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Semester 2 Medical School > Digestive > Flashcards

Digestive Flashcards

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USMLE® Step 1 flashcards
1
Q

What separates the anterior/oral and posterior/pharyngeal surfaces of the tongue?

A

The sulcus terminalis. (Foramen cecum at its apex is the origin of the thyroid gland).

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2
Q

What is the epithelial lining of the anterior 2/3 of the tongue?

A

Ventral - nonkeratinized stratified squamous. Dorsal - keratinized stratified squamous.

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3
Q

How many tongue muscles are there - how are they aligned and with what nerve are they controlled?

A

3, orthogonally, CN XII.

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4
Q

What are the types of papillae and which have taste buds?

A

Filiform (most abundant), Fungiform (taste buds on dorsal surface, less keratin), Circumvallate (generally nonkeratinized, 250 taste buds/papilla facing laterally), Foliate (rudimentary in human).

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5
Q

What kind of glands are in circumvallate papillae?

A

Serous Von Ebner’s glands.

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6
Q

What kind of secretions are in sublingual, submandibular, parotid glands?

A

Sublingual - mixed, mainly mucous Submandibular - mized, mainly serous Parotid - just mucous

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7
Q

What sort of cells surround salivary secretory portions?

A

Myoepithelial cells.

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8
Q

Describe the salivary intralobular ductal system.

A

Acini empty into intercalated ducts (cuboidal epithelium), which join to form striated ducts (has basal striations, actively moves Na+ from saliva into the EC space).

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9
Q

What is the lining of the salivary interlobular ductal system?

A

Variable, but right before emptying into the oral cavity, the main duct if each gland is stratified squamous nonkeratinized epithelium.

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10
Q

What are the four layers of the gut tube?

A

Mucosa, submucosa, muscularis externa, adventitia/serosa?

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11
Q

Where is the Meissner’s plexus located?

A

In the submucosa.

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12
Q

Where is the Myenteric/Auerbach’s plexus located?

A

In the muscularis externa.

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13
Q

When is it adventitia and when is it serosa?

A

Adventitia when the outer layer is attached to the surrounding tissue. Serosa when the outer layer is adjacent to the peritoneal cavity.

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14
Q

Describe the mucosa of the esophagus.

A

Nonkeratinized stratified squamous epithelium, cardiac glands, thin lamina propria. Upper esophagus has no muscularis mucosa, lower has a single longitudinal layer. At the gastroesophageal junction it becomes simple columnar.

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15
Q

What is in the esophageal submucosa?

A

Esophageal glands that secrete mucus.

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16
Q

What kind of muscle is in the esophageal muscularis externa?

A

Starts out skeletal, then mixed, then just smooth.

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17
Q

When in the esophagus is it adventitia and when is it serosa?

A

Adventitia in the thorax, serosa in the abdomen.

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18
Q

What epithelium lines the stomach?

A

Simple columnar.

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19
Q

What is the mucosa like in the cardia of the stomach and what cell types are there?

A

No goblet cells, glands are as big as the pits, long, branched, coiled. Mucus secreting cells, SCs, EECs, few parietal cells.

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20
Q

What is the mucosa like in the fundus/body of the stomach and what cell types are there?

A

Shallow puts and deep glands (straight). Neck of glands has mucus cells, SCs, lots of parietal cells. Base of glands has few parietal cells, chief cells, mucus cells, EECs.

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21
Q

What is the mucosa like in the pylorus of the stomach and what cell types are there?

A

Deep pits and short glands (coiled). Mucus secreting cells are predominant, G cells, D cells.

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22
Q

What do parietal/oxyntic cells produce? In what part of the glands are they?

A

HCl and IF. Upper 1/2 of gland.

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23
Q

What do Chief cells produce and what are their alternate names? In what part of the glands are they? What do they look like in histological staining?

A

Peptic/Zymogenic cells. They produce pepsinogen and a weak lipase. Lower 1/3 of gland. Basophilic, granules are visible, triangular in shape, smaller than parietal cells.

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24
Q

What are EECs alternate names?

A

APUDs (Amine precursor uptake and decarboxylation), Gastro/entero endocrine cells.

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25
Q

Where are stem cells in gastric pits?

A

The neck region.

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26
Q

What is the difference between mucus made by mucus neck cells in the neck and base?

A

Neck ones secrete less viscous mucus than on the surface.

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27
Q

Desctibe the submucosa of the stomach.

A

No glands, large blood vessels, Meissner’s plexus.

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28
Q

Describe the muscularis externa of the stomach.

A

3 muscle layers - inner oblique, middle circular, outer longitudinal.

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29
Q

Does the stomach have adventitia or serosa?

A

Serosa.

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30
Q

What are the lengths of the duodenum, jejunum, and ileum?

A

Duodenum - 25cm Jejunum - 2.5m Ileum - 3.5m

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31
Q

Describe the cells in the mucosa of the small intestine.

A

Simple columnar absorptive enterocytes (striated brush border with microvilli, decrease in frequency towards LI, coated in glycocalyx). Goblet cells (increase in frequency towards LI). EECs (D cells, EC cells, G cells, S cells, I cells, K cells). Paneth cells (base of crypts). Stem cells.

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32
Q

Does the small intestine have a muscularis mucosa?

A

Yes.

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33
Q

Describe the submucosa of the small intestine.

A

Includes Meissner’s Plexus. Duodenum has Brunner’s Glands, ileum has Peyer’s patches covered by M (microfold) cells.

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34
Q

Describe the muscularis externa of the small intestine.

A

Has Myenteric Plexus between the two layers.

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35
Q

Is the small intestine serosa or adventitia?

A

Serosa where it lies free in the abdominal cavity, adventitia where it is attached to the body wall.

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36
Q

What does the small intestine mucosa look like in Celiac’s disease?

A

Flattened villi.

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37
Q

What is the primary function of the large intestine?

A

Resorbtion of water and salts.

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38
Q

Describe the mucosa of the large intestine.

A

Simple columnar epithelium, no villi just crypts, no plicae circularis. Goblet cells, EECs, SCs, lamina propria (cellular, prominent lymphocytes, scattered nodules).

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39
Q

Does the large intestine have a muscularis mucosa?

A

Yes.

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40
Q

Describe the muscularis externa of the large intestine.

A

The outer longitudinal layer is formed into 3 longitudinal strips - teniae coli.

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41
Q

What cells are in the crypts of the large intestine epithelia?

A

The lower 2/3 entirely goblet cells. Has EECs, SCs too.

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42
Q

What is Hirschprung’s disease?

A

The absence of parasympathetic cells in the myenteric and submucosal plexus of the distal colon/rectum. (due to the arrest of the migration of neural crest cells). This leads to an aganglionic region that cannot relax - functional colonic obstruction.

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43
Q

What is special about the appendix?

A

It has the most lymphatic nodules per unit area of any GI organ.

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44
Q

What is the epithelial lining of the rectum and anus?

A

Upper 1/2 of rectum - simple columnar, lower 1/2 of rectum - stratified squamous non keratinized, anus - stratified squamous keratinized.

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45
Q

What is the name of the capsule encapsulating the liver?

A

Glisson’s capsule.

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46
Q

What is the portal triad that all the portal canals contain areas of?

A

Portal vein, hepatic artery, bile duct.

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47
Q

What is the space of Mall?

A

The periportal space between the CT and hepatocytes, where lymph originates.

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48
Q

What drains into the central vein?

A

The hepatic artery (nutrient poor, oxygenated blood) and portal vein (nutrient rich, deoxygenated).

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49
Q

Where do the central veins drain into?

A

The hepatic veins, which go into the IVC.

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50
Q

How do blood and bile flow through the hepatocyte?

A

Blood goes into the center through the periphery, bile goes outward.

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51
Q

Describe the classic hepatic lobule. What does it emphasize?

A

Central vein in the center, hexagonal. Emphasizes the endocrine function of the hepatocyty.

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52
Q

Describe the portal lobule.

A

A triangle with a central vein at each vertex. Each triangle is drained by a single bile duct. It emphasizes exocrine areas and flow of bile.

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53
Q

Describe the hepatic acinus.

A

Blood from each acinus supports two or more classic lobules. It emphasizes the different oxygen and nutrient contents of blood. The closer to the central vein the lower the oxygen content - periportal, mid-zonal, centrilobular spaces.

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54
Q

Describe the structure of a hepatocyte.

A

Can be binucleated, are cube-like with 6 major surfaces (2 sinusoidal and 4 lateral). Sinusoidal domains covered in microvilli that project into the space of Disse. The lateral domains form the bile canaliculi.

