esophagus which is typically associated with systemic illness and includes achalasia, esophageal spasms, ineffective esophageal motility, or absent contractility

180
Q

achalasia

A

antibody-mediated autoimmune attack of the myenteric plexus causing decreased peristalsis, decreased relaxation of the LES, and obstruction of the lower esophagus resulting in pain associated with food bolus not reaching the stomach about 15 seconds after ingestion

181
Q

candidiasis

A

most commonly caused by candida albicans (gram-positive yeast with pseudohyphae) which thrives in warm, moist, and dark areas and is more likely under dentures, referred to as thrush when in the mouth but can also spread to the esophagus causing esophagitis where overgrowth creates pseudomembrane, erythema, discomfort, cotton feeling in the mouth, diminished taste, discomfort eating and swallowing, and often associated with angular cheilitis bilaterally

182
Q

gastritis

A

inflammation of the stomach lining which may affect any region and can be acute or chronic caused by disruption of the mucosal barrier that protects the stomach by H. pylori, NSAIDs (inhibit mucus secretion, cause hypermotility), ETOH, and immunologic cause (chronic) which leads to epigastric pain, ulceration, bleeding, and vague pain

183
Q

peptic ulcers

A

breakdown in the protective mucosal lining which can occur in the esophagus, stomach, and duodenum associated with NSAIDs, H. pylori, ETOH, and smoking which may be superficial (erosions) initially but deepen over time and become true ulcers when they penetrate into the muscularis mucosa which causes blood vessel damage and upper GI bleeding

184
Q

hiatal hernia

A

herniation of the upper stomach through the diaphragm caused by short esophagus, fibrosis, and diaphragm pathology, decreases LES pressures

185
Q

type 1 hiatal hernia

A

sliding hiatal hernia where part of the stomach and LES move through the diaphragm

186
Q

type 2 hiatal hernia

A

rolling hiatal hernia where part of the stomach creates an outpouching through the diaphragm but the LES remains in place

187
Q

type 3 hiatal hernia

A

mixed hiatal hernia where the LES and outpouching of the stomach move through the diaphragm

188
Q

location of AST in hepatocytes and other metabolically active tissues

A

mitochondria (has direct sensitivity to severity of disease)

189
Q

location of ALT in hepatocytes

A

cytosol

190
Q

AST half-life

A

short - will elevate 8 hours after cell damage and peak at 24-46 hours

191
Q

ALT half-life

A

longer than AST, also more specific to liver

192
Q

AST elevation seen with hepatitis

A

20X

193
Q

AST elevation seen with obstruction

A

10X

194
Q

AST/ALT ratio > 5 indicates

A

extrahepatic cause like rhabdo or vigorous exercise

195
Q

location of alkaline phosphatase

A

present in several tissues including bone but of the highest concentration in the biliary tract epithelium, also present within Kupffer cells of the liver (elevated in children and in pregnancy in placenta)

196
Q

alkaline phosphatase function

A

transports metabolites - increases with intrahepatic and extrahepatic obstruction and in cirrhosis (also with rapid bone turnover and in pregnancy)

197
Q

lactate dehydrogenase (LDH)

A

an enzyme found in many tissues, not very specific to one organ, functions to convert lactate to pyruvate

198
Q

bilirubin

A

a byproduct of RBC breakdown in the spleen and liver where heme oxygenase enzymes convert it into biliverdin in the bloodstream producing unconjugated bilirubin which becomes bound to albumin and transported to the liver for conjugation

199
Q

causes of indirect/unconjugated hyperbilirubinemia

A

increased production (hemolysis - megaloblastic anemia, sickle cell, trauma - extravasation/bruising, overactive spleen, liver, and bone), decreased hepatic uptake (sepsis - reduced circulation and with medications like Rifampin), and decreased conjugation in the liver by GT (Gilbert’s syndrome and Crigler-Najjar syndrome - complete or partial loss of GT function)

200
Q

causes of direct/conjugated hyperbilirubinemia

A

hepatocellular dysfunction causing intrahepatic cholestasis due to cirrhosis, hepatitis, NASH, ETOH, medications, etc., biliary duct compression due to malignancy or infection causing cholestasis, and biliary duct obstruction due to choledocholithiasis or PSC causing cholestasis

201
Q

jaundice

A

indicates direct or indirect hyperbilirubinemia usually > 2 mg/dL (normal = < 1 mg/dL)

