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Physiology 2 > Physiology from Midterm 2 to Final > Flashcards

Physiology from Midterm 2 to Final Flashcards

1
Q

What is digestion a combination of?

A

Mechanical and enzymatic processes

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2
Q

Where does digestion occur?

A

Mouth, stomach, and small intestine

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3
Q

What is the point of chewing food?

A

Exposes more surface area for enzymes

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4
Q

What does the emulsification of fat via bile do?

A

Exposes more surface area for enzymes

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5
Q

What is absorption?

A

Crossing the gut epithelium

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6
Q

Where does most digestion occur?

A

Small intestine

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7
Q

Where does most absorption occur?

A

Mostly in small intestine (some ions and water absorbed in large intestine)

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8
Q

Does fat enter the bloodstream?

A

NO, enters lymph as lacteals

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9
Q

What part of the GI system is directly regulated?

A

Motility and secretion, which are regulated by hormones, nervous system, and local mechanisms

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10
Q

Order of absoprtion in small intestine?

A

Lumen –> apical membrane –> epithelial cell (enterocyte) –> basolateral membrane –? interstitium –> capillary in hte villi or the lymph (fat)

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11
Q

What do goblet cells do in the small intestine?

A

Secrete mucous

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12
Q

What do crypt cells do in the SI?

A

secrete ions and water

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13
Q

What constitutes approx. 50% of our diet?

A

Carbs…mostly starch and sucrose (table sugar), followed by glycogen, cellulose, glucose, fructose, etc.

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14
Q

Membrane transporters for carbs can transport what>

A

MONOsaccharides

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15
Q

How do artificial sweeteners work?

A

Typically interact with “sweet” receptors, but cannot be digested to a form that can cross into enterocytes (have Cl- instead of OH- groups)

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16
Q

What enzyme breaks down starch to maltose?

A

Amylase

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17
Q

What breaks down disaccharides?

A

Disaccharidases (maltase, sucrase, and lactase) found on brush border

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18
Q

Glucose enters the intestinal enterocytes via what transporter and leaves via what transporter?

A

Enters with Na+ via SGLT and exits on GLUT2

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19
Q

Fructose enters SI enterocytes via what transporter and leaves on what?

A

Enters via GLUT5 and exits on GLUT2

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20
Q

Where are the Na+/K+ ATPase pumps found on intestinal cells?

A

Basolateral side

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21
Q

What are endopeptidases?

A

Attack peptide bonds in the interior of the AA chain and break long peptide chains into smaller segments

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22
Q

Examples of endopeptidases?

A

Pepsin (stomach) and Trypsin/chymotrypsin (pancreas)

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23
Q

What are exopeptidases?

A

Release single AA from peptides by chopping them off the ends, one at a time

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24
Q

Examples of exopeptidases?

A

Carboxypeptidase and aminopeptidase from the pancrease

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25
Q

Products of protein digestion?

A

Free AAs, di and tripeptides

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26
Q

How are di and tripeptides absorbed?

A

Cotransport with H+ on the apical and basolateral membranes

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27
Q

How are amino acids absorbed?

A

Cotransport with Na+ on apical side (like glucose) and antiport with Na+ on basolateral side

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28
Q

How do babies reabsorb immunoglobulins during the first few days after birth?

A

The small peptides are carried intact across the cell by transcytosis

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29
Q

Most of the fat calories in our diet come from?

A

Trigylcerides because it is the major lipid in both animals and plants…cholesterol, phospholipids, long chain fatty acids, fat soluble vitamins

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30
Q

Why is the digestion of fats complicated?

A

Because it isn’t soluble in water…have low surface area for digestion in stomach

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31
Q

What are bile salts?

A

Amphipathic derivatives from cholesterol that break down fats

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32
Q

How do bile salts work?

A

Bile salts coat lipids to make emulsions of large droplets. The hydrophobic side associates with lipids, and the polar side chains/hydrophilic side associates with water.

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33
Q

What do pancreatic lipases do?

A

Can act on trigylcerides, in droplets, aided by colipase from pancreas

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34
Q

What are micelles?

A

Smaller droplets of fat that contain smaller components of fat, except cholesterol.. Micelles can then move close to surface of enterocytes and lipids can diffuse across apical membrane into cells.

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35
Q

Steps in fat absorption?