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55
Q

What are hepatic sinusoids?

A

Specialized capillaries that carry blood through the parenchyma; have sinusoidal endothelium, Ito cells (fat storing in space of Disse, store vit A, secrete lipid collagen), and Kupffer cells (macrophaces, APCs).

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56
Q

What are bile canaliculi? Where do they drain into?

A

Small, tubular, PM-bound enlargements in the EC space between two adjacent hepatocytes, sealed by zonula occludens. They drain into the canals of Hering (short simple epithelia), which drain into bile ducts.

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57
Q

Does the gallbladder have all the layers of the gut tube>

A

Not submucosa.

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58
Q

What’s the gallbladder mucosa like?

A

Simple columnar, lamina propria, no muscularis mucosa.

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59
Q

What’s the gallbladder muscularis externa like?

A

Muscle fibers oriented in all directions to facilitate emptying.

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60
Q

Does the gallbladder have serosa or adventitia?

A

Adventitia when it’s in contact with the liver.

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61
Q

Does the pancreas have a capsule?

A

Yes it does, CT divides it into lobes and lobules.

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62
Q

How do the islets of Langerhans stain in the pancreas?

A

Light.

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63
Q

What is in the lumen of pancreatic acini?

A

Centroacinar cells that form the beginning of the duct system. They are a distinguishing characteristic of this gland.

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64
Q

Where do the pancreatic acinars drain into? How are those things lined?

A

Centroacinar cell into intercalated duct (squam or cuboidal) into intralobular duct (cuboidal) into small and then large interlobular ducts (columnar) then into the main pancreatic duct (of Wirsung) (cuboidal).

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65
Q

How do pancreatic acinar cells stain?

A

Blue at the base (more RNA/nuclei) and pink at the amex (lots of zymogens).

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66
Q

What do the different cells in the islets of langerhans produce?

A

Alpha cells make glucagon, beta cells make insulin, delta cells make somatostatin.

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67
Q

Does the GI tract net ingest or net secrete liquid?

A

Secrete.

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68
Q

Where do water and lipid soluble things go once they’re absorbed from the intestines?

A

Water soluble goes to blood. Lipid soluble are packaged into chylomicrons to join the lymph.

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69
Q

Describe the two muscle layers and how they act in peristalsis when there is a bolus.

A

Oral to bolus - circular SM contracts, longitudinal SM relaxes. Anal to bolus - circular SM relaxes, longitudinal SM contracts.

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70
Q

What does the Myenteric/Auerbach’s Plexus control?

A

GI motility.

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71
Q

What does the Meissner’s/Submucosal Plexus control?

A

GI secretions.

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72
Q

What is intrinsic and extrinsic control of the digestive system?

A

Intrinsic control is when it’s 100% mediated by the enteric NS “short loop”, extrinsic control is when the autonomic system is involved (can completely override the ENS) “long loop”.

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73
Q

What are the excitatory substances in the digestive system smooth muscle?

A

Acetylcholine, Substance P. Substance P made by myenteric stimulatory motor neurons.

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74
Q

What are the inhibitory substances in the digestive system smooth muscle?

A

Vasoactive Intestinal Peptide (VIP), NO. NO made by myenteric inhibitory motor neurons. NorE can also inhibit smooth muscle contraction but the ENS neurons typically do not use it.

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75
Q

Is salive hypo, iso, or hypertonic to plasma?

A

Hypotonic. Watery, contains ions.

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76
Q

Where is the water processed in salivary glands?

A

All in the acini. Ducts have tighter junctions than acini.

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77
Q

What is the primary salivary secretion?

A

Made by acinar cells, found in acinar lumen. Ions are similar to plasma, contains some proteins.

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78
Q

What is salivary ductal processing?

A

Na+ and Cl- reabsorbed from primary saliva.

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79
Q

What is saliva like at high and low flows?

A

Very hypotonic at the slowest flow (highest K+). At fastest flow, elevated bicarbonate and NaCl (inefficient reabsorption). Less hypotonic.

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80
Q

How do parasympathetic and sympathetic stimulation affect the medullary salivatory nucleus?

A

PNS increases flow and stimulates watery parotid secretions. SNS reduces flow (still flow though) and stimulates thicker, enzyme rich submucosal secretions. Both have both, neither have neither.

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81
Q

Where is the swallowing center? What’s it stimulated by?

A

Medulla and lower pons. Touch receptors in the oropharynx.

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82
Q

What is the position of things when the bolus of food is in the mouth and then the pharynx?

A

Mouth - nasopharynx closed, tongue up and back. Pharynx - larynx pulled up against epiglottis, UES relaxed.

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83
Q

What stimulates the lower esophageal sphincter between and during swallows?

A

Between swallows - vagal excitatory fibers (ACh, SP). During swallow - vagal inhibitory fibers (VIP, NO).

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84
Q

How are protein/peptide hormones metabolized?

A

Quickly - act fast and are secreted quickly, fast on and fast off.

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85
Q

What are enterogastrones?

A

Peptide hormones secreted by the duodenum to inhibit gastric function.

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86
Q

Where is gastrin made?

A

In G cells - most in the antrum of the stomach but some in the duodenum.

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87
Q

What is gastrin’s signal?

A

Main is oligopeptides and amino acids in the gastric lumen (minor is the in the duodenal lumen).

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88
Q

What does gastrin do?

A

Stimulates ECL (enterochromaffin-like) cells to secrete histamine, and parietal cells to secrete HCl-rich juice. This increases gastric motility but also pyloric constriction.

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89
Q

Where is CCK made?

A

I cells found mainly in the duodenum and jejunum

.

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90
Q

What is CCK’s signal?

A

Fatty acids in the duodenal/duodenal lumen. Minorly - oligopeptides and amino acids in duodenal lumen.

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91
Q

What does CCK do?

A

Acts on gallbladder smooth muscle and makes it contract and secrete bile,acts on pancreatic acinar cells and stimulates pancreatic enzyme secretion. Also acts on ANS sensory neurons and causes pylorus constriction and gallbladder contraction (ACh) and Sphincter of Oddi relaxation (VIP) - reduces gastric emptying and increases concentrated bile secretion. Reduces gastric secretions (parietal cells?)

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92
Q

Where is secretin made?

A

By S cells mainly in the duodenum (some in the jejunum).

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93
Q

What is secretin’s signal?

A

pH under 4.5 in the duodenal lumen - minorly in the jejunal lumen.

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94
Q

What does secretin do?

A

Target pancreatic acinar cells and ducts, gallbladder bile ducts - increases secretion of bicarbonate (increases glalbladder bile secretion?)

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95
Q

Where is GIP made?

A

K cels in the duodenum and jejunum.

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96
Q

What is GIP’s signal?

A

Carbs, proteins, lipids in the intestinal lumen.

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97
Q

What is GIP’s target?

A

Pancreatic beta cells (potentiates insulin secretion), parietal cells, G cells (inhibit gastric secretion and motility).

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98
Q

Where is motilin made?

A

M cells in the duodenum and jejunum.

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99
Q

What is the main signal of motilin?

A

Not very well understood, lack of nutrients.

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100
Q

What is motilin’s target?

A

Stimulates intense contractions in the migrating motor complex.

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101
Q

What is gastric accommodation and receptive relaxation.

A

Vagally mediated fundus gastric wall relaxation in the cephalic phase (before swallowing) and gastric phase (after food is swallowed) respectively.

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102
Q

What are the effects on fatty and acidic meals on digestion?

A

Slow it down - acidic meals moreso.

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103
Q

What receptors do parietal cells have?

A

CCK, M3, H2 (histamine).

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104
Q

What affect does aspirin have on the GI system?

A

Reduces bicarbonate secretion.

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105
Q

Describe the effect of vagal neurons on gastric acid secretion.

A

Increases - stimulate parietal cells, ECL cells, G cells, inhibit D cells.

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106
Q

How does somatostatin affect the GI system?

A

It inhibits parietal cells, inhibits ECL cells, inhibits G cells. Decreases acid.

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107
Q

How do prostaglandins affect the GI system?

A

Inhibit parietal cells. Decreases acid.

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108
Q

What % of acid secretion happens in what phases of swallowing?

A

30% in cephalic (mediated by vagal signals), 60% in gastric (feedback from stomach signals), 10% in intestinal (feedback from duodenal signals).

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109
Q

What is the sodium concentration in gastric juice at different flow rates?

A

High at low flow, low at high.

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110
Q

Describe glycerophospholipids and name the 4 relevant ones.

A

Glycerol backbone, 2FAs (middle one usually unsaturated) attached through ester bonds. Phosphatidylserine, phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol.