202
Q

form of bilirubin excreted in urine and feces

A

urobilinogen which is converted by bacterial enzymes in the intestine and urinary tract

203
Q

metabolism of ETOH in the liver

A

ETOH is absorbed in the stomach and travels through the bloodstream to the liver where it is converted to acetaldehyde in the cytosol of hepatocytes which can cause direct DNA damage to hepatocytes if in excess, this will lead to engorgement and eventual death of hepatocytes and the inflammation will trigger activation of Kupffer cells

204
Q

steatosis

A

reversible lipid deposition within the liver which begins at the central vein and spreads out through the lobule which will progress to steatohepatitis (inflammation and necrosis of hepatocytes due to acetaldehyde, genetic disposition, and oxygen radicals) and fibrotic liver disease (breakdown of deposited lipids to form free radicals and further inflammation) leading to cirrhosis (irreversible fibrosis) if the insulting agent (ETOH) is not stopped

205
Q

cirrhosis

A

irreversible inflammation leading to Kupffer cell activation, the release of inflammatory mediators, activation of fibrogenic hepatic stellate cells, and fibrosis of the liver which changes or blocks the flow of bile and blood within the liver lobule causing hepatic impairment with increased levels of toxins (ammonia), metabolic changes, jaundice, and portal HTN - usually secondary to another liver disease such as ETOH liver disease, HCV, or NASH

206
Q

cirrhosis complications

A

jaundice, portal HTN, ascites, varices, hepatorenal syndrome, hepatopulmonary syndrome, portopulmonary syndrome, and hepatic encephalopathy

207
Q

NAFLD

A

triglyceride infiltration into hepatocytes with no ETOH involvement which can progress to nonalcoholic steatohepatitis and cirrhosis

208
Q

NAFLD risk factors

A

genetic disposition, obesity, hypercholesterolemia, hypertriglyceridemia, and change in gut microbiome

209
Q

portal hypertension

A

pressure > 5 mmHg in portal vein due to resistance in flow which is usually a downstream effect of a prehepatic, intrahepatic, or posthepatic disease process

210
Q

normal portal system pressure

A

3 - 5 mmHg

211
Q

prehepatic causes of portal HTN

A

portal vein thrombosis due to malignancy, hypercoagulable state, septicemia, decreased flow (cirrhosis), trauma/inflammation (pancreatitis, hepatitis)

212
Q

intrahepatic causes of portal HTN

A

thrombosis, inflammation, cirrhosis, infectious hepatitis, and schistosomiasis

213
Q

posthepatic causes of portal HTN

A

Budd-Chiari syndrome (hepatic vein thrombosis), posthepatic thrombosis, and RV failure

214
Q

ascites

A

excess fluid from the vascular system, the intestines, and liver lymph secretion causing a transudative effusion, associated with a change in hydrostatic pressure that outweighs capillary osmotic pressure, within the peritoneal cavity secondary to increased portal pressure (portal HTN) and decreased albumin, may also be associated with malignancy, nephrotic syndrome, malnutrition, and right heart failure

215
Q

complications of ascites

A

decreased intravascular volume and renal blood flow resulting in increased ADH release and activation of RAAS which leads to increased Na+ and H2O reabsorption worsening the problem, translocation of bacteria from the intestines due to increased intraluminal pressure can result in spontaneous bacterial peritonitis (BAD!!!)

216
Q

ascites presentation

A

distended abdomen, weight gain, SOB b/c of decreased diaphragmatic excursion, peripheral edema, and hyponatremia

217
Q

hepatitis A virus

A

nonenveloped RNA picornavirus (hepatovirus) transmitted via fecal-oral route that causes acute infections but no chronic disease processes most commonly associated with travel to endemic areas, at risk groups include MSM, IVDU, and those working with primates, has a 28-day incubation period which is when patient is the most contagious due to amount of fecal shedding

218
Q

hepatitis A presentation

A

acute onset of fever/chills, N/V, clay-colored stools, arthralgias, abdominal discomfort, jaundice, dark urine, and hepatomegaly

219
Q

time at which hepatitis A antibodies develop

A

anti-HAV IgM antibodies develop at 4 weeks and decline following acute infection and viral clearance, IgG develops later and remains elevated for years (long-term immunity) - can prevent infection with HAV vaccine

