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Medical Physiology I > Block 6 Exam > Flashcards

Block 6 Exam Flashcards

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USMLE® Step 1 flashcards
1
Q

Mouth

A

Mechanical homogenization of food

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2
Q

Salivary glands

A

Salivary secretion

Hydration, lubrication, Amylase

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3
Q

Esophagus

A

Propulsion of food

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4
Q

Stomach

A

Gastric acid & pepsinogen secretion, mechanical churning to reduce particle size

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5
Q

Pancreas

A

Pancreatic secretion of bicarbonate, propeptidases, amylase, prolipases

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6
Q

Liver and Gall bladder

A

Bile acid secretion

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7
Q

Small intestine

A

Digestion and absorption of nutrients (proteins, fats, sugars), electrolytes, and water

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8
Q

Anus

A

Defecation of fecal waste

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9
Q

Villi cells

A

Primarily nutrient and electrolyte absorption

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10
Q

Crypt or gland cells

A

Primarily secretion

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11
Q

Features that increase surface area of small and large intestine

A 
Folds of Kerckring
Semilunar folds
Villi
Crypts or glands
Microvilli
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12
Q

Transcellular

A

Through the cell

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13
Q

Paracellular

A

Between the cell

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14
Q

Blood flow in fasting state

A

30mL/min/100g of tissue

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15
Q

Blood flow after a meal

A

Can reach 250mL/min/100g of tissue

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16
Q

Which locally produced hormones and kinins cause vasodilation during digestion

A

Cholecystokinin

Neurotensin

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17
Q

Submucosal plexus

A

Meisner’s

Only found in small and large intestine

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18
Q

Myenteric plexus

A

Auerbach’s

Found throughout GI tract

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19
Q

Vagovagal reflex

A

Sensory afferents from chemoreceptors, osmoreceptors, and mechanoreceptors in the mucosa are carried by the vagus nerve to autonomic centers in the brain, which in turn sends efferents via the vagus nerve to change secretion and motility

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20
Q

Acetylcholine (ACh) source

A

Cholinergic neurons

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21
Q

Acetylcholine (ACh) Actions

A 
Contraction of smooth muscle in wall
Relaxation of sphincters
Increase salivary secretion
Increase gastric secretion
Increase pancreatic secretion
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22
Q

Norepinephrine (NE) source

A

Adrenergic neurons

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23
Q

Norepinephrine (NE) actions

A

Relaxation of smooth muscle in wall
Contraction of sphincters
Increase salivary secretion

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24
Q

Vasoactive intestinal peptide (VIP) source

A

Neurons of mucosa and smooth muscle

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25
Q

Vasoactive intestinal peptide (VIP) actions

A

Relaxation of smooth muscle
Increase intestinal secretion
Increase pancreatic secretion

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26
Q

Gastrin-Releasing Peptide (GRP), or Bombesin source

A

Neurons of gastric mucosa

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27
Q

Gastrin-Releasing Peptide (GRP), or Bombesin actions

A

Increase gastrin secretion

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28
Q

Enkephalins (opiates) source

A

Neurons of mucosa and smooth muscle

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29
Q

Enkephalins (opiates) actions

A

Contraction of smooth muscle

Decrease intestinal secretion

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30
Q

Neuropeptide Y source

A

Neurons of mucosa and smooth muscle

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31
Q

Neuropeptide Y actions

A

Relaxation of smooth muscle

Decrease intestinal secretion

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32
Q

Substance P source

A

Cosecreted with ACh

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33
Q

Substance P actions

A

Contraction of smooth muscle

Increase salivary secretion

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34
Q

Cholecystokinin source

A

I cells in duodenum and jejunum

Neurons in ileum and colon

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35
Q

Cholecystokinin target

A

Pancreas

Gall bladder

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36
Q

Cholecystokinin action

A 
Increase enzyme secretion (pancreas)
Increase contraction (gall bladder)
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37
Q

Gastric inhibitory peptide source

A

K cells in duodenum and jejunum

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38
Q

Gastric inhibitory peptide target

A

Pancreas

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39
Q

Gastric inhibitory peptide action

A

Exocrine: decrease fluid absorption
Endocrine: increase insulin release
Suppresses glucagon secretion

