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Semester 2 > Pathophys - 3, 4, and 5 > Flashcards

Pathophys - 3, 4, and 5 Flashcards

1
Q

valvular function of illeocecal junction

A

prevents backflow into SI mechanically

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2
Q

sphincter function of illeocecal junction

A

regulates movement of ileal contents into large intestines

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3
Q

functions of LI SM

A

mixes chyme (enhances fluid/electrolyte absorption), propels fecal material

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4
Q

parasympathetic input of LI

A

vagus innervates proximal colon, pelvic nerves (S2-4) distal colon and rectum/anus

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5
Q

what innervates the external anal sphincter

A

puedenal nerves

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6
Q

what is the purpose of haustral contractions

A

mixing movements facilitate fluid and electrolyte reabsorption

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7
Q

what is the purpose of propulsive movements

A

move feces to rectum/stimulate defecation reflex

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8
Q

what is the distance of the propulsive movements

A

transverse colon to sigmoid colon or rectum

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9
Q

when do propulsive movements occur

A

after meals, reflexes - gastocolic, duodenocolic reflex

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10
Q

what are the three levels of control of defecation

A

intrinsic reflex, spinal cord reflex, involvement of higher centers

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11
Q

valsalva maneuver

A

deep breathe, closure of glottis, and increased abdominal pressure ; work to move fecal contents downward

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12
Q

_____ can make defecation difficult

A

spinal injury (need digitally or edema)

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13
Q

digestion involves what process to absorb nutrients in small intestines

A

hydrolysis (addition of water)

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14
Q

monomer for carbs

A

monosaccharides

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15
Q

monomer for proteins

A

small peptides and amino acids

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16
Q

monomer for fats

A

2-monoglycerides and fatty acids

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17
Q

digestive enzymes in stomach

A

pepin

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18
Q

digestive enzymes in salivary glands

A

a-amylase, lingual lipase

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19
Q

digestive enzymes in pancreas

A

amylase, trypsin, chymotrypsin, carboxypeptidase, elastase, lipase-collapse, cholesterol esterase

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20
Q

what digestive enzymes are in the intestinal mucosa

A

enterokinase; sucrase, maltase, lactase, trehahalse, isomaltese, amino-oligopeptidase dipeptidase

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21
Q

how does enterokinase activate trypsinogen

A

cleaving hexapeptide from N-terminal end to form trypsin

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22
Q

what is the surface area increase for SI

A

1000-fold

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23
Q

increase in folds of kerckring

A

3-fold increase in SA

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24
Q

what are folds of kerckring controlled by

A

muscularis mucosa

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25
Q

what is the fold increase in villi

A

10-fold increase

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26
Q

what is the fold increase in SA

A

20-fold increase

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27
Q

site at which alot of enzyme reaction details occur

A

microvilli brush border

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28
Q

what happens for babies to allow large proteins (immunoglobins) in

A

endocytosis

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29
Q

where does endocytosis occur in adults

A

ileum for absorption of vitamin B12

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30
Q

what is the most important process in SI to make absorption of nutrients possible

A

sodium electrochemical gradient

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31
Q

what can be use for drug absorption if someone has N/V or problems swallowing

A

rectal catheter

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32
Q

a nutrient must cross ____ barriers to be absorbed by blood or lymph

A

8

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33
Q

where do lactose and sucrose get digested

A

only at brush border

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34
Q

where does starch digestion occur

A

begins with a-amlyase in salvia, continues in SI with pancreatic amylase, final digestion at brush border

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35
Q

what is the final product of carb digestion

A

monosaccharides, mostly glucose

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36
Q

what is the rate-limiting step in carb assimilation

A

absorption

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37
Q

how is fructose getting across the membrane

A

facilitated diffusion (no energy needed, just concentration gradient)

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38
Q

how are glucose and galactose getting across the membrane

A

secondary active transport, SGLUT-1 (energy from NA+/K+ ATPase)