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111
Q

What lipid does E. coli not have in its membrane?

A

Cholesterol.

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112
Q

How are phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol synthesized?

A

G3P is made from DHAP (or straight from glycerol in the liver) then 2FAs are added to make phosphatidic acid (DAG phosphate). Phosphatidic acid can also be converted to DAG. Either the lipid or the headgroup are primed with cytidine triphosphate.

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113
Q

How is phosphatidylserine synthesized?

A

From phosphatidylethanolamine in the liver using phosphatidylethanolamine serine transferase. PS can also be decarboxylated to PE which can then be methylated to PC.

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114
Q

What does phospholipase A do?

A

Cleaves FAs from glycerol (A2 can release arachidonic acid from PI or PE).

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115
Q

What does phospholipase C do?

A

Cleaves the headgroup in a glycerophospholipid between glycerol and the phosphate.

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116
Q

What does phospholipase D do?

A

Cleaves the headgroup in a glycerophospholipid after the phosphate. Found primarily in plants.

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117
Q

What is a sphingolipid?

A

Ceramide (sphingosine + FA) + headgroup.

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118
Q

What is the headgroup on sphingomyelin?

A

Choline.

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119
Q

What is an important role that glycerosphingolipids play?

A

They are in the PM outer membrane, play an important role in intracellular communication. ABO blood groups, essential membrane component (6% of gray matter membrane lipids).

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120
Q

How is sphingosine synthesized?

A

Serine and palmitoyl CoA are combined to make sphingamine (C-C bond with serine). Then a second hydrocarbon chain is added to the amine (forming and amide bond) and this makes sphingosine. The first hydrocarbon is oxidized to introduce a double bond, while another fatty acyl CoA is added (making ceramide).

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121
Q

What is the glycocalyx?

A

Outer carb coating on membranes, made from glycolipids. It is dark staining on EM.

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122
Q

What enzymes make a type A blood antigen and which make type B?

A

A = N acetylgalactosamine B = galactose trasferase Added onto terminal galactose.

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123
Q

What is a ganglioside?

A

A type of glycosphingolipid. A ceramide group, branch structure of sugars, first sugar typically glucose. Key feature is 1 or more N-acetylneuraminic acid (NANA/sialic acid) residues. It is broken down in lysosomes.

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124
Q

When sphingomyelin is made from phosphatidylcholine, what is the other product?

A

DAG.

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125
Q

What is a ceramide (not the group, the lipid).

A

A ceramide group, with a linear chain of sugars starting with glucose.

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126
Q

What are cerebrosides?

A

Ceramides with a single sugar residue (usually glucose or galactose).

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127
Q

What are globosides?

A

Ceramides with more than one sugar in a linear linkage.

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128
Q

In Tay-Sach’s disease, what enzyme is defective and what accumulates?

A

Defective - Hexasominisade A Accumulates - GM2 ganglioside

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129
Q

How is Tay-Sachs inherited and what are the symptoms?

A

Autosomal recessive. Classic version is infantile onset (3-6mo), death by 3 years. Growth retardation, dysphagia, seizures, decreaed mental skills and muscle tone, deafness, blindness, paralysis, cherry red spot in the macula surrouned by grey-white.

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130
Q

In Gaucher’s disease, what enzyme is defective and what accumulates?

A

Defective - glucocerebrosidase Accumulates - glucocerebroside in spleen, liver, lungs, bone marrow, brain.

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131
Q

How is Gaucher’s inherited and what are the symptoms?

A

Autosomal recessive. Hepatosplenomegaly, mental retardtion in type 2 and 3, skeletal disorders and anemia in type 1.

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132
Q

In Fabry disease, what enzyme is defective and what accumulates?

A

Defective - alpha galactosidase A Accumulates - globosides in eyes, kidneys, cardiovascular, autonomic NS.

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133
Q

How is Fabry Disease inherited and what are the symptoms?

A

X-linked. Kidney failure, heart failure/stroke, burning in hands, red-purple skin rashes.

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134
Q

In Niemann-Pick disease, what enzyme is defective and what accumulates?

A

Defective - sphingomyelinase Accumulates - sphingomyelin in spleen, liver, lungs, brain, bone marrow

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135
Q

How is Niemann-Pick disease inherited and what are the symptoms?

A

Autosomal recessive. Type A - jaundice, hepatomegaly, profound infantile brain damage. Type B - hepatosplenomegaly in teens. Type C/D - moderate splenohepatomegaly, extensive brain damage as an adult. Bone marrow transplant can be done.

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136
Q

In Krabbes disease, what enzyme is defective and what accumulates?

A

Defective - beta galactosidase Accumulates - galactocerebroside. Presence of globoid cells, breakdown of myelin in nerves, destruction of brain cells.

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137
Q

How is Krabbes inherited and what are the symptoms?

A

Autosomal recessive. Mental and motor deterioration, irritability, fever, seizures, vomiting, weakness, feeding issues, deafness, blindness. Presence of globoid cells, breakdown of myelin in nerves, destruction of brain cells.

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138
Q

In Sandhoff disease, what enzyme is defective and what accumulates?

A

Defective - Hex A and B (A has alpha and beta subunits, B is beta homodimer). Accumulates - GM2 and globosides.

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139
Q

How is Sandhoff disease inherited and what are the symptoms?

A

Autusomal recessive. More severe than Tay-Sachs, also includes macrocephaly.

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140
Q

In Metachromatic Leukodystrophy (MLD), what enzyme is defective and what accumulates?

A

Defective - arylsulfatase A Accumulates - sulfatides in liver, kidney, nervous system

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141
Q

How is Metachromatic Leukodystrophy (MLD) inherited and what are the symptoms?

A

Autosomal recessive. Difficulty walking, muscle wasting, blindness, convulsions, dysphagia, paralysis, dementia (infantile or juvenile), psychiatric disorder (in adults).

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142
Q

In Farber disease, what enzyme is defective and what accumulates?

A

Defective - ceraminidase Accumulates - ceramides in joints, CNS, liver, heart, kidney

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143
Q

How is Farber disease inherited and what are the symptoms?

A

Autosomal recessive. Impaired motor and mental ability, dysphagia, arthritis, swollen lymph nodes and joints, hoarness (infantile).

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144
Q

What is the regulated step in cholesterol synthesis?

A

HMG CoA (made from Ac CoA) being made into mevalonate by HMG CoA reductase.

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145
Q

What are the two important primary bile acids to know?

A

Cholic acid/cholate and chenodeoxycholic acid.

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146
Q

How is cholesterol made into primary bile acids?

A

Double bond on the B ring is reduced, 3 carbons removed from the hydrocarbon chain, carboxyl group introduced at the end of the chain.

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147
Q

What are the two important bile salts to know?

A

Glycocholic acid, taurochenodeoxycholic acid.

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148
Q

How is a bile salt made from a bile acid?

A

Amide bond added - conjugated to glycine or taurine or to sulfate or glucuronate.

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149
Q

Where in the body can bile salts be deconjugated?

A

In the small intestine, by bacteria.

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150
Q

What is cardiolipin?

A

A 4 FA lipid with a polar head that is made in the mitochondria and makes membranes permeable to ions.

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151
Q

What are plasmalogens?

A

Similar to phospholipids except the end FA group has an ether linkage and a double bond rather than an ester linkage.

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152
Q

How does platelet activating factor (PAF) differ from plasmalogen structure?

A

Has no double bond and the middle FA is replaced by acetate.

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153
Q

What part of the GI system is responsible for most absorption?

A

Small intestine.

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154
Q

All the metabolic breakdown reactions are hydration reactions.

A

Just a reminder.

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155
Q

How is trypsinogen made into trypsin (active form)?

A

Cleaved by enterokinase/enteropeptidase. Can also cleave and activate it back. It is also able to autocatalyze in the presence of bile salts or weak acid conditions (pH 5.4-7.8)

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156
Q

What enzyme in the GI besides trypsin can autocatalyze in acidic conditions? And where is it activated?

A

Pepsin. In the stomach (the rest of the enzymes are cleaved in the SI).

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157
Q

What percentage of transporter defect diseases are due to amino acid malabsorption?

A

60%.

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158
Q

How are proteins usually absorbed in the GI tract?

A

As mono/dipeptides.

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159
Q

What sort of transporter are peptide transporters usually?

A

Antiports using H+, Na+, K+ and their counter ion.

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160
Q

Where is carbohydrate absorption done?

A

In the duodenum and jejunum.

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161
Q

What enzymes break down carbohydrates?