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40
Q

Gastrin source

A

G cells, antrum of stomach

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41
Q

Gastrin target

A

Parietal cells in body of stomach

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42
Q

Gastrin action

A

Increase H+ release

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43
Q

Gastrin-releasing peptide source

A

Vagal nerve endings

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44
Q

Gastrin-releasing peptide target

A

G cells in antrum of stomach

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45
Q

Gastrin-releasing peptide action

A

Increase gastrin release

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46
Q

Guanylin source

A

Ileum and colon

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47
Q

Guanylin target

A

Small and large intestine

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48
Q

Guanylin action

A

Increase fluid absorption

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49
Q

Motilin source

A

Endocrine cells in upper GI tract

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50
Q

Motilin target

A

Esophageal sphincter
Stomach
Duodenum

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51
Q

Motilin action

A

Increase smooth-muscle contraction

Migrating motor complex

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52
Q

Neurotensin source

A

Endocrine cells

Widespread in GI tract

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53
Q

Neurotensin target

A

Intestinal smooth muscle

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54
Q

Neurotensin action

A

Vasoactive stimulation of histamine release

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55
Q

Peptide YY source

A

Endocrine cells in ileum and colon

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56
Q

Peptide YY target

A

Stomach

Pancreas

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57
Q

Peptide YY action

A

Decrease vagally mediated acid secretion (stomach)

Decrease enzyme and fluid secretion (pancreas)

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58
Q

Secretin source

A

S cells in small intestine

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59
Q

Secretin target

A

Pancreas

Stomach

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60
Q

Secretin action

A

Increase HCO3 - and fluid secretion by pancreatic ducts (pancreas)
Decrease gastric acid secretion (stomach)

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61
Q

Somatostatin source

A

D cells of stomach and duodenum

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62
Q

Somatostatin target

A

Stomach
Intestine
Pancreas
Liver

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63
Q

Somatostatin action

A

Decrease gastrin release (stomach)
Increase fluid absorption/decrease secretion (intestine)
Increase smooth-muscle contraction (intestine)
Decrease endocrine/exocrine secretions (pancreas)
Decrease bile flow (liver)

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64
Q

Substance P source

A

Enteric neurons

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65
Q

Substance P target

A

Enteric neurons

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66
Q

Substance P action

A

Neurotransmitter

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67
Q

VIP source

A

ENS neurons

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68
Q

VIP target

A

Small intestine

Pancreas

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69
Q

VIP action

A

Increase smooth-muscle relaxation (small intestine)
Increase secretion by small intestine (small intestine)
Increase secretion by pancreas (pancreas)

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70
Q

Peristalsis

A

Propulsion of chyme in the caudal direction

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71
Q

Segmentation

A

Mixing or churning of chyme

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72
Q

Gastric accommodation

A

Active dilation or relaxation of the fundus of the stomach in response to entry of food

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73
Q

Internal anal sphincter

A

Circular and longitudinal smooth muscle

Involuntary control

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74
Q

External anal sphincter

A

Striated muscle only

Voluntary and involuntary control

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75
Q

What portions of the human digestive system contain striated muscle

A

Upper esophageal sphincter
Upper third of esophagus
External anal sphincter

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76
Q

Principal functions of stomach

A

Stores and mixes food
Secretes intrinsic factor for vitamin B12 absorption
Secretes HCl and proteolytic enzymes

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77
Q

Exocrine secretions of stomach

A

Facilitate iron absorption

Secretes mucus to protect mucosa against noxious agents

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78
Q

Endocrine secretions of stomach

A

Miscellaneous functions

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79
Q

Gastric Sympathetic innervation function

A

Decrease motility
Decrease secretion
Constrict vasculature

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80
Q

Where is pepsinogen I released from

A

Oxyntic mucosa only

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81
Q

Where is pepsinogen II released from

A

Throughout gastric mucosa

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82
Q

Gastric endocrine cells neurotransmitters

A 
Vasoactive intestinal peptide (VIP)
Galanin
Serotonin
Pituitary adenylate cyclase activating peptide (PACAP)
Gastrin-releasing peptide (GRP)
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83
Q

Gastric endocrine cells paracrine mediators and hormones

A

Ghrelin
Gastrin
Somatostatin

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84
Q

Loss of sonic hedgehog

A

Loss of acidity
Diminished production of somatostatin
Increase in serum gastrin levels

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85
Q

What do parietal cells release

A

intrinsic factor

HCl

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86
Q

What do chief cells release

A

pepsinogen

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87
Q

What do ECL cells release

A

histamine

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88
Q

What do G cells release

A

gastrin

GF

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89
Q

What do D cells release

A

somatostatin

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90
Q

What cells does ACh act on

A

Parietal cell
ECL cell
D cell

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91
Q

ACh receptor

A

M3

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92
Q

What cells does GRP act on

A

G cell

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93
Q

Atropine

A

Blocks M3 receptor

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94
Q

Cimetidine, Ranitidine (-dine)