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39
Q

lactose intolerance

A

acquired lactase deficiency caused by absence of brush border lactase

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40
Q

Glut-1 deficiency

A

lack of glucose galactose carrier

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41
Q

where does the digestion of AA occur

A

intestinal lumen, stomach (pepsin, digests collagen), SI

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42
Q

what is at the brush border (proteins)

A

oligopeptidases, dipeptidases

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43
Q

what is digested in cytoplasm of mucosal cells (proteins)

A

(Di, tri-peptidases)

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44
Q

how do proteolytic enzymes get digested

A

digest themselves

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45
Q

pancreatic insufficiency

A

decreased absorption of protein - nitrogen in stool
pancreatitis or CF

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46
Q

congenital absence of trypsin

A

no trypsin - no other proteolytic enzymes, protein malabsorption

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47
Q

Hartnup disease

A

cannot absorb neutral AA (tryptophan); neutral AA can still be absorbed as di- and tri-peptides (proof of separate carrier system)

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48
Q

where does the first step of fat absorption occur

A

SI

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49
Q

where are chylomicrons secreted

A

lymph system and go to thoracic duct where they enter the subclavian vein

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50
Q

what does LDL do

A

takes cholesterol from the liver to the rest of the body

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51
Q

what does HDL do

A

primarily takes cholesterol form body tissue back to liver

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52
Q

difference between HDL and LDL

A

high amount increase risk of HD, high amounts reduce risk

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53
Q

hypertriglyceridemia

A

accumulation of large quantities of fat (lipoproteins) in the blood

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54
Q

what are the three main processes must occur for triglyceride to be absorbed in the blood

A

emulsification, enzymatic digestion, reconstitution of triglyceride and chylomicron formation

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55
Q

Cirrhosis of the liver ____ resistance

A

increases

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56
Q

Ascites

A

accumulation of fluid in the gut coming from liver disease

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57
Q

what is the resistance, pressure, and flow of liver?

A

low resistance, low pressure, high flow

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58
Q

Major functions of the liver

A

filtration and storage of blood, formation of bile, storage of vitamins/iron, formation of coagulation factors, metabolism

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59
Q

what is the liver lobule a pathway for

A

blood and lymph

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60
Q

Kupffer cells

A

phagocytic cell forming lining of sinusoids in liver to breakdown RBCs

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61
Q

what can decrease liver blood volume

A

exercise/hemorrhage (sympathetic stimulation)

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62
Q

what can increase liver blood volume

A

heart failure (as much as 1 L)

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63
Q

___% of body lymph is formed in the liver

A

50

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64
Q

where does lymph flow in the liver

A

through the space of Disse and collects in lymph vessels

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65
Q

what does increased sinusoidal pressure increase

A

lymph production (liver sweats lymph, fluid accumulates in abdominal cavity)

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66
Q

what leaks fluid and proteins into space of disse

A

porous fenestrations

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67
Q

where are Kupffer cells located

A

liver sinusoids

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68
Q

what compromises liver reticuloendothelial system

A

tissue macrophages (Kupffer cells)

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69
Q

what is the main cellular system for removal of particulate materials and microbes from circulation

A

kupffer cells

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70
Q

what can you make glucose out of

A

fat and protein (liver breaks it down and spits out new glucose)

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71
Q

where does gluconeogenesis occur

A

only in the liver

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72
Q

what can the liver form (metabolism)

A

intermediate metabolites and glucose from galactose/fructose

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73
Q

what does excess glucose after meals get converted to

A

glycogen (glycogenesis)

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74
Q

what does decreased glucose between meals cause

A

stimulation of depolymerization of glycogen (glycogenolysis)

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75
Q

what does liver do to amino acids

A

removes the nitrogen from the molecule

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76
Q

what is the liver’s function in metabolism of proteins

A

demination of amino acids, formation of plasma proteins, synthesis of nonessential amino acids (12 that we can make), removal of ammonia by synthesis of urea

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77
Q

what does the liver require to make prothrombin, Factors VII, VIII, IX, and X

A

vitamin K

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78
Q

liver disease or vitamin K def lead to

A

bleeding abnormalities

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79
Q

Hemophilia

A

recessive X-linked disorder(rare in females); cannot make Factor XIII, cannot coagulate blood well