A
  1. Bile salts coat fat droplets 2. Pancreatic lipase and colipase break down fats into monoglycerides and fatty acids stored in micelles 3. Monoglycerides and fatty acids diffuse from micelles and cross cell membranes 4. Cholesterol is actively transported into cells 5. Absorbed fats combine with cholesterol and proteins in intestinal cells to form chylomicrons 5. Chylomicrons removed by lymphatic system, and short fatty acids can travel solo, entering capillaries rather than lymph
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36
Q

Steps in nucleic acid digestion?

A

Digested into nucleotides, then bases, and monosaccharides. Bases absorbed via ACTIVE transport. Sugars absorbed via same transporters as other monosaccharides

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37
Q

How are fat soluble vitamins reabsorbs?

A

Absorbed in SI with fats

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38
Q

Fat soluble vitamins?

A

A, D, E, K

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39
Q

How are water soluble vitamins absorbed?

A

Typically absorbed in SI via membrane transporters

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40
Q

Water soluble vitamins?

A

C, most Bs

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41
Q

Where is Vitamin B12 absorbed?

A

In the ileum

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42
Q

What does vitamin B12 require to be absorbed in the ileum?

A

Requires protein secreted by gastric parietal cells called intrinsic factor

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43
Q

What does deficiency of intrinsic factor lead to?

A

Deficiency of B12 that cannot be corrected by oral B12 supplemenntation

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44
Q

What 2 substances are homeostatically regulated in SI?

A

Iron and Calcium…decreased levels –> detectors –> signal –> increased intestinal uptake

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45
Q

How is absorption of ions and water caused in the small and large intestine?

A

Ions (esp Na+) move across apical side via various transporters; main driver in basolateral side in Na/K ATPase; water follows by osmosis

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46
Q

In the regulation of GI function, what are long reflexes?

A

Reflexes integrated in the CNS; sensory from GI tract to CNS and feedforward relfexes that originate outside the GI tract

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47
Q

What are cephalic reflexes?

A

Long reflexes that occur completely outside the digestive system…feedforward responses in response to sight, smell, thought of food, effects of emotion

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48
Q

What limb of the autonomic nervous system is excitatory in the GI tract?

A

Parasympthathetic

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49
Q

What are short reflexes in the GI tract?

A

Integrated within the gut in the enteric nervous system

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50
Q

WHat do neurons in submucosal plexus do?

A

Receive signals from lumen, regulate secretion

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51
Q

What do neurons in the myenteric plexus do?

A

Regulate motility

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52
Q

Reflexes involving gut peptides act where, and effect what?

A

Can act locally (paracrine) or travel via blood (endocrine) and can effect motility (altered peristalsis, gastric emptying, etc) and effec both exocrine and endocrine secretion…some gut peptides can also act on brain or are produced there

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53
Q

What are the parallels between the enteric and central nervous systems?

A

Intrinsic neurons lie entirely within gut, similar to interneurons within gut and autonomic neurons that bring signals from CNS to gut are extrinsic neurons 2. Release more than 30 different NT and neuromodulators that are not NE/E/Ach, similar to those in CNS 3. Has glial cupport cells, similar to astrocytes in CNS 4. Diffusion barries with capillaries surrounding glanglia that are not very permeable, like blood-brain barrier 5. Acts as an integrating centre, gut function can be regulated without CNS

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54
Q

What did the Bayliss and Starling experiment determine?

A

Acidic chyme entering the small intestine caused pancreatic secretion even when all nerves to the pancreas were cut. Applied extract of duodenum to pancreas, and it caused pancreatic secretion. Therefore, the factor from the intestine that stimulated secretion was called secretin.

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55
Q

3 families of gut hormones?

A

Gastrin family, secretin family, and motilin

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56
Q

Gastin family gut hoemones?

A

Gastrin, CCK, et al.

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57
Q

Targets of the gastrin family hormones?

A

Stomach for gastrin and intestine and accessory organs for CCK

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58
Q

Secretin family gut hormones?

A

Secretin, vasoactive intentestinal peptide (VIP), gastric inhibitory peptide (GIP), glucagon like peptide (GLP-1)

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59
Q

Targets of secretin family?

A

BOth endocrine and exocrine

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60
Q

What is motilin and what does it do?

A

Family of gut hormone that acts on gut smooth muscle and regulates migrating motor complexes

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61
Q

Role of oral cavity and esophagus in GI function?

A

M: swallowing, chewing S: saliva D: carbs (salivary amylase) A: none

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62
Q

Role of stomach in GI function?