A

Block H2 receptor

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95
Q

Omeprazole, Pantoprazole (-azole)

A

PPI

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96
Q

ANTGIP effect on plasma insulin

A

Decreases

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97
Q

ANTGIP effect on serum glucose levels

A

Decrease

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98
Q

Gastrin’s role in duodenal ulcer

A

Basal levels slightly elevated
Meal-stimulated elevated, prolonged
Autoregulatory defect
Increased responsiveness of parietal cells to circulating gastrin

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99
Q

Somatostatin Inhibits which GI functions

A

GI peptides
Gastric acid secretion
Motility
Pancreatic enzyme and HCO3- secretion

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100
Q

Somatostatin mode of action

A

Neurotransmitter
Hormone
Paracrine

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101
Q

Duodenal ulcer phenotype

A

Antral predominant gastritis
High gastrin and acid secretion
Impaired inhibitory control of acid secretion
Protection from gastric cancer

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102
Q

Simple gastritis phenotype

A

Mild mixed gastritis
High gastrin but normal acid secretion
No gastric atrophy
No significant clinical outcome

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103
Q

Gastric cancer phenotype

A 
Corpus-predominant gastritis
Multi-focal atrophic gastritis
High gastrin
Hypo/achlorhydria
Low pepsinogen I and pepsinogen I/II ratio
Increased risk of gastric cancer
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104
Q

Invasive methods to diagnose H. pylori

A

Histology
Culture
Rapid urease test (CLOtest)

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105
Q

Serology to diagnose H. pylori

A

ELISAs detect IgG

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106
Q

Best test for evaluating eradication of H. pylori

A

Urea breath tests

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107
Q

Past treatment of peptic ulcer

A

No acid, no ulcer

Acid suppression

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108
Q

Present treatment of peptic ulcer

A

Cure H. pylori, heal ulcer

H. pylori eradication and acid suppression

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109
Q

Future treatment of peptic ulcer

A

No H. pylori, no ulcer

Prevent ulcer by preventing H. pylori

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110
Q

What are incretins

A

Hormones mediating the enteroinsular axis

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111
Q

Incretin stimulus

A

Glucose containing meal

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112
Q

Site of release of incretins

A

Small intestine

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113
Q

Effect of incretin release

A

Stimulated pancreatic beta islet cells to release insulin

114
Q

Pathologies of Gastric Inhibitory Polypeptide

A

Obesity and type 2 Diabetes mellitus

Cushing’s syndrome

115
Q

GIP synthestized/secreted by what?

A

K cells in upper small intestine

116
Q

GIP biological properties

A

Delays gastric emptying

Stimulates insulin release in response to glucose

117
Q

Effects of GIP on metabolism

A

Increase insulin release
Increase glucose absorption
Decrease lipolysis
Increase lipogenesis/fat storage

118
Q

Effects of ANTGIP on metabolism

A

Decrease GIP stimulated insulin release
Decrease serum glucose levels
Decrease d-glucose absorption from the small intestine
Increase lipolysis

119
Q

Metabolic syndrome characterized by

A

Obesity
Nonalcoholic fatty liver disease (NAFLD)
Insulin resistance with hyperinsulinemia

120
Q

Duodenal ulcer

A

Damage to duodenal mucosa via excessive gastric acid secretion

121
Q

Gastric ulcer

A

Damage to gastric mucosa via cytotoxic atrophy

122
Q

H. pylori in Duodenal ulcer

A

Inhibits somatostatin and HCO3- secretion

123
Q

Hypersecretory states in duodenal ulcer

A

Elevated basal gastrin

Significantly increased postprandial gastrin secretion

124
Q

H. pylori in gastric ulcer

A

Release cytotoxins that damage gastric mucosa

125
Q

Decrease in gastric [H+] in gastric ulcer

A

H. pylori migrates to corpus and damages/inhibits parietal cells and increases gastric secretion

126
Q

Functions of saliva

A 
Moisten and lubricate foodstuffs
Facilitate speech
Dissolve food for taste
Begin digestion of carbohydrates and lipids
Antibacterial/immunologic
Retards dental caries
Washes out substances
127
Q