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80
Q

Factor VIII

A

anti hemophilic factor; encoded by F8 gene on X chromosome

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81
Q

what is the liver’s role in fat metabolism

A

conversion of carbs and proteins to fat, beta oxidation of fatty acids, synthesis of special lipids (cholesterol - 80% converted into bile salts, phospholipids, lipoproteins)

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82
Q

what is the main form of fat used in the body

A

triglycerides

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83
Q

what do phase 1 reactions do to parent drug

A

convert it into polar metabolite with functional group; metabolite usually inactive

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84
Q

what do phase 2 reactions do to parent drug or phase 1 metabolite

A

an endogenous substrate is attached to a functional group (going to plasma)

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85
Q

bilirubin plays a role in ____

A

anti-oxidation, inflammation

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86
Q

what are the forms of bilirubin

A

conjugated and unconjugated (direct and indirect)

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87
Q

what is the number 1 protein in blood

A

albumin

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88
Q

direct bilirubin

A

conjugated

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89
Q

where does bile go when it leaves the gut

A

feces, urine, enterohepatic circulation

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90
Q

what do liver cells do with bilirubin

A

uptake, conjugation, and excretion

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91
Q

what does too much bilirubin cause

A

jaundice

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92
Q

overproduction of bilirubin

A

hemolysis (UC)

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93
Q

defection excretion of bilirubin

A

obstruction - cancer, gallstones
cirrhosis, hepatitis
C

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94
Q

defection conjugation of bilirubin

A

neonatal jaundice (UC)

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95
Q

treatment for neonatal jaundice

A

exposure to blood light from fluorescent tubes; transforms unconjugated bilirubin into a water-soluble photoisomer that can be excreted by kidneys

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96
Q

what is the cause of jaundice in new-borns

A

underdeveloped state of smooth endoplasmic reticulum (makes bilirubin soluble)

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97
Q

what is the role of bile

A

fat emulsification and absorption; medium for excretion of bilirubin and cholesterol

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98
Q

what does the gallbladder store

A

stores and concentrates bile

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99
Q

what does gallbladder mucosa absorb

A

water and most electrolytes (not Ca+)

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100
Q

when does gallbladder begin to empty

A

when food, esp fat, enter duodenum (CCK, nervous - Vagus/ENS)

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101
Q

what is the most abundant solute in bile

A

bile salts

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102
Q

what does CCK do

A

contracts gallbladder and relaxes sphincter of Oddi

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103
Q

what has a major effect on emptying gallbladder

A

duodenal peristaltic waves

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104
Q

what are the two stages bile is secreted in

A

hepatocytes - secrete primary bile constituents, bile ducts- addition of water, Na+, HCO3-

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105
Q

what does the formation of bile salts start with

A

cholesterol

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106
Q

bile salts are ____

A

amphipathic

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107
Q

what does the amphipathic nature of bile enable it to do

A

emulsify lipids, transport lipids

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108
Q

black, foul-smelling stool (melena)

A

intestinal bleeding (stomach and upper SI), due to ulcers, tumors; ingestion of iron and bismuth

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109
Q

maroon stool

A

intestinal bleeding (middle intestine or prox colon due to ulcers, tumors, Crohn’s disease, ulcerative colitis

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110
Q

Clay-colored stool

A

lack of bile due to blockage of main bile duct

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111
Q

pale, yellow, greasy, foul-smelling stool

A

malabsorption of fat due to pancreatic insuff, as seen with pancreatitis, pancreatic caner, CF, and celiac disease

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112
Q

what is the most common cause of cirrhosis

A

excessive alc use

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113
Q

steatohepatitis

A

fatty liver accompanied by inflammation, which leads to scarring of liver and cirrhosis

114
Q

what do complications of cirrhosis include

A

jaundice, ascites, peripheral edema, bleeding esopha varices, blood coagulation abnormalities, coma and death

115
Q

what are the majority of gallstones

A

cholesterol

116
Q

what is the key event leading to most gallstones

A

precipitation of cholesterol in bile

117
Q

what are the causes of cholesterol precipitation

A

too much water reabsorbed, too much cholesterol, inflammation of gallbladder, too much absorption of bile salts and lecithin

118
Q

what are 10% of gallstones

A

pigment stones

119
Q

What are the segments of the alimentary tract?