A

Salivary amylase (ptyallin) - active at pH >4, still slightly active in fundus. Pancreatic amylase takes over. They are both alpha amylases, digest starches and glycogens into di/trisaccharides. Digestion into monosaccharides requires additional glycosidases.

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162
Q

What happens to carbs that weren’t digested in the small intestine?

A

In the large intestine, enterobacteria help break them down (indigestible carbs) to short chain fatty acids which are absorbed by the colonic mucosa.

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163
Q

How is lactose intolerance diagnosed?

A

With the H2 test (exhaled in breath in the case of lactose intolerance).

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164
Q

What enzymes break down lipids?

A

Lingual (~pH 5) and gastric lipases (pH 3-6) - 10% digestion in the stomach. Pancreatic lipase in the duodenum (uses colipase and cholesterol esterase and PLA). Colipase attaches to a TG on the surface of an emulsion droplet, and serves as an anchor for lipase which hydrolyzes the ester bonds.

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165
Q

How does PLA2 act on lecithin?

A

Makes FAs and lysolecithin.

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166
Q

How do lipolytic digestion products (FAs) enter enterocytes? Where do they go?

A

Through FAT or just through diffusion. They reform as triglycerides and go to golgi, released as chylomicrons that go into lymph.

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167
Q

Are bile salts absorbed in digestion?

A

No, they always stay in the lumen.

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168
Q

Are all size fatty acids made into chylomicrons?

A

No, just ones 14-18 carbons. Small and medium FAs just go to the liver.

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169
Q

What is Olestra?

A

An 8 FA indigestible disaccharide.

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170
Q

What is orlistat?

A

A competitive inhibitor of most lipases.

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171
Q

Where is pepsin made and what is its target?

A

The chief cells of the stomach. N-terminal of aromatic aas.

172
Q

What does esophageal pepsin exposure in the absence of low pH result in?

A

Downregulation of protective proteins.

173
Q

What does larynx/hypopharynx pepsin exposure in the absence of low pH result in?

A

The upregulation of inflammarion, may lead to tumours.

174
Q

Where is trypsin made and what does it target?

A

The acinar cells of the pancreas. Stored in granular vesicles in the duodenum, where it acts. C-term of Lys or Arg.

175
Q

Where is chymotrypsin made and what is its target?

A

The acinar cells of the pancreas. ALpha is the active form, pi can cleave. Phe, Trp, Tyr.

176
Q

Where is elastase made and where does it act? What does it target?

A

Made in the acinar cells of the pancreas. Acts in duodenum and jejunum, target is the c-term of any hydrophobic AA.

177
Q

Where is carboxypeptidase A made? Where does it act? What does it target?

A

Made in the acinar cells of the pancreas. Acts in duodenum. Targets c-term of aliphatic and aromatic AAs.

178
Q

Where is carboxypeptidase B made? Where does it act? What does it target?

A

Made in the acinar cells of the pancreas. Acts in duodenum. Targets c-term of Basic AAs.

179
Q

Where is enteropeptidase made and as what zymogen? What does it target?

A

Made in the duodenal and jejunal brush border cells as proenteropeptidase. Targets a residue of 4XAsp Lys, hydrolysis occurs on the Lys c-term.

180
Q

Where are aminopeptidases made and as what zymogen? What does it target?

A

Made in IC compartments and have no zymogen. A brush border enzyme. Target is amino terminal peptide bonds.

181
Q

Where is dipeptidase made and as what zymogen? What does it target?

A

Made in SI enterocytes, acts in and on brush border. Has no zymogen. Targets dipeptides.

182
Q

What is the specific target of salivary alpha amylase?

A

alpha 1->4 glycosidic linkages in starch. Produce is maltose and smaller starches.

183
Q

What is the specific target of pancreatic alpha amylase?

A

alpha 1->4 glycosidic linkages in amylose. Product is maltose and smaller starches.

184
Q

Where is isomaltase made, where does it act, and what is the specific target?

A

Made in enterocytes, acts in SI. Targets alpha 1->6 glycosidic linkages in starch, product is maltose.

185
Q

Where is glucoamylase/ glucan alpha 1->4 glucosidase made, where does it act, and what is the specific target?

A

Made in brush border enterocytes, acts in SI. Targets alpha 1->4 glycosidic linkages of alpha 1->6 linkages right next to the alpha 1->4 ones. Produce is D-glucose.

186
Q

What is the contraction pattern of sphincter smooth muscle?

A

Normally contracted, relaxes for a short burst.

187
Q

What is the contraction pattern of blood vessels/airways?

A

Normally partially contracted, has tone/

188
Q

What is the contraction pattern of the esophagus and bladder?

A

Normally relaxed, tightens for short bursts - opposite of sphincters.

189
Q

What is the contraction pattern of the gut wall from the stomach down (besides the sphincters).

A

Phasic. A slow wave - phasically changing membrane potential. A spike (AP) is a consequence of the slow wave reaching the threshold.

190
Q

What sets the pace for slow waves? What are the paces n the different organs?

A

Insterstitial cells of Cajal (ICCs) in the stomach and within the walls of the SI and LI. Stomach - 3-4/min Duodenum - 10-12/min Colon - 3-7/min

191
Q

What is the motility pattern the SI in the fasting state?

A

90-120 min pattern of virtually no activity followed by a short intense peristalsis (migrating motor complex).

192
Q

Where does the migrating motor complex begin?

A

In the proximal stomach.

193
Q

Wheat are the phases of the migrating motor complex?

A

I - quiescent, little activity II - increasing activity III- peak electrical/mechanical activity IV - declining activity transitioning into quiescence

194
Q

What are the three types of intestinal segmentation movements?

A

Regularly spaces, isolated, irregularly spaced.

195
Q

What controls the ileocecal sphincter?

A

The SNS, vagus, ENS. Ileal distension/irritation leads to relaxation, cecal distension/irritation leads to contraction.

196
Q

Are the IAS and EAS voluntary or involuntary?

A

IAS is involuntary, EAS is voluntary.

197
Q

What is the parasympathetic and sympathetic control of the colon?

A

Vagal and sacral PNS fibers, SNS fibers are mesenteric and hypogastric plexi.

198
Q

How does too little propulsion in the colon affect stool?

A

Too-hard stools.

199
Q

How frequently does the proximal colon do mass peristalsis?

A

1-3x a day. May move the contents 20cm or more.

200
Q

What stimuli trigger vomiting/emesis?

A

Gastric/upper intestinal irritation, vestibular stimuli, gastric outlet constriction.

201
Q

Describe vomiting/emesis.

A

Peristalsis suppressed, powerful abdominal muscle contraction creating strong pressure gradient, stomach, LEX, esophagus relax. Sometimes there is antiperistalsis/retroperistalsis.

202
Q

What is the difference between vomiting and retching?

A

If the UES is closed, retching occurs.

203
Q

How much fluid does the small intestine secrete per day?

A

~1L a day.

204
Q

How does bicarbonate secretion change as you move down the colon?

A

Decreases (highest in proximal colon).

205
Q

How does K+ secretion change as you move down the colon?

A

Decreases. Passive secretion paracellular and greatest in distal colon. Active secretion transcellular and greatest in proximal colon.

206
Q

What increases CFTR activity?

A

ACh (M3 ENS receptors), VIP, prostaglandins, histamine, (AC action), serotonin (5HT, PLC), anything that increases guanylyl cyclase.

207
Q

How is colonic active potassium secretion stimulated?

A

By aldosterone (epithelial cells) or cAMP in crypt cells. There is also more secretion in dehydration.

208
Q

Which side of the cell does minor hormone guanylin come from?

A

The apical side.

209
Q

How much fluid does the pancreas exocrinely secrete per day?

A

~1.5L

210
Q

Describe low basal pancreatic juice secretions.

A

Mostly acinar fluid, high in Cl-, low in bicarbonate.

211
Q

Describe high flow rate pancreatic juice.

A

Mostly from ducts, high in bicarbonate and low in Cl-.

212
Q

Is the stuff coming out of pancreatic ducts acidic or basic?

A

Basic.

213
Q

What percentage of max enzyme secretion is the pancreas at at the different stages of digestion?

A

Cephalic - 25%, gastric - 10-20%, intestinal - 50-80%.

214
Q

How much fluid does the small intestine absorb per day?

A

6.5L

215
Q

What are the 5 patterns of digestion/absorption?

A
  1. monomer, no digestion needed 2. digestion in lumen into monomers 3. digestion in lumen into oligomers, further digestion at brush border into monomers 4. dimers and trimers absorbed into enterocyte, digested into monomers inside cells 5. digested into monomers in lumen, absorbed into enterocytes, repackaged into larger molecules before exiting enterocytes
216
Q

What follows what in absorption?