A

M: mixing and propulsion (peristalsis) S: HCl, pepsinogen and gastric lipase, mucus and HCO3-, gastrin, histamine D: proteins and fasts A: lipid soluble substances such as alcohol and aspirin

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63
Q

Role of SI in GI function?

A

M: mixing and propulsion mostly by segmentation S: enzymes, HCO3-, bile, mucus, CCK, secretin, GIP, etc. D: carbs, fats, polypeptides, nucleic acids A: peptides, AA, glucose, fructose, fats, water, ions, minerals, vitamins

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64
Q

Role of large intestine in GI function?

A

M: segmental mixing; mass movement for propulsion S: mucus D: none, except for my bacteria A: ions, water, minerals, vitamins, small organicc molecules produced by bacteria

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65
Q

What is the cephalic phase of GI function?

A

Anticipation of food/presence of food in mouth –> activation of neurons in medulla –> efferent signals to salivary glands and autonomic signals via vagus to enteric nervous system –> increase in motility and secretion in stomach, intestine, and accessory organs

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66
Q

When do short reflexes in the GI tract occur?

A

When food hits the stomach/distension

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67
Q

Where does digestion begin?

A

In the mouth

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68
Q

What controls the secretion of saliva?

A

Autonomic nervous system

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69
Q

What does saliva do?

A

Softens and lubricates food. Chemical digestion via salivary amylase and some lipase. Also, antimicorbial through lysozyme and immunoglobulins.

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70
Q

What is the proper name of chewing?

A

Mastication

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71
Q

What is the proper name for swallowing?

A

Deglutition

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72
Q

Steps in the swallowing reflex?

A
  1. Tngue pushes bolus against soft palate and back of mouth, triggering swallowing reflex. Soft palate elevates closing off nasopharynx. 2. Breathing inhibited as bollus passes airway. Epiglottis folds down to help keep swallowed material out of airways, and upper esophageal sphincter relaxes.
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73
Q

Where is the swallowing reflex integrated?

A

The medulla. Sensory afferents in cranial nerve IX and somatic motor neuron and autonomic neurons mediate reflex.

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74
Q

What is gastroesophageal reflux disease?

A

Heartburn. Caused by the splashing up of acid from the stomach into lower esophagus during respiration (intrathoracic pressure drops) or during churning of the stomach.

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75
Q

What initiates digestive activity in stomach?

A

Long vagal reflex of the cephalic phase. Once food enters the stomach, series of short reflexes constitute gastric phase.

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76
Q

3 functions of the stomach?

A
  1. Storage 2. Digestion 3. Protection
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77
Q

Why is the storage function of the stomach so important?

A

Its neurally mediated receptive relaxation of upper stomach helps to keep undigested food blasting into the SI, which causes numerous problems (dumping syndrome)

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78
Q

Do secretions happen before food arrives?

A

Yeah

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79
Q

How does the stomach offer protection?

A

Antimicrobial via acid, and self-protection through teh mucus-bicarb barrier

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80
Q

What cells secrete gastric acid?

A

Parietal cells in tummy

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81
Q

What does gastric acid do?

A

Activates pepsin, denatures proteins to make them more accessible to pepsin, and acts as an anti-microbial agent

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82
Q

What cells secrete pepsinogen?

A

Chief cells

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83
Q

What is pepsinogen cleaved into?

A

Pepsin

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84
Q

What does pepsinogen do?

A

An endopeptidase that is particulary effective on collagen (meat digestion)

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85
Q

What cells secrete gastric lipase?

A

Chief cells…co-secreted with pepsinogen

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86
Q

What does gastric lipase do?

A

MINOR contribution to fat digestion

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87
Q

What cells secrete histamine in the GI tract?

A

Enterochromaffin-like cells (ECL)

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88
Q

What does histamine do in the GI tract?

A

Binds to H2 receptors in parietal cells, which promotes acid secretion

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89
Q

What cells secrete somatostatin?

A

D cells

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90
Q

What does somatostatin do?

A

Shits down secretion of acid and pepsinogen

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91
Q

What cells secrete gastrin?

A

G cells

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92
Q

What triggers the release of gastrin?

A

Both long and short loop reflexes

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93
Q

Steps in the integration of cephalic and gastric phases?

A
  1. Food or cephalic reflexes initiate gastric secretion 2. Gastrin stimulates acid secretion by direct action on parietal cells or indirectly through histamine 3. Acid stimulates short reflex secretion of pepsinogen 4. Somatostatin release by H+ is negative feedback signal that modulates acid and pepsin release.
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94
Q

What is the mucus bicarb barrier in the stomach?