Types of acinar cells

A

Serous

Mucus

128
Q

Serous acinar cell

A

water
salts
protin

129
Q

Mucus acinar cell

A

Mucins

130
Q

Exocrine pancreas function

A

Secretion of bicarbonate to neutralize gastric acid

Secretion of digestive enzymes

131
Q

Ductal cell bicarbonate secretion inhibited by

A

substance p

132
Q

Ductal cell bicarbonate secretion stimulated by

A

ACh

Secretin

133
Q

Parotid acinar cell

A

alpha-amylase

134
Q

Sublingual acinar cell

A

Mucin glycoprotein

135
Q

Aldosterone effect on salivary ductal cells

A

Increase absorption of NaCl and secretion of K+

Increase ENaC

136
Q

Most important regulator of Protein secretion by pancreatic acinar cells

A

ACh

137
Q

Most potent regulator of Protein secretion by pancreatic acinar cells

A

CCK

138
Q

Most potent 2nd messenger of Protein secretion by pancreatic acinar cells

A

Ca2+

139
Q

Ductal cell Cl- secretion facilitated by

A

Apical CFTR and CaCC

140
Q

Basolateral channels on ductal cells

A

Sodium bicarb co-transporter

Bicarb from CO2 and carbonic anhydrase

141
Q

Apical channels on ductal cells

A

Leaves by anion exchanger

142
Q

Pancreatic secretion cephalic phase regulated by

A

ACh

143
Q

Pancreatic secretion intestinal phase regulated by

A

CCK
Secretin
Vagovagal enteropancreatic reflex

144
Q

What does CCK cause exocrine pancreas

A

Maximal acinar release of digestive enzyme

145
Q

What does secretin cause exocrine pancreas

A

Maximal ductal secretion of HCO3- and fluid

146
Q

CCK effect on bile release

A

Contraction of gallbladder

Relaxes sphincter of Oddi

147
Q

ACh effect on bile release

A

Contraction of gall bladder

148
Q

Principle roles of bile

A

Gastric acid neutralization

Assist with lipid absorption

149
Q

Nutrients that trigger GIP release

A

Proteins
Lipids
Carbohydrates

150
Q

Nutrients that trigger Secretin release

A

H+

Fatty acids

151
Q

Nutrients that trigger Gastrin release

A

Amino acids/peptones

Vagal stimulation

152
Q

Nutrients that trigger CCK release

A

Fatty acids&raquo_space; proteins

153
Q

Na/glucose or Na/Amino acid cotransporters timing

A

Primary mechanism after a meal

154
Q

Na/glucose or Na/amino acid cotransporters location

A

Duodenum
Jejunum (main)
Ileum

155
Q

Na-H exchanger timing

A

Postprandial

156
Q

Na-H exchanger location

A 
Duodenum
Jejunum (main)
157
Q

Parallel Na-H and Cl-HCO3 exchanger timing

A

primary mechanism during interdigestive period

158
Q

Parallel Na-H and Cl-HCO3 exchanger location

A

Ileum

Proximal colon

159
Q

Epithelial Na+ channel (ENaC) location

A

Distal colon

160
Q

Passive K+ absorption location

A

Jejunum

Ileum

161
Q

Passive K+ secretion location

A 
Proximal colon
Distal colon (main)
162
Q

Active K+ secretion location

A 
Proximal colon (main)
Distal colon
163
Q

Active K+ absorption location

A

Distal colon

164
Q

Na/Glucose or Na/Amino acid cotransporters enterotoxin effect

A

No effect

165
Q

Parallel Na-H and Cl-HCO3 exchanger enterotoxin effect

A

Decreases Na+ absorption

166
Q

What inhibits ENaC

A

Amiloride

167
Q

What enhances ENaC

A

Aldosterone

168
Q

Active K+ secretion stimulation

A

cAMP, Ca2+

169
Q

Active K+ secretion enhanced by

A

Aldosterone

170
Q

Small intestine K+ transport

A

Net absorption

171
Q

Large intestine K+ transport

A

Net secretion

172
Q

Passive Cl- absorption timing

A

During a meal

173
Q

Passive Cl- absorption location

A

Jejunum (main)
Ileum (limited)
Distal colon (main)

174
Q

Cl-HCO3 exchanger timing

A

Interdigestive

175
Q

Cl-HCO3 exchanger location

A

Ileum
Proximal colon (main)
Distal colon

176
Q

Cl- Secretion location

A 
Duodenum
Jejunum
Ileum
Proximal colon
Distal colon
177
Q

Bacterial enterotoxins secretagogue

A

Cholera toxin
E. coli; heat labile and heat stable
Yersinia toxin
Clostridium difficile toxin