220
Q

hepatitis B virus

A

double-stranded DNA virus that is transmitted via mucosal contact or blood-borne with high rates of vertical transmission (mom-baby) and also transmitted sexually, via contaminated needles and open sores, can survive for 7 days on fomites and has a 1-4 month incubation period, most common liver infection worldwide, linked with hepatocellular carcinoma, and more infectious than hepatitis C

221
Q

hepatitis B infection

A

infiltrates the hepatocytes where it replicates and causes an inflammatory response in the liver, lysis of hepatocytes, and release of ALT and AST resulting in scarring, this causes decreased liver function and production of albumin, clotting factors, gluconeogenesis, toxin (bilirubin, ammonia) excretion, resistance to blood flow resulting in portal HTN, encephalopathy, and cirrhosis

222
Q

hepatitis B presentation

A

most commonly subclinical infection but later symptoms include ascites, fatigue, anemia, and encephalopathy, rarely causes fulminant hepatic failure

223
Q

hepatitis C virus

A

enveloped ss-RNA virus (flavivirus) that is blood-borne similar to hepatitis B with a high rate of chronic liver disease which can lead to cirrhosis and hepatocellular carcinoma, has a 4-12 week incubation period

224
Q

hepatitis C presentation

A

abdominal discomfort, N/V, jaundice, and fatigue which may develop into chronic infection, can also be asymptomatic with chronic infection or have intermittent flares

225
Q

hepatitis D virus

A

hepatovirus that usually occurs concomitantly with hepatitis B and increases patient’s risk for hepatocellular carcinoma

226
Q

hepatitis E virus

A

hepatovirus transmitted via fecal-oral route through contaminated water in endemic areas, typically self-limited

227
Q

hepatic failure

A

may be fulminant, non-fulminant, chronic, or acute where acute disease lasts < 26 weeks, often occurs acutely with an underlying chronic liver condition causing acute hepatic necrosis

228
Q

liver abscess

A

most commonly causes a visceral abscess that is polymicrobial involving anaerobic organisms, streptococci, and staph seen in immunocompromised patients, DM, transplant patients, patients on PPIs, hepatobiliary disease, and pancreatic disease, occurs via contiguous spread with SBP and biliary infection due to obstruction or gallstones or hematogenous spread with endocarditis (strep/staph)

229
Q

liver abscess presentation

A

abdominal pain, fever, N/V, weight loss, and elevated AST, ALT

230
Q

pancreas

A

made of head, neck, body, and tail where the head is attached to the duodenum, the uncate process extends inferiorly, the neck lies next to the stomach pylorus, and the tail is anterior to the kidney

231
Q

cells within the pancreas

A

Islets of Langerhans which produce insulin and glucagon and make up 1% of the total pancreas volume and acinar cells which produce digestive enzymes and make up 99% of the total pancreas volume

232
Q

CCK functions

A

stimulates gallbladder contraction and relaxation of the sphincter of Oddi, augments trypsin output from acinar cells, increases bicarbonate secretion from ductal cells, increases pancreatic mass, relaxes the proximal stomach and stimulates contraction of the pylorus (delaying gastric emptying), and induces satiety

233
Q

secretin function

A

released into bloodstream by intestinal mucosa and stimulates the pancreas to secrete pancreatic juice rich in bicarbonate ions which neutralizes acidic chyme

234
Q

pancreatitis

A

inflammation of the pancreas due to acinar cellular injury or pancreatic duct issue which is associated with ETOH, biliary obstruction, trauma, hyperlipidemia, smoking, and medications

235
Q

acute pancreatitis

A

blockage of CBD due to gallstones or increased toxic metabolites within the pancreas due to chronic ETOH use resulting in sphincter of Oddi spasms (protein buildup and obstruction) which leads to a backup of pancreatic secretions and increased pressure in the pancreas, the pressure compresses blood vessels causing tissue ischemia and activates of proteases which digest pancreatic tissue and inflammation worsens causing systemic response (cytokine release) and severe epigastric pain due to stimulation of nerves in parietal peritoneum

236
Q

Cullen’s sign

A

bruising in the peri-umbilical region suggesting intra-abdominal hemorrhage (seen in pancreatitis)

237
Q

Grey-Turner’s sign

A

bruising along both flanks suggesting intra-abdominal hemorrhage (seen in pancreatitis)