A

Gastric mucous cells produce mucus that lies in a layer above the cells, allowing the pH to be 7 at the cell surface vs. pH 2 in lumen of stomach

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95
Q

What is a peptic ulcer>

A

Acid and pepsin damage mucosal surface, creating holes that extend into submucosa and muscularis layers

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96
Q

Prevention and treatment of peptic ulcers?

A
  1. Ingestion of anti-acids that neutralize gastric acid 2. H2 receptor antagonists that block the action of histamine, so parietal cells don’t release H+ 3. Proton pump inhibitors that block the H+/K+ ATPase
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97
Q

Method of acid secretion in parietal cells?

A

H+/K+ ATPase on apical membrane exports H+ in exchange for K+. HCO3-/Cl- on basolateral side pumps in CL- in exchange for bicarb. Cl- leaves parietal cells via a open CL- channel

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98
Q

What begins the intestinal phase of GI function?

A

Controlled entry of chyme into small intestine. Sensors in duodenum feed back to stomach to control dilvery of chyme, feed forward to intestine to promote digestion, motility and nutrient utilization

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99
Q

What is secreted during the intenstinal phase of GI function?

A

Bicarb, mucus, bile, and enzymes as zymogens

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100
Q

Carbs in the small intestine activate what hormones?

A

GIP and GLP-1

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101
Q

What do GIP and GLP-1 stimulate?

A

Release of insulin from pancrease

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102
Q

What do fats and proteins in the SI activate?

A

CCK release

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103
Q

What does CCK secretion activate?

A

Pancreatic enzyme secretion

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104
Q

What does secretin do?

A

Activates pancreatic bicarb secretion

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105
Q

What stimulates the release of bibarb from the pancreas’ duct cells?

A

Neural signals and secretin

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106
Q

What is the function of bicarb in GI function?

A

Neutralize chyme

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107
Q

What is the stimulus of release of mucus from goblet cells?

A

Increase inflammation…for protection and lubrication

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108
Q

What stimulates the release of bile from gall bladder?

A

CCK, presence of fats and proteins

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109
Q

Purpose of bile>

A

Fat digestion

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110
Q

Where is bile reabsorbed?

A

In the ileum, enters circulation, and travels back to liver. Recycled several times during a meal.

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111
Q

Steps in activation of pancreatic zymogens?

A
  1. Pancreatic secretions including zymogens enters small intestine through the pancreatic duct 2. Enteropeptidases in brush border activate trpysinogen into trypsin 3. Trypsin activates zymogens (chymotrypsinogen/chymotrypsin, procarboxypeptidase/carboxypeptidase, procolipase/colipase, and prophospholipase/phospholipase)
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112
Q

Where is most fluid absorbed?

A

Small intestine

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113
Q

What causes absorption in the SI?

A

Transport of organic nutrients and ions create osmotic gradient

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114
Q

Where do most nutrients absorbed in small intestine go?

A

Move into capillaries in villi, then into hepatic portal vein. Fats go into lymphatic systems. Xenobiotics must first pass through the liver before reaching the systemic circulation

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115
Q

Where does food enter the large intestine?

A

Iliocecal valve

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116
Q

What are the incomplete muscles on the LI that create haustra called?

A

Tenia coli

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117
Q

What is the main role of the large intestine?

A

Removes most of remaining water and forms feces

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118
Q

What is the motility like in the large intestine?

A

Iliocecal valce relaxes each time a peristalic waves reaches it and contracts when food leaves stomach (gastroileal reflex). Segmental contractions with little forward movement except when mass movements occur (3-4 times/day). Waves of contraction send bolus forward and triggerdistension of rectum…defacation reflex

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119
Q

What is osmotic diarrhea?

A

Unabsorbed, osmotically active solutes such as undigested lactose, sorbitol, olestra, or osmotic laxatives draw water into large intestine and cause excessive defecation

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120
Q

Secretory diarrhea?

A

Bacterial toxins, such as cholera, increase Cl- secretion. Diarrhea can be adaptive but can also lead to dehydration and metabolic acidosis

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121
Q

To be absorbed in the SI, carbs must be broken down to ______ and moved across the apical membrane of intestinal epithelium by ______

A

Monosaccharide units and 2ndary active transport

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122
Q

Order of protein digestion

A

Acid denaturation, endopeptidases, exopeptidases

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123
Q

Bile salts are…

A

Amphipathic derivatives of cholesterol that are stored in and secreted by the gall bladder

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124
Q

What is homeostatic eating?