A

Chloride follows sodium, water follows NaCl

217
Q

Where is the ENaC found and what is it?

A

Epithelial sodium channel. Found in the distal colon.

218
Q

Where is K+ absorption?

A

In the distal colon only. Exchanged with hydrogen at surface epithelial cells.

219
Q

In which parts of the small intestine is calcium absorbed?

A

The whole thing.

220
Q

In which parts of the small intestine is cobalamin/B12 absorbed?

A

Terminal ileum.

221
Q

In which parts of the small intestine is iron absorbed?

A

Duodenum.

222
Q

In which parts of the small intestine is folate/B9 absorbed?

A

Duodenum.

223
Q

How is calcium kept in the cell before being moved across the basolateral membrane? How does it come into the cell?

A

Held in place with calbindin. It can come in paracellularly or transcellularly.

224
Q

How does calcium leave the cell?

A

Basolaterally - via a calcium/hydrogen exchanger (primary active transport) or a Na+/Ca++ antiport using the sodium potassium pump.

225
Q

Where does the liver get its blood supply?

A

From all of the abdominopelvic GI prgans and the spleen. It gets 1/4 of the body’s cardiac output.

226
Q

What vitamins/things does hte liver store?

A

Vitamin A, D, B9, B12, glycogen, iron.

227
Q

What does the liver do?

A

Makes and secretes bile acids and pigments, excretes heavy metals, cholesterol, bile pigments, drugs and hormones, detoxifies, has hematopoietic functions in fetal life, some defense (Kupffer cells), activates Vitamin D.

228
Q

How much hepatic bile is secreted every day?

A

~900mL, about half is diverted to the gallbladder.

229
Q

How does bile go from the canaliculi?

A

Interlobular ducts, septal ducts, lobar ducts, R&L hepatic ducts.

230
Q

What are the components of bile?

A

Cholesterol, cholesterol-derived bile acids/salts, bile pigments (from hemoglobin), phospholipids, ions, water. It is pH 6.0-7.5

231
Q

What are primary vs secondary bile acids?

A

Primary is made by hepatocytes - enhances solubility, allows for ‘soap action’. Secondary is primary modified by intestinal bacteria (generally slightly reduces solubility).

232
Q

What are the four steps of processing for secretion in hepatocytes?

A

Uptake from basolateral blood, transport within cell, chemical modification, secretion through apical membrane.

233
Q

How do free bile acids enter hepatocytes?

A

With a sodium dependent transporter (secondary active transport).

234
Q

How are bile salts moved into the lumen from the hepatocytes?

A

Transporter Z ATPase moves the ones conjugated to taurine/glycine, Transporter Y ATPase moves the ones conjugated to sulfate/glucuronate.

235
Q

If the Sphincter of Oddi is closed, where does bile back up into?

A

The gallbladder.

236
Q

What does the gallbladder reabsorb?

A

NaCl and water.

237
Q

How can you tell apart gallbladder and hepatic bile? How much gallbladder bile is secreted every day?

A

Hepatic bile is yellow-green, gallbladder is dark green - osmotically similar but just less Cl- and typically with more green bile acids. The gallbladder secretes ~50mL of bile a day.

238
Q

How much bile reaches the duodenum?

A

~500mL

239
Q

How do ACh, VIP, and NO affect gallbladder bile secretion.

A

All increase, ACh stimulates GB muscle contraction, VIP&NO inhibit sphincter of Oddi contraction.

240
Q

How are bile acids and salts reabsorbed?

A

Through enterohepatic circulation, reabsorbed in the terminal ileum. Primary and secondary bile acids passively diffuse in. Na+ dependent carrier mediated secondary active transport beings in primary bile salts only.

241
Q

Where do most secondary bile acids go?

A

Mostly lost in feces.

242
Q

What percent of secreted bile acids and salts are returned ot the liver on each pass?

A

95%. About 20% of the bile acid pool is replaced every day through synthesis of new bile acids.

243
Q

How do bacteria aid in digesting lipids?

A

It makes SCFAs that the colon can absorb via secondary active transport. Byproducts can be gas, pain, etc.

244
Q

What is the average male and female BMR?

A

1 and 0.9 kcal/kg/hr

245
Q

How is total metabolic energy calculated?

A

BMR + thermic effect of food (5-10% BMR) + physical activity (light is 30-50% BMR, active is 100% BMR, can be up to 800%).

246
Q

How much energy is obtained from carbs?

A

4kcal/g

247
Q

What percent of the diet should be carbs? How many grams?

A

45-65%. Should be >130g/day.

248
Q

How much energy is obtained from alcohol?

A

7kcal/g

249
Q

How much energy is obtained from protein?

A

4kcal/g

250
Q

What percent of the diet should be protein? How many grams?

A

10-30%. About 56g for males, 46g for females

251
Q

How much energy is obtained from fat?

A

9kcal/g

252
Q

What percent of the diet should be fat?

A

25-35%.

253
Q

What percent of daily calories should be gotten from simple sugars and disaccharides?

A

<10%

254
Q

What much happen to starches to be effectively digested?

A

They must be cooked!

255
Q

What’s the difference between amylose and amylopectin?

A

Amylose is linear and digested slower, amylopectin is branched and digested faster.

256
Q

What are the sources of dietary fiber?

A

Bran, navy beans, shredded wheat, cranberry beans, lentils, peas.

257
Q

What effects do dietary fiber have?

A

Decreases absorption of dietary fat and cholesterol, delays gastric emptying, generates feelings of fullness, reduces post prandial blood glucose.

258
Q

What is a glycemic load?

A

How much a typical serving of a food raises blood [glucose].

259
Q

What is a glycemic index?

A

How quickly glucose is absorbed from a certain food.

260
Q

How much dietary fiber should be obtained per day in the diet?

A

25-35g

261
Q

What are the essential amino acids?

A

Ones that must be obtained from the diet. Val, Ile, Leu, His, Lys, Met, Thr, Phe, Trp, .

262
Q

What is PDCAAS?

A

Protein digestibility corrected amino acid score - the proportion of amino acids that are needed by the body. 1.0 is the highest. Gelatin and plants have a poor score.

263
Q

What is kwashiorkor?

A

A diet inadequate in protein (high carb subsistence diet) resulting in a pot belly, fatty liver, hypoalbuminemia, edema.

264
Q

What is marasmus?

A

Calorie intake is relatively less than protein intake (weaning to low calorie foods) resulting in emaciation, anemia, low subcutaneous fat, weakness.

265
Q

What are the two essential fatty acids?

A

Linoleic acid (C 18:2 cis 9,12) - omega 6. Linelenic acid (C 18:3 cis 9,12,15) - omega 3

266
Q

How much linoleic acid is needed in the daily diet?

A

12g or 17g

267
Q

How much linolenic acid is needed in the daily diet?

A

1.1 or 1.6g

268
Q

What is the effect of dietary cholesterol on serum cholesterol?

A

Currently we think none.

269
Q

What kind of ingested fats affect the serum cholesterol and how?

A

Saturated and trans increase, unsaturated decrease.

270
Q

How do the mediterranean and vegetarian diets differ from the normal recommended diets?

A

In the mediterranean one, there’s more seafood and fruit and less dairy. In the vegetarian one it’s less protein and dairy is back up.

271
Q

How is the recommended daily intake determined for vitamins/minerals?

A

Such that 98% of people won’t show signs of a deficiency.

272
Q

What are the fat-soluble vitamins?

A

A (Retinol), D (Cholecalciferol), E (Tocopherol), K (Quinone).

273
Q

Of the water-soluble vitamins, which areconsidered energy-releasing?

A

B1 (Thiamine), B2 (Riboflavin), B3 (Niacin), B5 (Pantothenic acid), B7 (Biotin).

274
Q

Of the water-soluble vitamins, which are considered hematopoietic?

A

B9 (Folate) and B12 (Cobalamin).

275
Q

What are the food sources of Vitamin C (Ascorbic Acid)?

A

Many fresh fruits and vegetables.

276
Q

What are the functions of Vitamin C (Ascorbic Acid)?

A

It functions as an antioxidant, and is required as a coenzyme to hydroxylate Pro and Lys in collagen. Required in carnithine, NorE, and bile acid synthesis.

277
Q

Describe a deficiency in Vitamin C (Ascorbic Acid).

A

Scurvy - sore and spongy gums, loose teeth, fragile blood vessels, swollen joints, microcytic anemia.