A

mouth, pharynx, esophagus, stomach, SI, LI, spinchters between segments

120
Q

What are the layers of the GI Tract (outside to inside)?

A

serosa, longitudinal muscle, myenteric nerve plexus, circular muscle, submucosa, submucosal nerve plexus, muscular mucosa, mucosa, epithelial lining

121
Q

What are the parts of the ENS?

A

Myenteric & submucosal (meissner’s) nerve plexus

122
Q

What are the two structurally related families of GI Peptides?

A

Gastrin & CCK
- Secretin, GIP, VIP, glucagon

123
Q

preprohoromone

A

precursor protein to one or more prohormones, which are in turn precursors to peptide hormones

124
Q

What is the hypokalemia associated with gastrinoma caused by?

A

loss of GI secretions in the stool

125
Q

What do all molecular forms of gastrin share?

A

AA seq

126
Q

What are the four steps required to establish existence of GI hormone?

A

physiological release, effects independent of nervous system, isolated substance has physiological effect, chemical identification and synthesis

127
Q

What are all horomones in the GI?

A

peptides

128
Q

What are the symtpoms of Gastrinoma: Zollinger-Ellison Syndrome?

A

duodenal ulcers, diarrhea, steatorrhea, hypokalema

129
Q

What does hypergastrinemia cause?

A

hypersecretion of acid, increased parietal cell mass, constant stimulation of hyperpastic mucosa

130
Q

What happens if too much gastrin is secreted (gastrin-secreting tumor)?

A

mucosal hyperplasia and hypertrophy

131
Q

What do you use to diagnose Gastrinoma?

A

ChiRhoStim (synthetic secretion); blood test (> 120 pg/mL gastin)

132
Q

Where is somatostatin (peptide) found?

A

gastric/duodenal mucosa and pancreas

133
Q

What is somatostatin (peptide) release stimulated/inhibited by?

A

acid, inhibited by Ach

134
Q

What does somatostatin (peptide) do?

A

Inhibits parietal cell acid secretion, gut hormones, and gastrin

135
Q

What does Histamin do?

A

stimulates acid secretion, H2 receptor blockers

136
Q

What causes Histamines release?

A

Gastrine and Ach cause release from pariteal cells in stomach

137
Q

Where is VIP?

A

gut mucosa and SM

138
Q

Where is GRP (Bombsein)?

A

Gastric mucosa

139
Q

Where is Enkephalins?

A

Gut mucosa and SM

140
Q

What does VIP do?

A

relaxation of gut SM

141
Q

What does GRP do?

A

increase gastrin release

142
Q

What does Enkephalins do?

A

increases SM tone

143
Q

What plexuses are involved in intrisic control?

A

Myenteric and Submucosal plexus

144
Q

What does the parasympathetic system do in terms GIT?

A

mainly stimulates (Ach)

145
Q

What does sympathetic system do? (GIT)

A

mainly inhibits (NE)

146
Q

What is the composition of the ENS?

A

cell bodies, axons, dendrites, nerve endings

147
Q

Where is the innervation of the ENS?

A

gut cells, sensory nerves, other neurons

148
Q

What is the integration of the ENS?

A

can occur entirely within ENS, can function independent of ANS

149
Q

What are the transmitters in the ENS?

A

many excitatory and inhibitory

150
Q

What is the location of the ENS?

A

What is the location of the ENS?

151
Q

What is the main function of the myenteric plexus?

A

controls GI motility

152
Q

What are stimulatory influences of myenteric plexus?

A

increased tonic control, increased contraction frequency/intensity

153
Q

What are inhibitory influences of myenteric plexus?