A

Eating when energy fuels are depleted and not eating when energy fuels are sufficient…metabolically driven eating

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125
Q

What is non-homeostatic eating?

A

Eating in the complete absence of hunger, and eating despite large fat reserves. Involves cognitive, reward, and emotional factors. Also, has neural parallels with addiction mechanisms. “Hedonic” eating.

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126
Q

What are the two control centres for homeostatic eating, and where are they located?

A

Hunger/feeding centre and satiety centre in the hyopthalamus

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127
Q

What is the glucostatic theory?

A

Food intake is regulated by glucose levels, monitored by centres in the hypothalamus. When plasma glucose is low, satiety centre is depressed and feeding centre is dominant.

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128
Q

What is the lipostatic theory?

A

Signal from fat stores to the brain modulates eating behaviour. Leptin, synthesized in white adipose tissue, tells the brain to stop eating.

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129
Q

What happens if the “ob” gene is knocked out?

A

There is a mutation in making leptin, which means leptin isn’t produced, so no signal to stop eating, causing extreme obesity and voracious eaters/

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130
Q

What happens id the db/db receptor is knocked out?

A

No receptor for leptin, so you don’t stop eating.

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131
Q

Peptides that increase food intake and their location?

A

Ghrelin, released from cells in an emptystomach. Neuropeptide Y, released from hypothalamus. Orexins, released from hypothalamus.

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132
Q

Singals from the gut that decrease appetite and their location?

A

Inc. stretch of stomach and acid secretion in stomach. Increased CCK and increased glucose in lumen of upper SI. Increased GLP-1 in the lower small intestine/colon.

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133
Q

Energy input comes from?

A

Diet (hunger/appetite, satiety, and social/psychological factors)

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134
Q

How much of the energy output comes from heat? Work?

A

50% for both

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135
Q

What is the energy output for work used for?

A

Transport across membranes, mechanical work (movement), Chemical work (synthesis for growth and maintenance, energy storage, such as ATP and PCr, and chemical bonds, such as glycogen and fat)

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136
Q

How is metabolic rate estimated?

A

Rate of oxygen consumption and CO2 production, and how much O2 is produced fro macronutrients other than glucose.

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137
Q

Equation for reaction of glucose to yield energy?

A

C6H1206 + O2 + ADP + Pi —> CO2 + H2O + ATP + heat

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138
Q

Factors affecting metabolic rate?

A

Age, sex, lean muscle mass (muscle has higher O2 consumption than adipose at rest), activity level, diet (heat production increases after eating, extent depends on what was eaten), hormones, gut peptides, and genetics/

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139
Q

3 fates of ingested biomolecules?

A
  1. Energy to do mechanical work 2. Synthesis for growth and maintenance 3. Storage as glycogen (liver, skeletal muscles) or fat
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140
Q

2 states of metabolism?

A
  1. Fed/absorptive state 2. Fasted/postabsorptive state
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141
Q

What is the fed/absorptive state?

A

Anabolic, products of digestion being absorbed and used or stored

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142
Q

What is the fasted/postabsorptive state?

A

Catabolic, body taps into stores to maintain blood glucose levels, even though no food is coming into the body.

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143
Q

What are the nutrient pools that are available for immediate use (mostly in plasma)?

A

Glucose pool, amino acid pool, and free fatty acid pool

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144
Q

In the fed-state what enzymes are active and which are deactivated?

A

Insulin is active, leading to net glycogen synthesis, whereas enzymes for glycogen breakdown are inhibited.

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145
Q

In the fasated-state metabolism, what enzymes are active, and which are inactive?

A

Glucagon is active, and enzymes that break down glycogen are more active. Enzymes for glycogen synthesis are inhibited.

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146
Q

In the fed state, how much of the absorbed glucose in the liver passes through to brain, muscles, and other tissues?

A

Approx. 70%

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147
Q

In the fed-state, how much of the absorbed glucose in the liver travels into the interstitium and then into hepatic cells via GLUT transporters?

A

Apprx. 30%

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148
Q

Glucose that moves into hepatic cells via GLUT transporters during the fed state is used for?

A
  1. ATP synthesis or 2. Stored as glycogen or fat
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149
Q

What is the main source of glucose in the post-absorptive state?