278
Q

What are the food sources of Vitamin B1 (Thiamine)?

A

Most foods, yeast, lean pork, legume seeds.

279
Q

What are the functions of VItamin B1 (Thiamine)? And what’s its active form?

A

Thiamine pyrophosphate. It is a cofactor in several metabolic enzymes carrying out aldehyde transfer or oxidative decarboxylation. E.g. PDH, alpha KG dehydrogenase, transketolase (in HMP, assayed by erythrocyte transketolase reaction).

280
Q

Describe a deficiency in Vitamin B1 (Thiamine).

A

Can occur if polished rice is the primary diet. Can cause Beriberi - mild has GI complaints, weakness, burning feet sensation. Severe has peripheral neuropathy, mental abnormality, ataxia. Dry beriberi means there are neurological deficits, wet beriberi means there is edema due to cardiac dysfunction. Can also cause Wernicke-Korsakoff syndrome (common in alcoholics). Acute has Wernicke encephalopahty (mental deramgement, ataxia, eye paralysis), chronic has Korsakoff psychosis (severe debilitating anterograde amnsia, frontal lobe damage). Mamillary bodies disappear.

281
Q

Which vitamins can have toxicity?

A

A (Retinal), D (Cholecalciferol), K (Quinone), B3 (Niacin), B6 (Pyridoxine).

282
Q

What are the food sources of Vitamin B2 (Riboflavin)?

A

Liver, eggs, yeast, milk, enriched breads and cereals.

283
Q

What are the functions of Vitamin B2 (Riboflavin)?

A

Redox cofactor in many enzymes in the form of FMN, FAD - typically remains tightly bound to the enzyme. E.g. succinate dehydrogenase, NADH dehydrogenase.

284
Q

Describe a deficiency in Vitamin B2 (Riboflavin).

A

Deficiency is rare, more common in alcoholics. Assayed in urine. Causes dermatitis, glossitis, cheilosis, sore throat.

285
Q

What are the food sources of Vitamin B3 (Niacin)?

A

Unrefined grains, milk, lean meat, liver.

286
Q

What are the functions of Vitamin B3 (Niacin)?

A

Converted to NADH and NADP - coenzymes for numerous reactions and also redox carriers. Can also be used to treat hyperlipidemia.

287
Q

Describe Vitamin B3 (NIacin) deficiency.

A

Pellagra - dermatitis, diarrhea, dementia, death, sun sensitivity. It is poorly absorbed from maize unless the maize has been treated with lye.

288
Q

Describe the functions of Vitamin B5 (Pantothenate).

A

Part of CoA, coenzyme in FA synthetase.

289
Q

Describe a Vitamin B5 (Pantothenate) deficiency.

A

There is no deficiency of B5.

290
Q

What are the food sources of Vitamin B7 (Biotin)?

A

Yeast, liver, eggs, peanuts, milk, chocolate, fish.

291
Q

What are the functions of Vitamin B7 (Biotin)?

A

Prosthetic group for many ATP-dependent carboxylases, typically covalently bound.

292
Q

Describe a Vitamin B7 (Biotin) deficiency.

A

Virtually unknown unless consuming raw eggs (avidin is high affinity for biotin and can deplete it). Glossitis, dermatitis, appetite loss, nausea.

293
Q

What are the food sources of Vitamin B9 (Folate)?

A

Green leafy vegetables, yeast, liver, fruits.

294
Q

What are the functions of Vitamin B9 (Folate)? What is the active form?

A

Tetrahydrofolate is the active form. Participates in 1-carbon transfer reactions.

295
Q

What do sulfonamates do?

A

Interfere with B9 synthesis in bacteria.

296
Q

Describe a Vitamin B9 (Folate) deficiency.

A

Common in pregnant women and alcoholics. Causes megaloblastic anemia - can leadt to neural tube abnormalities in the fetus.

297
Q

What are the food sources of Vitamin B12 (Cobalamin)?

A

Animal products.

298
Q

What are the functions of Vitamin B12 (Cobalamin)? What is the active form?

A

Common in -CN, CH3, -deoxyadenosyl forms. Required only for methionine synthase (get 5-methyl THF to THF) and methyl malonyl CoA mutase.

299
Q

How is Vitamin B12/Cobalamin absorbed?

A

Initially bound to salivary transcobalamin I, then in stomach it binds IF and after absorption is swapped onto transcobalamin II and carried through the blood with it.

300
Q

Describe a deficiency of Vitamin B12 (Cobalamin).

A

Pernicious anemia, later stages show neuropsychiatric symptoms.

301
Q

What are the food sources of Vitamin B6 (Pyridoxine)?

A

Liver, fish, whole grains, nuts, egg yolk.

302
Q

What is isomazid?

A

A tuberculosis drug that reacts with vitamin B6, lowering bioavailability.

303
Q

What are the functions of Vitamin B6 (Pyridoxine)? What is the active form?

A

Found as pyridoxine (plants), pyridoxal, and pyridoxamine (ianimal products). Active form is pyridoxal phosphate (PLP). PLP it the cofactor for many enzymes - e.g. decarboxylation, transamination, deamination, condensation. In high doses can be used to treat carpal tunnel.

304
Q

Describe a Vitamin B6 (Pyridoxine) deficiency.

A

Rare but can occur with alcoholics, infants with deficient formula, women on oral contraceptives. Glossitis, dermatitis, sideroblastic anemia.

305
Q

Describe Vitmain B6 toxicity.

A

Toxic in high doses (400X RDA, 500mg/day), can have neuro symptoms. But in less high doses (100mg.day_ can be used to treat carpal tunnel.

306
Q

What are the food sources of ‘Vitamin’ B4 (Choline)?

A

Trick question! Not a real vitamin, is made de nobo.

307
Q

What are the functions of ‘Vitamin’ B4 (Choline)?

A

Needed in acetylcholine, phosphatidylcholine synthesis, source of methyl groups for 5-adenosylmethionine.

308
Q

What are the food sources of Vitamin A (Retinol)?

A

Carrots, vegtables, yellow/gree/orange fruits, liver, kidney, meat, eggs, cream, butter.

309
Q

What are the functions of Vitamin A (Retinol)? What is its active form?

A

Found as retinol, retinoic acid, retinal, beta-carotene. Retinol and retinoic acid act as transcription factors. It is critical for epithelial cell development, mucus secretion, spematogenesis. Retinal is a bound cofactor to rhodopsin - important in vision. Retinoic acid can treat psoriasis and acne.

310
Q

Describe a Vitamin A (Retinol) deficiency.

A

Common in developing countries. Night lindness, eventual loss of retinal cells, xeropthalmia.

311
Q

Describe Vitamin A (Retinol) toxicity.

A

Dry skin, enlarged and eventually cirrhotic liver, increaesd intracranial pressure.

312
Q

What are the food sources of Vitamin D (Cholecalciferol)?

A

Fatty fish, liver, egg yolk, milk (if fortified). Gotten from diet as ergocalciferol, can be made in the skin.

313
Q

What are the functions of Vitamin D (Cholecalciferol)? What is its active form?

A

Active form is calciferol. Maintains plasma calcium concentration - increases intestinal absorption, mininmizes kidney loss through resorption.

314
Q

Describe a Vitamin D (Cholecalciferol) deficiency.

A

Rickets (lack of bone mineralization) if in a child, but in adults it is osteomalacia (demineralization).

315
Q

Describe a Vitamin D (Cholecalciferol) toxicity.

A

Toxic in very high doses. Is stored in body fat. Loss of appetite, nausea, thirst, stupor, hypercalcemia.

316
Q

What are the food sources of Vitamin E (Tocopherol)?

A

Vegetable oil, oil seeds, wheat germ.

317
Q

What are the functions of Vitamin E (Tocopherol)? What is the active form?

A

alpha-tocopherol is the most active. Works as an antioxidant, scavenges free radicals.

318
Q

Describe a Vitamin E (Tocopherol) deficiency.

A

Rare but can occur in newborns before they have developed their own stores, otherwise it would be due to poor absorption of chylomicrons.

319
Q

What are the food sources of Vitamin K (Quinone)?

A

Cabbage, spinach, kale, egg yolk, liver, is also synthesized by gut flora.

320
Q

What are the functions of Vitamin K (Quinone)? WHat is the active form?

A

K1/phylloquinone is found in plants, K2/menaquinone, K3/menadione is synthetic. It acts as a substrate for gamma-glutamyl carbozylase which matures clotting factors II, VII, IX, X.

321
Q

What does warfarin do?

A

Blocks Vitamin K epoxide reductase, which regenerates Vitamin K.