A

decreased sphincter tone (relax) - pyloric, ileocecal, LES

154
Q

Where is the submucosal plexus located?

A

mucosal layer from esophagus to anus

155
Q

What is the function of the submucosal plexus?

A

local control (secretion, absorption, contraction of mucular mucosa)

156
Q

What is the cranial divison of the parasympathetic innervation?

A

Vagus N. - first half of gut

157
Q

Where do PS neurons synapse?

A

closer to organ

158
Q

What is the first half of the gut innervated by?

A

vagus n.

159
Q

What is the sacral divison of the parasympathetic innervation?

A

second half of the gut - pelvic n.

160
Q

What does parasympathetic innveration stimulate?

A

excites ENS

161
Q

What other fibers PS neurons contain?

A

afferent sensory fibers (per–> central)

162
Q

What is the pattern of neurons in SI?

A

short pregang, long postgang

163
Q

What does SI do in GI tract?

A

inhibits activity of ENS and inhibits SM

164
Q

What neurotransmitters cause excitatory affects in the ENS

A

ach, substance P, serotonin

165
Q

What are the purposes of chewing?

A

break cells, increases surface area (decreases particle size), mixes food with saliva

166
Q

What does salvia mixing with food do?

A

starts breaking down carbs and fat (a-amylase, linguial lipase)

167
Q

What is the innervation of chewing

A
168
Q

cystic fibrosis

A

salivary Ca+, Na+, and protein are elevated (also true for bronchial secretions, pancreatic juices, and sweat)

169
Q

what can cause xerostomia

A

drugs, capillary perfusion decreased, radiation, autoimmume

170
Q

xerostomia

A

dry mouth

171
Q

what directly increases salivation

A

symp NS

172
Q

why is mucous composition essential for digestion

A

adherees, body (coat well), low resistance, self adherent, resistant to digestion, buffering capacity

173
Q

what is the composition of mucus

A

thick secretion that is mainly water, electrolytes, and glycoproteins

174
Q

where are the main secretions coming from for saliva

A

parotid and submandibular gland

175
Q

what is serous secretion

A

watery secretion, a-amylase and lingual lipase

176
Q

what are the two types of salvia secretions

A

serous and mucus

177
Q

where is the biggest pH jump in GI tract

A

stomach –> small intestines

178
Q

Chewing reflex

A

food –> muscles of mastication relax –> jaw drops –> stretch reflex –> rebound contraction –> lining of mouth

179
Q

What is the innervation of chewing

A

5th crainal nerve (trigeminal), controlled by nuceli in brain

180
Q

What are the purposes of chewing?

A

break cells, increases surface area (decreases particle size), mixes food with saliva

181
Q

what is the treatment of drooling

A

anticholingeric drugs, surgical removal of the sublingual glands, retroposition submandibular ducts

182
Q

what do CF patients lack

A

chloride transporters (CFTR)

183
Q

primary aldosteronism

A

excess aldosterone; salivary NaCl close to zero, salivary K+ high

184
Q

What is the PNS pregang eff neuron neurotransmitters?

A

ach

185
Q

What is the PNS postgang eff neuron neurotransmitters?

A

ach

186
Q

What are the inhibiory neurotransmiters for the ENS?

A

VIP, NO

187
Q

What stimulates GI afferent neurons?

A

distention of gut wall, irritation, chemical stimuli

188
Q

What can stimulation of sensory afferent neurons (GI) do?

A

excite or inhibit (intestinal movements & secretions)

189
Q

Pathway of vagovagal reflexes

A

stomach/duodenum –> aff. n —> brain stem –> eff n–> stomach/duodenum

190
Q

Defecation reflexes pathway

A

colon/rectum –> aff n. –> spinal cord –> eff. n. –> colon/rectum

191
Q

What do pain reflexes do to the GI tract?

A

overall inhibition

192
Q

What are the gastrointestinal reflexes?

A

gastrocolic, enterogastric, colonileal (vagovagal, defecation, pain)

193
Q

ong loop GI reflexes pathway

A

gut –> aff. n –> prevertebral ganglia –> eff n. —> gut

194
Q

What are local GI reflexes?