178
Q

Cholera toxin second messenger

A

cAMP

179
Q

E. coli heat labile second messenger

A

cAMP

180
Q

E. coli heat stable second messenger

A

cGMP

181
Q

Yersinia toxin second messenger

A

cGMP

182
Q

Clostridium difficile toxin second messenger

A

Ca2+

183
Q

Hormones and neurotransmitters secretagogue

A 
VIP
Guanylin
Acetylcholine
Bradykinin
Serotonin (5-HT)
184
Q

VIP second messenger

A

cAMP

185
Q

Guanylin second messenger

A

cGMP

186
Q

Acetylcholine second messenger

A

Ca2+

187
Q

Bradykinin second messenger

A

Ca2+

188
Q

Serotonin (5-HT) second messenger

A

Ca2+

189
Q

Immune cell products secretagogue

A

Histamine

Prostaglandins

190
Q

Histamine second messenger

A

cAMP

191
Q

Prostaglandins second messenger

A

cAMP

192
Q

Laxatives secretagogue

A

Bile acids

Ricinoleic acid

193
Q

Bile acid second messenger

A

Ca2+

194
Q

Lamina Propria cells affect on intestinal ion transport Macrophages

A

Prostaglandins

O2 radicals

195
Q

Lamina Propria cells affect on intestinal ion transport Mast cells

A

Histamine

196
Q

Lamina Propria cells affect on intestinal ion transport neutrophils

A

Eicosanoids

Platelet-activating factor

197
Q

Lamina Propria cells affect on intestinal ion transport fibroblasts

A

Eicosanoids

Bradykinin

198
Q

Sucrose

A

Glucose + fructose

199
Q

Lactose

A

Glucose + Galactose

200
Q

Maltose

A

2 glucose

201
Q

Maltotriose

A

3 glucose

202
Q

Lactase deficiency causes

A

Physiological
Familial
Decreased mucosal surface area
Damage to enterocytes

203
Q

Lactase deficiency problems

A

Milk intolerance
Flatulence/distention
Diarrhea
Cramps

204
Q

Trypsinogen activating agent

A

Enteropeptidase

Trypsin

205
Q

Trypsinogen active enzyme

A

Trypsin

206
Q

Trypsinogen action

A

endopeptidase

207
Q

Trypsinogen products

A

Oligopeptides (2-6 amino acids)

208
Q

Chymotrypsinogen activating agent

A

Trypsin

209
Q

Chymotrypsinogen active enzyme

A

Chymotrypsin

210
Q

Chymotrypsinogen action

A

Endopeptidase

211
Q

Chymotrypsinogen products

A

Oligopeptides (2-6 amino acids)

212
Q

Proelastase activating agent

A

Trypsin

213
Q

Proelastase active enzyme

A

Elastase

214
Q

Proelastase action

A

Endopeptidase

215
Q

Proelastase products

A

Oligopeptides (2-6 amino acids)

216
Q

Procarboxypeptidase A activating agent

A

Trypsin

217
Q

Procarboxypeptidase A active enzyme

A

Carboxypeptidase A

218
Q

Procarboxypeptidase A Action

A

Exopeptidase

219
Q

Procarboxypeptidase A products

A

Single amino acids

220
Q

Procarboxypeptidase B activating agent

A

Trypsin

221
Q

Procarboxypeptidase B active enzyme

A

Carboxypeptidase B

222
Q

Procarboxypeptidase B action

A

Exopeptidase

223
Q

Procarboxypeptidase B products

A

Single amino acids

224
Q

Peyer’s patches

A

Aggregated lymphoid tissue in lamina propria

225
Q

Detergents

A

Amphipathic molecules that are water-soluble below CMC and form micelles above CMC

226
Q

Emulsifiers

A

Amphipathic molecules that can be incorporated into micelles

227
Q

Surfactants

A

Amphipathic molecules that helps stabilize two non-mixable fluids

228
Q

Why do we need cholesterol

A

Makes membranes pliable, yet tight

229
Q

Where does cholesterol come from

A

Synthesized by liver

Diet

230
Q

How do we get rid of cholesterol

A

Predominantly by bile acid synthesis

231
Q

Bad properties of cholesterol

A

Insoluble in water
Limited lipid solubility
Forms crystals when lipids are saturated