322
Q

Describe a Vitamin K (Quinone) deficiency.

A

Unusual, can occur in newborns (usually get a shot of Vitamin K), can result in clotting disorders.

323
Q

Describe Vitamin K (Quinone) toxicity.

A

Large menadione doses can cause jaundice and hemolytic anemia.

324
Q

What is the difference between a trace element and a trace mineral?

A

Trace element is RDA <100mg, trace mineral is RDA <1mg.

325
Q

What are the trace elements?

A

Fe, Zn, Cu, Mn.

326
Q

What is the recommended iron intake?

A

Males 8g, females 18g.

327
Q

.What does a lack if iron/hemoglobin result in?

A

Microcytic hypochromic anemia.

328
Q

Describe hemochromatosis.

A

Iron overload. More prevalent in older men from northern Europe - exacerbated by a mutation in the HFE gene. Liver, heart, endocrine glands affected.

329
Q

What are the dietary sources of zinc?

A

Seafood, eggs, meat, legumes, cereals.

330
Q

What is zinc needed for?

A

300+ proteins including DNA Polymerase, Carbonic Anhydrase, carboxypeptidase, DNA regulatory proteins, Superoxide dismutase.

331
Q

Describe zinc deficiency.

A

Loss of taste (dysgeusia), anosmia, poor wound healing, peroral rash.

332
Q

What is acrodermatitis enteropathica?

A

A defect in zinc absorption. Results in inflammation with pimples, diarrhea, abnormal nails. Congenital form is chromosome 8 SLC39A mutation.

333
Q

What are the dietary sources of copper?

A

Meats, shellfish, nuts, cereals.

334
Q

What is copper needed for?

A

Cofactor in oxygen binding enzymes, required for cytocorome c oxidase, superoxide dismutase, lysyl oxidase, ferroxidase/ceruloplasmin, dopamine oxidase, tyrosinase (makes melanin). Important for healthy nerves and joints.

335
Q

What is WIlson’s disease?

A

An autosomal recessive mutation in ATP7B which encodes a Cu@+ ATPase that transports copper into the ER/golgi. Copper accumulates in the liver and brain leading to dementia, movement disorders, Kayser-Fleisher rings. Will result in high blood copper, low blood ceruloplasmin. Treat with penicillamine (Cu chelator).

336
Q

What is Menkes Disease?

A

X-linked recessive mutation in ATP7A gene, wwhich encodes an intestinal Cu2+ translocase. Cupper accumulates in the small intestine and kidneys, lowly in the brain. Results in kinky hair, seizures, unstable body temperature. Will result in low blood copper and ceruloplasmin. Poor prognosis, usualy death by 3 years of age, give copper supplements.

337
Q

What are the food sources of manganese?

A

Grains, nuts, leafy vegetables, soy.

338
Q

What is manganese needed for?

A

Many enzymes - ATPases, arginase, pyruvate carboxylase, peptidases, etc. Important in healthy bones and cartilage, metabolism and reproductive functions.

339
Q

Describe manganese deficiency. Can there be a toxicity?

A

Deficiency can cause osteoporosis. There can be toxicity.

340
Q

What is iodine needed for? What can deficiency cause?

A

Thyroid hormone - goiter.

341
Q

What is selenium needed for? What can deficiency cause?

A

Oxidoreductases (can substitute sulfur) - hypothyroidism.

342
Q

In what foods is selenium found?

A

Nuts, cereals, meats, mushrooms, fish, eggs/

343
Q

What is cobalt needed for? Where is it found? What can deficiency cause?

A

Needed in B12. Found in meat and dairy. Deficiency can lead to pernicious anemia.

344
Q

What is molybdenum needed for? Where is it found?

A

Nitrogenases and oxidizing proteins. Found in legumes, grains, nuts.

345
Q

What does fluoride do? What can deficiency cause?

A

It helps form hard bones and teeth. fluoroapatite is harder than hydroxyapatite. Deficiency can cause tooth decay.

346
Q

Where are there lipases?

A

In the intestine, but also muscle and adipose have it in their capillary lumen.

347
Q

What do lipases break triglycerides into?

A

Two fatty acids and a monoglyceride.

348
Q

What is a chylomicron remnant?

A

A chylomicron that has been depleted of triglyceride. It goes to the liver, fatty acids are repackaged back into VLDLs.

349
Q

When insulin drops, what tends to last longer, glucose or chylomicrons?

A

Chylomicrons.

350
Q

What does fatty acid synthesis require and where is it done?

A

Requires ATP and reducing equivalents NADPH. It takes place in the cytosol.

351
Q

How is Acetyl Coa moved out of the mitochondria for fatty acid synthesis to begin?

A

A pyruvate is turned into oxaloacetate with pyruvate carboxylase. Then Citrate is made with AcCoA and the oxaloacetate and this is exported out to the cytosol and turned back into acetylCoA and oxaloacetate at the cost of 1 ATP. The oxaloacetate is made into malate at the cost of an NADH and the malate comes back in and turns to pyruvate, generating an NADPH.

352
Q

Desribe fatty acid synthesis.

A

Acetyl CoA is turned into Malonyl CoA using Acetyl CoA carboylase. Then the FAS enzyme cysteine site is primed with a starter chain, and the malonyl CoA is added to the ACP on the pantethiene arm of the enzyme. A condensation reaction adds the starter chain to the malonyl CoA (one CO2 lost). THen there is a reduction with ketoreductase, a dehydration, and a reduction with enoyl reductase (each reduction is at the cost of an NADPH). The new chain is translocated to the enzyme Cys-SH and everything is repeated until there is a saturated 16 carbon palmitate.

353
Q

Where is triglyceride synthesis carried out?

A

In the liver, and a little in the muscle and adipose.

354
Q

Describe the structure of FAS (Fatty Acid Synthase).

A

Giant, has an acyl carrier protein domain covalently bound to a long phosphopantathiene arm.

355
Q

Describe triglyceride synthesis.

A

A G3P backbone (made from DHAP or glycerol in the liver) is taken. A FA Coa is added (usually unsaturated at the middle position) and then the phosphate is removed to add the third fatty acid.

356
Q

What does Adipose Triglyceride Lipase (ATGL) have a preference for?

A

End FA.

357
Q

Describe Hormone sensitvive Lipase (HSL).

A

Has a preference for the middle position FA. Epinephrine (cAMP) stimulates its activity by the kinase action, insulin activates phosphatase.

358
Q

What are free fatty acid bound to in the blood?

A

Albumin.

359
Q

How do fatty acids enter the mitochondria?

A

First they enter the cell and immediately have a CoA added. THen they diffuse into the OM and CPTI exchanges carnithine for CoA, creating FA-carnithine. On the IM, CPTII brings FA-carnithine in.

360
Q

Describe beta oxidation.

A

Acyl CoA dehydrogenase oxidizes the FA (creating an FADH2) into enoy-CoA (2-trans, unsaturated). Next an enoyl-CoA hydratase turns it into 3-hydroxyacyl CoA. 3-hydroxyacyl CoA dehydrogenase oxidizes (makes an NADH) and turns it into 3-ketoacyl CoA. 3-ketoacyl CoA thiolase removes the Ac CoA.

361
Q

What enzyme do you use in beta oxidation is there is an odd double bond?

A

cis delta3 enoyl CoA isomerase.

362
Q

What enzyme do you use in beta oxidation is there is an even double bond?

A

2,4 dienoyl CoA isomerase. Uses NADPH.

363
Q

What is the end result of beta oxidation of an odd chain fatty acid and how do you deal with it?

A

Propionyl CoA. Propionyl CoA carboxylase (B7 cofactor) uses ATP to turn it into methylmalonyl CoA which is processed by methylmalonyl CoA mutase (B12 cofactor) into succinyl CoA.

364
Q

Is the muscle sensitive to glucagon?

A

No.

365
Q

Describe the regulation of Acetyl CoA carboxylase.

A

Activated by citrate and in dephosphorylation. Downregulated by accumulation of LCFAs and AMP kinases.

366
Q

How is the carnithine shuttle regulated?

A

Malonyl CoA inhibits CPTI.

367
Q

What is Zellweger syndrome?

A

A peroxisomal assembly issue “empty peroxisomes”. VLCFAs are not oxidized. Adrenal insufficiency, reduction in plasmalogens, white matter insufficiency.

368
Q

What is medium chain AcCoA desaturase deficiency?

A

An autosomal recessive condition. Medium chain AcCoA desaturase is used in all fatty acid processing. It causes sudden death, hypoketotic hypoglycemic state, seizures, coma at 2 months - 6.5 years.