A

Glycogen

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150
Q

How many hours of energy does liver glycogen provide?

A

Apprx 4 hours

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151
Q

In the fed state, where do absorbed AAs travel to?

A

To the liver, where some pass through, used for synthesis of structural proteins, enzymes, hormones, amines, and others move into interstitium then into hepatic cells for synthesis of liver enzymes, plasma proteins, and lipoproteins.

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152
Q

What happens to excess proteins?

A

Converted to FAT

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153
Q

Where are chlyomicrons formed?

A

Enterocytes

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154
Q

What makes up a chylomicron?

A

Cholesterol, TGs, phospolipids plus lipid binding proteins (apoproteins)

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155
Q

What happens to chylomicrons ater they enter the circulation from lymphatic drainage?

A

Acted upon by lipases in capillary endothelium—FFA can be oxidized for energy (most cells), FFA plus glycerol can be re-esterfied and stores as TG (adipose), and remaining particles (HDL, chylomicron remnants) taken up by liver

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156
Q

What can the liver do in regards to fat?

A

Metabolize fat, store fat as TGs, use cholesterol to form bile salts, which are released into gut lumen, and package FFA and cholesterol as LDL particles, which are releaed into circulation as sources of cholesterol and FAs

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157
Q

How are LDL-C particles taken into the cell?

A

By receptor mediated endocytosis when apoproteins interact with receptors.

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158
Q

Steps in Fat Synthesis

A
  1. Glycerol can be made from glucose through glycolysis 2. Fatty acids made when 2-carbon acyl units from acetyl CoA link together 3. One glycerol plus 3 FAs —> triglyceride (happens in smooth ER) 4. Even with 0 dietary cholesterol, colesterol can and will be synthesized from Acetyl CoA (HMG Co-Reductase)
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159
Q

During the fasted-state, what pathways are used to maintain plasma glucose levels?

A

Glycogenolysis, lipolysis, amino acids, and gluconeogenesis

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160
Q

What is glycogenesis?

A

Making glycogen from glucose molecules via glycogen synthase

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161
Q

What is glycogenolysis?

A

Breaking down glycogen into glucosyl units via phosphorylase

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162
Q

What is glycolysis?

A

Forming 2, 3C pyruvates from glucose

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163
Q

Steps in the overview of fasted-state metabolism?

A
  1. Liver releases glucose from stored glycogen 2. TGs in adipose broken down into FFAs and glycerol 3. Glycogen used for energy in muscle. Muscles also used FAs and break down their proteins to amino acids that enter the blood in extreme cases 4. Brain can only use glucose and ketone bodies
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164
Q

How can muscle contribute to plasma glucose?

A

Only indirectly by exporting pyruvate or lactate. Cannot release glucose because it doesn’t have glucose-6-phosphatase

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165
Q

2 options for formation of G-6-P from glycogen?

A
  1. Splitting off glucose by addition of Pi (90% of the time) 2. Splitting off glucose then spending an ATP to phosphorylate (only 10% of the time)
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166
Q

Amino acids are deaminated, giving rise to intermediates that can be?

A

Directly sent to glycolysis or TCA cycle or be sent to the liver to be converted to glucose (gluconeogenesis)

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167
Q

Proteolysis occurs when?

A

During extended fasts. Free AA pool is normally used for ATP production during fasted state.

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168
Q

What causes the formation of ketone bodies?

A

If lipolysis occurs faster than acetyl CoA can be used in TCA cycle, ketone bodies are formed. They can enter blood and serve as energy substrates for brain during times of starvation.

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169
Q

What type of diet increases ketone production?

A

Low carb/high fat, protein diets

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170
Q

Why can ketogenesis become dangerous?

A

Certain ketone bodies (acetoaceti acid, beta-hydroxybutyric acid) are strong metabolic acids that can disrupt acid-base balance

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171
Q

With respect to regulation of GI function, “long reflexes” refer to…

A

PNS efferent info from brainstem to GI tract that stimulates GI activity and cephalic relfexes of digestion such that the sight, smell, or through of food stimulate GI activity

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172
Q

Gastric acid secretion is stimulated by…

A

Histamine from ECL cells, PNS stimulation, and gastrin from G cells

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173
Q

Which secreted products of the intestine inhibit gastric acis secretion?

A

CCK, Secretin, and GLP-1

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174
Q

Which digestive hormone stimulates gall bladder contraction and pancreatic enzyme secretion?