A

afferent fibers from gut terminate in ENS, affect (+/-) secretion, peristalsis mixing movements

195
Q

syncytium

A

nucleated mass of protoplasm produced by merging of cells

196
Q

why are gap junctions important in GI SM?

A

signal propogation, unitary

197
Q

what are the pacemaker cells of GI slow waves

A

interstitial cells of cajal

198
Q

what dictates the max frequency of SM contraction

A

pacemaker (interstital) cells

199
Q

what are rhythmical changes in membrane potential caused by variations in

A

sodium conductance

200
Q

what is variable amplitude in slow waves affected by

A

nervous/hormonal stimuli

201
Q

what are the frequency of spike potentials affected by

A

nervous/hormonal stimuli;

202
Q

what happens when frequency of spike potentials increases

A

stronger contraction

203
Q

what cause SM contraction

A

true APs

204
Q

what are spike potentials stimulated by

A

stretch, ach, PS

205
Q

what are hyperpolarizations of SM stimulated by

A

noreip, symp

206
Q

what are stimuli that initiate peristalsis

A

distention, irritation, PS

207
Q

what is required for peristalsis

A

myenteric plexus

208
Q

what decreases peristalsis

A

atropine

209
Q

what does atropine do

A

blocks Ach receptors

210
Q

what are the main feed arteris of the GI

A

celiac a., SMA, IMA

211
Q

whats the venous drainage of GI

A

portal vein –> liver sinusoids –> hepatic vein

212
Q

what is gut blood flow proportional to

A

local acitivity

213
Q

what causes activity - induced blood flow

A

vasodilator hormones (gastrin, secretin, CCK), low oxygen

214
Q

what is the PNS control of GI blood flow

A

increases gut activity and increases blood flow

215
Q

what is SNS control of gut blood flow

A

decreases blood flow

216
Q

fatty acids and triglycerides

A

high density energy storage

217
Q

phopholipids

A

membrane component, contain precursors for bio active substances, modulate activities of membranes enzymes&transporters

218
Q

cholesterol

A

impt part of membranes, control fluidity and protein function. precursor for bile acids and liver makes most of it (most cells can syn from acetyl CoA)

219
Q

what are most dietary lipids

A

neutral fat or triglyceride

220
Q

acini

A

grape-like clusters of cells that store and secrete digestive enzymes

221
Q

ducts

A

secrete bicarbonate

222
Q

two types of pancreatic ducts

A

intercalated ducts (acini), intralobular ducts (intercalated)

223
Q

role of pancreas in chyme going into SI

A

bicarb solution to neutralize acid chyme, digestive enzymes for all food types

224
Q

what cleaves proteins to polypeptides

A

trypsin and chymotrypsin

225
Q

what cleaves polypeptides to AA

A

carboxypeptidase

226
Q

what is the only luminal enzyme for carb digestion

A

amylase

227
Q

what digests starches and glycogen to disaccharides

A

starches and glycogen

228
Q

what enzymes digests fat into fatty acids and monoglycerides

A

pancreatic

229
Q

what helps the pancreas to not digest itself

A

pancreatic proteolytic enzymes are stored and secreted in an inactive form (also, trypsin inhibitor is present)

230
Q

what converts trypsinogen to trypsin

A

enterokinase

231
Q

where is enterokinase located

A

intestinal mucosal cells

232
Q

what does trypsin

A

autocatalytic activation (breakdown proteins in intestines)

233
Q

what neutralizes acid chyme

A

bicarb (secretin-induced)

234
Q

where does the pancreas receive signals from for regulation

A

stomach and intestines

235
Q

what hormones potentiate effects of secretin on water and bicarb secretion

A

CCK and ach

236
Q

chronic pancreatitis causes

A

alcohol (adults) and CF (children)

237
Q

acute pancreatitis causes

A

gallstones

238
Q

what do brunner’s glands secrete

A

alkaline mucus (protect intestines from acid)

239
Q

what are brunners glands stimulated and inhibited by

A

stimulated - local irritatation (vagus, Ach)
inhibited - sympathetics (NE)

240
Q

mucous/goblet cells

A

secrete mucus that lubricates and protects the intestinal surfaces

241
Q

intestinal stem cells

A

differentiate into the special cells of the intestinal epithelium, which renews throughout life

242
Q

paneth cells

A

secrete anti-microbial compounds and other compounds known to be important in immunity and host defense, thereby contributing to maintenance of the GI barrier

243
Q

how does SI motility contribute to digestion and absorption?