232
Q

Gut derived lipoproteins

A

Chylomicrons

Remnant chylomicrons

233
Q

Liver derived lipoproteins

A

VLDL
LDL
HDL

234
Q

Chylomicrons core

A

TAGs
Vitamins A, E, and K
Cholesterol
Cholesterol esters

235
Q

Chylomicrons surface

A

Apolipoprotein A1
Phospholipids
Cholesterol

236
Q

Cl- secretion stimulators

A

cAMP
cGMP
Ca2+

237
Q

Carbohydrate absorption

A

Duodenum (main)
Jejunum
Ileum

238
Q

Alpha-amylase produces:

A

Maltose
Maltotriose
alpha-limit dextrins

239
Q

SGLT1 functions

A

Mediates glucose and galactose into enterocytes

240
Q

GLUT5 function

A

Facilitated diffusion of fructose into enterocytes

241
Q

GLUT2 function

A

Facilitated diffusion of all three monosaccharides out of the enterocytes

242
Q

Isomaltase function

A

Breaks alpha 1,6 linkages

243
Q

Oligopeptide abosrption

A

H/oligopeptide cotransporter

244
Q

Amino acid absorption

A

Na/AA cotransporter

245
Q

Where is cobalamin absorbed

A

Ileum

246
Q

What stimulates intrinsic factor release

A

Histamine
ACh
Gastrin

247
Q

Ca2+ absorption

A

Passive throughout small intestine

Active in duodenum

248
Q

How does Ca2+ enter enterocyte

A

TRPV6 channel

249
Q

How does Ca2+ exit enterocyte

A

Ca-H pump

Na-Ca exchanger

250
Q

What is required for active Ca2+ absorption

A

Vitamin D

251
Q

Calbindin

A

Keeps [Ca2+]i low
Driving force for more absorption
Ca2+ crucial second messenger to many pathways

252
Q

Absorption of Folate location

A

Duodenum

253
Q

Which form of iron is absorbed

A

Ferrous (Fe2+)

254
Q

How does Fe2+ exit enterocyte

A

Ferroportin

255
Q

Water soluble vitamins

A

B and C

256
Q

Fat soluble vitamins

A

A
D
E
K

257
Q

Anabolic functions in fed state

A

Glycogen synthesis
Lipogenesis
Protein synthesis

258
Q

Catabolic functions in fasting state

A

Glycogenolysis
Lipolysis + Ketogenesis
Proteolysis

259
Q

What ketone bodies do our bodies produce

A

Acetone
Acetoacetate
3-beta hydroxybutyrate

260
Q

Glucose Homeostasis phase I

A

Brain uses glucose
Excess stored as glycogen
Cutoff @ 4 hours

261
Q

Glucose Homeostasis Phase II

A

Short-term fasting between meals
Glycogen is used for glucose synthesis
Cutoff @ 16 hours

262
Q

Glucose Homeostasis Phase III

A

Glycogen is depleted
Gluconeogenesis increases
Cutoff @ 2 days

263
Q

Glucose Homeostasis Phase IV, V

A

Fuel sparing
Gluconeogenesis dips
Body relies on fats (keto acids)

264
Q

What important gluconeogenic enzyme is the muscle missing

A

Glucose-6-Phosphatase

265
Q

Phosphoglycerate kinase

A

1,3-BPG => 3-phosphoglycerate

266
Q

Pyruvate kinase

A

PEP => Pyruvate

267
Q

Glucokinase and Hexokinase

A

Glucose => Glucose-6-P

268
Q

Phosphofructo-kinase-1

A

Fructose-6-P => Fructose-1,6-BP

269
Q

Pyruvate dehydrogenase

A

Pyruvate => Acetyl CoA

270
Q

Pyruvate carboxylase

A

Pyruvate => OAA

271
Q

PEP carboxykinase

A

OAA => Phosphoenolpyruvate

272
Q

Fructose bisphosphatase

A

Fructose-1,6-P => Fructose-6-P

273
Q

Glucose 6-Phosphatase

A

Glucose-6-P => Glucose

274
Q

Rate limiting step of glycolysis

A

PFK-1

275
Q

Glucokinase glucokinase affinity

A

Low

Not easily saturated

276
Q

Hexokinase glucose affinity

A

High

Saturable

277
Q

Which enzyme is inhibited by G6P

A

Hexokinase

278
Q

What upregulated PFK-1

A

F-2,6-BP

279
Q

Malate-aspartate shuttle location

A

Liver and heart

280
Q

What does the malate-aspartate shuttle produce

A

NADH

281
Q

alpha-Glycerol phosphate shuttle location

A

Brain and muscle

282
Q

What does the alpha-glycerol phosphate shuttle produce

A

FADH2

Medical Physiology I (8 decks)

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