A

CCK

175
Q

Insulin is release in response to…

A

Presence of carbs in SI, which stimulates GIP and GLP-1

176
Q

What is metabolism?

A

Whether transformations of energy substrates (carbs, fats, proteins) are biased toward storage/anabolism or breakdown/catabolism

177
Q

How is metabolism regulated?

A

Primarily through endocrine pancreas (insulin and glucagon) and neural (regulation of food intake and autonomic innervation of endocrine pancreas)

178
Q

What is the endocrine pancreas?

A

Endocrine cells found in Islets of Langerhans

179
Q

What do alpha cells in the endocrine pancreas to?

A

Secrete glucagon

180
Q

What do beta cells do in the endocrine pancreas?

A

Secrete insulin

181
Q

What do D cells do in the endocrine pancreas?

A

Secrete somatostatin

182
Q

What processes does insulin increase?

A

Glucose oxidation, glycogen synthesis, fat synthesis, and protein synthesis

183
Q

What processes does glucagon increase?

A

Glycogenolysis, gluconeogenesis, and ketogenesis

184
Q

What is insulin’s structure?

A

51 amino acids, A and B chains linked by two disulfide bridges. Tends to form dimers (A+B) x2, and hexamers in solution

185
Q

What is insulin secreted as?

A

Preproinsulin

186
Q

What is proinsulin cleaved into?

A

C peptide and insulin peptide

187
Q

What form of insulin can bind to receptors?

A

Only monomers

188
Q

Factors affecting release of insulin?

A

Increased plasma glucose (greater than 100 mg/dL), plasma AAs, GLP-1 and GIP, and parasympathetic activity (inhibited by SNS)

189
Q

Targets of insulin?

A

Striated muscle, fat, liver (NOT brain, kidney, intestine)

190
Q

Actions of insulin in adipose and muscle?

A

Increase glucose transport into cells, increase glucose metabolism, glycogenesis, fat synthesis, and protein synthesis

191
Q

Actions of insulin on hepatocytes?

A

Increase glucose metabolism, increased glyocgenesis, fat synthesis, and protein synthesis

192
Q

How is insulin release stimulated in pancreation beta cells?

A
  1. High blood glucose 2. Metabolism within hepatocyte increases 3. Increase ATP 4. ATP gated K+ channels close 5. Cell depolarizes and calcium channels open 6. Ca2+ enters 7. Exocytosis of insulin
193
Q

GLUT transporters found in hepatocytes?

A

GLUT-2

194
Q

Does insulin cause a recruitment of GLUT transporters to the membrane in the liver?

A

NO. Insulin activates hexokinase, to add a phoshpate to glucose, which maintains low [glucose] in cell and starts glycolysis/energy production

195
Q

How does the insulin receptor work?

A

Enzyme coupled receptor tyrosine kinase. When activated, RTKs transfer phosphate groups to insulin receptor substrates, which alter protein/enzyme activity, causing cell responses

196
Q

Where does insulin bind on its receptor?

A

The 2 alpha sub-units located extracellularly

197
Q

What are the beta subunits in the insulin receptor?

A

Penetrate through the membrane…ATP-binding and tyrosine kinase domains found there

198
Q

Steps in insulin mechanism of action

A
  1. Insulin binds to tyrosine kinase receptor 2. Receptor phosphorylates insulin-receptor substrates (IRS) 3. Seconds messenger pathways alter protein synthesis and existing proteins 4. Membrane transport is modified 5. Cell metabolism is changed
199
Q

What is the effect of insulin on adipose and muscle cells?

A
  1. Insulin binds to receptor 2. Singal transduction cascade 3. GLUT4 inserted to membrane 4. Glucose enters the cell
200
Q

Role of liver in a fasted state (no insulin)?

A

Hepatocytes make glucose and export it via GLUT2 transporters

201
Q

Effects of insulin in liver?

A

Gardient favours glucose import into hepatocyte via GLUT2. Insulin signalling activates hexokinase to start glycolysis/energy storage and making processes, and also keeps free glucose low in cell to maintain gradient)

202
Q

Insulin activates enzymes that enhance?

A

glycolysis (glucose oxidation), glycogenesis (storage), AA utilization/protein synthesis, lipogenesis (conversion of excess glucose and AA into triglycerides)

203
Q

Insulin inhibits enzymes that enhance?

A

Glucogoneogenesis, glycogenolysis, proteolysis, ketogenesis, lipolysis, and beta-oxidation of fatty acids

204
Q

When insulin is low or absent, what type of pathways dominate?