238
Q

pancreatitis complications

A

pancreatic pseudocysts and pancreatic necrosis/abscesses

239
Q

chronic pancreatitis

A

fibrotic destruction of the pancreas with calcification associated with ETOH use, smoking, recurrent acute pancreatitis, often idiopathic, results in pain with intraductal pressure and ischemia

240
Q

chronic pancreatitis presentation

A

weight loss (malnutrition, poor absorption), decreased vitamin absorption, exocrine and endocrine pancreatic dysfunction and breakdown of acinar cells, Islets of Langerhans, ductal cells, and increased fibrosis

241
Q

acute pancreatitis presentation

A

sudden, severe epigastric pain which may radiate to the back, fever, N/V, diminished bowel sounds, and profound dehydration

242
Q

cholelithiasisis

A

gallstones that form as a result of decreased cholesterol, bilirubin, and bile acid metabolism which also contain fatty acids, unconjugated bilirubin, calcium, and phosphate where the type is determined based on the percentage of composition plus appearance - cholesterol are the most common (supersaturation of cholesterol forming crystals, microstones, and then macrostones), pigmented types are brown (soft) and black (hard) stones, form during times of fasting when GB is non-contractile and cholesterol can pool

243
Q

biliary colic

A

temporary pain due to stone lodging in the cystic duct most commonly after a fatty meal when GB contracts, stone then becomes dislodged and pain improves

244
Q

cholecystitis

A

gallstone within the cystic duct which causes obstruction, inflammation, and GB distention leading to swelling and ischemia, can cause necrosis and perforation

245
Q

cholecystitis presentation

A

radiating pain to the back and right shoulder, initially dull, diffuse abdominal pain referred to the epigastric region, fever, N/V, tachycardia, positive Murphy’s sign, later persistent RUQ pain, abdominal guarding and peritoneal signs, and dehydration

246
Q

choledocholithiasis

A

gallstone within the CBD causing prolonged RUQ pain associated with consistent blockage (not biliary colic) and elevated AST/ALT, and with time alk phos and bilirubin due to cholestasis

247
Q

complications of choledocholithiasis

A

acute pancreatitis and ascending cholangitis

248
Q

cholangitis

A

partial obstruction of the CBD typically caused by gallstones but also can be due to malignancy, stricture, iatrogenic, parasites, or sclerosis where increased pressure in the bile duct leads to reduced flushing of bile out, damaged biliary ductal epithelium, and ascension of bacteria from duodenum through the sphincter of Oddi most commonly E.coli, Klebsiella, Strep, and Pseudomonas which reduces excretion of bile leading to hyperbilirubinemia and jaundice, increased Alk phos and GGT, fever, increased WBCs, tachycardia, hypotension, confusion, and oliguria which can lead to septic shock

249
Q

phenylketonuria (PKU)

A

congenital amino acid metabolism disorder that is autosomal recessive causing a deficiency in tyrosine due to phenylalanine hydroxylase deficiency leading to elevated levels of phenylalanine which can cause oxidative stress, intellectual disability, and decreased brain development, myelination and neurotransmitter synthesis issues, heart defects, and skins changes which can be fatal, varies in severity - causes musty odor to urine, sweat, and breath

250
Q

tyrosine functions

A

made from phenylalanine and functions in protein, hormone, and neurotransmitter synthesis and regulation including epinephrine, dopamine, norepinephrine, and melanin

251
Q

hereditary hemochromatosis

A

congenital abnormality leading to increased iron absorption and iron overload due to autosomal recessive HFE gene disorder which modulates (reduces) the expression of hepcidin which is made in the liver and regulates iron homeostasis, when iron is high hepcidin gene (HAMP) is typically upregulated and slows or stops absorption

252
Q

Wilson’s Disease

A

autosomal recessive genetic disorder leading to copper metabolism mutation and dysfunction of hepatic copper transporter gene ATP7B leading to accumulation of copper in tissues such as the brain, liver, and cornea (typically excreted in bile) resulting in hepatocyte injury, necrosis, and apoptosis, increased circulating copper, and deposits within the brain and eye (Kayser-Fleischer rings)

253
Q

Wilson’s Disease lab findings

A

decreased serum ceruloplasmin, increased AST, ALT, and bilirubin, and increased free copper

254
Q

ulcerative colitis presentation

A

bloody diarrhea, weight loss, abdominal cramping, tenesmus, urgency, and frequency where ulcerations and pseudopolyps may be seen on colonoscopy

CABS III (5 decks)

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