A

mixing chyme, circulation of chyme, propulsion of chyme

244
Q

Most water and electrolyte recovery occurs in what GI section?

A

LI

245
Q

What “glands” in small intestine secrete alkaline mucus?

A

Brunners

246
Q

The swallowing center is located where?

A

Medulla (of brain stem)

247
Q

Dehydration has what effect on salivary flow?

A

Inhibits

248
Q

True or false? The intrinsic defecation reflex is controlled within the enteric nervous system

A

True

249
Q

Blood returning to liver from circulation comes through which common vein?

A

Portal

250
Q

Rhythmical changes in membrane potential in smooth muscle caused by variance of sodium conduction are called:

A

Slow waves

251
Q

Intrinsic neural control of GI tract is via which system?

A

ENS

252
Q

Which accessory organ stores bile?

A

Gallbladder

253
Q

Q: The parotid gland secretes what?

A

Saliva (serous)

254
Q

Parasympathetic stimulation does what to mucus secretion in large intestine?

A

Increases

255
Q

The cephalic phase of gastric secretion relies on what nerve?

A

vagus

256
Q

HCl is formed in what cells in the stomach?

A

Parietal

257
Q

The G cells in the antrum and duodenum release what?

A

Gastrin

258
Q

Luminal digestion of proteins produces a majority of what product?

A

A: Di- and tri-peptides

259
Q

Final digestion of CHO happens at what location?

A

Brush border

260
Q

Which structures increase the surface area of the SI 10x and contain capillaries and a lacteal?

A

villi

261
Q

The majority of nutrient absorption in the gut happens where?

A

SI

262
Q

Which buffer helps neutralize acid to create optimal conditions for digestive enzymes?

A

bicarb

263
Q

Which enzyme is the first to start breaking down fats?

A

lingual lipase

264
Q

What enzyme breaks down phospholipids?

A

A: Phospholipase

265
Q

Amylase is a common term for an enzyme that breaks down what macronutrient?

A

CHO

266
Q

What word describes enzymes that cleave proteins to polypeptides?

A

Proteolytic

267
Q

Lipids must form which structures to be absorbed into enterocytes?

A

Micelles

268
Q

Which peptide is released by the duodenum in response to acid and the presence of fatty acids?

A

Secretin

269
Q

Lipids form which structures to be transported from the enterocyte through lymphatic circulation?

A

Chylomicrons

270
Q

In arterioles, which enzyme binds chylomicrons and hydrolyzes triglycerides to FFA + glycerol?

A

lipoprotein lipase

271
Q

Which type of lipid synthesis is blocked by statin drugs?

A

Cholesterol

272
Q

Which receptor is used to transport glucose and galactose across the brush border into the intestinal cells?

A

SGLUT1

273
Q

Which hormone is most active in the antrum of the stomach?

A

Gastrin

274
Q

Which hormone stimulates insulin release?

A

Glucose-Dependent Insulinotropic Peptide

275
Q

What part of the pancreas secretes bicarbonate?

A

Ducts

276
Q

Vitamin K is needed by the liver to form what?

A

Coagulation factors

277
Q

The liver conversion of a parent drug to a more polar metabolite is called what?

A

Phase 1 or first pass metabolism

278
Q

Which duct combines secretions of the pancreas and the gallbladder?

A

Common bile duct

279
Q

The majority of all gallstones are composed of what substance?

A

Cholesterol

280
Q

What term describes the location where the intestinal lumen meets SI epithelial cells ?

A

Brush border

Semester 2 (6 decks)

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