369
Q

What are the three ketone bodies?

A

Acetoacetate, 3-hydroxybutyrate, acetone/

370
Q

How is acetoacetate ketone body generated?

A

Ac CoA is made into acetoAcCoA, which is then made into HMG COA with HMG CoA Synthase. Then HMG CoA Lyase catalyzes it into AcCoA and acetoacetate.

371
Q

How do you generate 3-hydroxybutyrate and acetone from acetoacetate?

A

It takes an NADH to make it into 3-hydroxybutyrate, and it can spontaneously decarboxylate into acetone which cannot be metabolized.

372
Q

What is arachidonic acid?

A

Linoleic acid has 2 carbons and 2 double bonds added. to make it. Arachidonic acid is typically bound to the middle position of phospholipids and typically releaed in response to PLA2.

373
Q

How is arachidonic acid turned into prostaglandin G2 and leukotrienes?

A

COX1 and COX2 convert it to prostaglandin E2 (which can be made into thromboxanes)/ Aspirin blocks the action of COX1 and COX2. Lipoxygenase will convert it to leukotrienes.

374
Q

What class of drug is aluminum hydroxide and how is it administered?

A

Antacid, oral.

375
Q

What are some adverse effects of aluminum hydroxide?

A

Constipation.

376
Q

What class of drug is magnesium hydroxide and how is it administered?

A

Antacid, oral. Also considered an osmotic laxative.

377
Q

What are some adverse effects of magnesium hydroxide?

A

Diarrhea.

378
Q

What does magnesium hydroxide treat?

A

GERD, PUD, acid peptic diseases. Also good for imagine procedures.

379
Q

What class of drug is calcium carbonate and how is it administered?

A

Antacid, oral.

380
Q

What does calcium carbonate treat?

A

Acid peptic diseases, hypocalcemia, osteoporosis prevention, hyperphosphatemia.

381
Q

What are some adverse effects of calcium carbonate?

A

Hypercalcemia, cnostipation, hypophosphatemia, milk-alkali syndrome (alkalosis, hypercalcemia, renal insufficiency).

382
Q

What class of drug is sodium bicarbonate and how is it administered?

A

Antacid, oral.

383
Q

What are some adverse effects of sodium bicarbonate?

A

Hypernatremia, edema, heart failure exacerbation.

384
Q

What are the H2 receptor antagonists and how are they administered? What sort of antagonists are they?

A

Cimetidine, Ranitidine, Famotidine. Oral, IV, IM. Competitive inhibitors.

385
Q

What are some adverse effects of Cimetidine?

A

Inhibits several enzymes of the hepatic cyt p450 metabolism pathways. Inhibits binding of DHT to androgen receptors and inhibits estradiol metabolism - gynecomastia, loss of libido, impotence.

386
Q

What class of drug is Omeprazole and how is it administered?

A

PPI, oral. Given as acid-resistant enteric coated formulation.

387
Q

What class of drug is Esomeprazole and how is it administered?

A

PPI, oral, IV. IV given as prodrug, oral as acid-resistant enteric coated formulation.

388
Q

How do omeprazole and esomeprazole work?

A

They are proton pump inhibitors on the apical parietal cell H+/K+ ATPase. They covalently, irreversibly bind.

389
Q

What is the preferred gastric drug type for severe conditions?

A

PPI.

390
Q

What are the adverse effects of PPIs?

A

Reduced B12, increased rick of hip fracture for >1 year PPI therapy (possibly due to decreased calcium absorption), increased risk of community acquired respiratory infections/nosocomial pneumonia, increased risk of ECL and parietal hyperplasia in >2 year PPI therapy.

391
Q

What class of drug is sucralfate and how is it administered?

A

Mucosal protective agent, oral.

392
Q

How does sucralfate work and what is it best used to treat?

A

It is negatively charged and binds to positively charged proteins on ulcerated tissue. It is best as a short term therapy for duodenal ulcers, also reduces incidence of upper GI bleeding in critically ill patients.

393
Q

What are some adverse effects of sucralfate?

A

Bezoar formation, constipation.

394
Q

What class of drug is misoprostol and how is it administered?

A

Mucosal protective agent, oral, vaginal, rectal.

395
Q

How does misoprostol work and what is it best used to treat?

A

It is an analog of PGE1 - an agonist of prostaglandin receptors (EP3 on parietal cell). It stimulates mucus, electrolyte, bicarbonate, and fluid secretion, enhances mucosal blood flow, reduces histamine-stimulated cAMP production and gastric acid secretion, stimulates intestinal motility, stimulates uterine contractions. It is best used to treat as a prophylactic for NSAID-induced ulcers.

396
Q

What are the adverse effects of misoprostol?

A

Stimulates uterine contractions! If given with mifepristone it will terminate a pregnancy <70 days. Should start on 2nd or 3rd day of period.

397
Q

What class of drug is bismuth subsalicylate and how is it administered?

A

A musosal protective agent, oral.

398
Q

What is bismuth subsalicylate used to treat?

A

H. pylori, dyspepsia, diarrhea.

399
Q

What is an adverse effect of bismuth subsalicylate?

A

Black stool.

400
Q

What class of drug is metoclopramide and how is it administered?

A

A prokinetic drug.Oral, IM, IV.

401
Q

How does metoclopramide work?

A

A dopamine D2 receptor antagonist. It enhances gastric emptying, speeds up digestion, antinausea and antiemetic action.

402
Q

What is metoclopramide used to treat?

A

Diabetic gastroparesis, good for advancement of nasoenteric feeding tube, can do GERD but is not preferred - may be given with a PPI in patients with reractory heartburn or regurgitation.

403
Q

What are adverse effects of metoclopramide? Any contraindications?

A

Tardive dyskinesia, also possibly depression, extrapyramidal symptoms, parkinsonian-like symptoms. GI obstruction is a contraindication.

404
Q

What class of drug is erythromycin and how is it administered?

A

A prokinetic drug, oral, IV.

405
Q

How does erythromycin work? What is it good for treating?

A

Stimulates motilin on the GI smooth muscle. Good for before an endoscopy, gastroparesis. It is also an antibiotic.

406
Q

What class of drug is pancrelipase and how is it administered?

A

A prokinetic drug, oral.

407
Q

What is pancrelipase good for treating?

A

Pancreatic insufficiency - can be caused by CF, pancreatic resection, chronic pancreatitis.

408
Q

What class of drug is methylcellulose` and how is it administered? How does it work?

A

Bulk-forming laxative, oral. Is indigestible colloids and fibers that absorb water - forms a bulk and distends the abdomen.

409
Q

What class of drugs are docusate and mineral oil and how are they administered?

A

Stool softeneres, oral and rectal.

410
Q

How do stool softeners work?

A

Allows water and lipids to penetrate stool, prevents water loss.

411
Q

What are the adverse effects of mineral oil?

A

Impaired absorption of fat-soluble vitamins, pneumonitis upon aspiration.

412
Q

What class of drug is polyethylene glycol and how is it administered?

A

Osmotic laxative, and oral.

413
Q

What class of drug is lactulose and how is it administered?

A

Osmotic laxative, oral and rectal.

414
Q

What are osmotic laxatives good for?

A

Clearing for imaging procedures.

415
Q

What class of drug are bisacodyl and senna and how is it administered?

A

A stimulant laxative. Oral.

416
Q

What class of drug is lubiprostone and how is it administered?

A

Chloride channel activator laxative, oral.

417
Q

What are the effects of chloride channel activators (including lubiprostone)? What are they good for treating?

A

Stimulate intestinal motility, shorter transit time - good for opioid induced constipation, IBS with predominant constipation, IBS with predominant constipation, chronic idiopathic constipation.

418
Q

What is an adverse effect of lubiprostone?

A

Nausea.

419
Q

What are the transporters involved in small intestine carbohydrate absorption?

A

Apital GLUT5 (brings in fructose), apical SGLT1 (brings in sodium with glucose or gapactose), basal GLUT5 (sends fructose into blood), basal GLUT 2 (sends glucose, galactose, fructose into blood)

420
Q

What are the transporters involved in small intestine amino acid absorption?

A

Apical sodium/AA symporter, PepT1 H+/di or tri peptide symporter, basal channel bringing out amino acids (peptides digested inside cell).

421
Q

List the salivary acinar and ductal cell channels.

A
422
Q

List the pancreatic acinar and ductal cell channels.

A
423
Q

List the parietal cell channels.

A
424
Q

List the gastric mucosal barrier cell channels.

A
425
Q

List the crypt cell channels.

A

Semester 2 Medical School (7 decks)

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