A

Catabolic

205
Q

Glucagon is a member of what gut hormone family?

A

Secretin, along with secretin, GIP, and GLP-1

206
Q

What is the main trigger of glucagon release?

A

Low plasma blood glucose

207
Q

What is the main target of glucagon?

A

Liver

208
Q

What type of receptor does glucagon work on?

A

G protein-coupled receptors, cyclic AMP

209
Q

What is the main function of glucagon?

A

To prevent hypoglycemia

210
Q

During an overnight fast, how much glucose from the liver comes from glyocogenolysis and glucoenogenesis?

A

75% and 25%

211
Q

Why do AAs stimulate insulin and glucagon release?

A

If a meal containing protein, but no carbs is ingested, insulin will lower blood sugar, even though there are no carbs to replace the lost blood glucose, so glucagon is released to insure blood glucose doens’t drop too low

212
Q

Type 1 diabetes?

A

Inadequate insulin secretion

213
Q

Type 2 diabetes?

A

Inadequate insulin secretion and/or abnormal target cell respsonsivenss

214
Q

What is metabolic syndrome?

A

At least 3 of: central obesity, hypertension, fasting blood glucose greater than 110 mg/dL, elevated fasting triglycerides, and low plasma HDL-cholesterol

215
Q

Is there ketoacidosis in Type 2 diabetes?

A

Not usually, because insulin IS still present, so liver can uptake glucose, meaning it doesn’t increase ketone production

216
Q

During the absoptive state in a person at rest, the liver…

A

forms glycogen

217
Q

CCK, a hormone from the SI…

A

slows gastric activity, decreases appetite, and increases secretion of enzymes from pancreatic acini cells

218
Q

Possible fats of FAs include…

A

beta-oxidation for energy, being re-esterified to TAGs and stored in adipose, or circulating in blood with lipoprotein particles

219
Q

What is the most readily available pool of lipids?

A

LDL

220
Q

During the fasting/post asborbitive state, muscle can contribute to maintenance of blood glucose levels by…

A

breaking down proteins and exporting AAs as gluconeogenic substrates to the liver, carrying out glycogenesis and sending pyruvate as glucoenogeneic substrate to the liver

221
Q

Ketogenesis occurs in a situation in which…

A

more acetyl CoA is formed than can be oxidized and rates of lipolysis are high

222
Q

A human with the same condition as an ob/ob mouse would be…

A

obese and would respond to treatment with exogenous leptin

223
Q

the sequence that best describes the path of a triglyceride as it is digested and absorbed.

A

Fat droplet, micelle, smooth ER of enterocyte, chylomicron, interstitium, lacteal

224
Q

Order of the layers of the adrenal gland starting with the outermost layer?

A

Capsule, Zona glimerulosa, Zone fasciculata, Zone reitcularis, and adrenal medulla

225
Q

What is made in the zona glomerulosa?

A

Aldosterone

226
Q

What is made in the zona fasciculata?

A

Glucocorticoids (cortisol and cotricosterone)

227
Q

What is made in the zona reticularis?

A

Sex hormones (various weak androgens)

228
Q

What is made in the adrenal medulla?

A

Mostly epinephrine

229
Q

Order of hormones made in the adrenal gland from the zona glomerulosa to the adrenal medulla?

A

Aldosterine, glucocorticoids, sex hormones, catecholamines

230
Q

What enzyme changes progesterone into glucocorticoids?

A

21-hydroxylase

231
Q

What is the first biologically active hormone?

A

Progesterone

232
Q

Hypothalamic-Pituitary-Adrenal Axis for cortisol?

A

Circadian rhythm, stress, or low blood glucose —> CRH in hypothalamus —> ACTH (from POMC) in ant. pit. —> cortisol in adrenal cortex (zona fasciculata) —> immunse system, liver, muscle, and adipose tissue

233
Q

Cortisol effect on immune system?

A

Supression

234
Q

Cortisol effect on liver?

A

Gluconeogenesis

235
Q

Cortisol effect on muscle?

A

Protein catabolism

236
Q

Cortisol effect on adipose tissue?

A

Lipolysis

237
Q

When do cortisol level peak>

A

early morning (4 - 8 am)

238
Q

What cells express glucocorticoid receptors?

A

All nucleated cells

239
Q

Whatt type of efects do glucocorticoids have?

A

Mostly longer term/genomic effects such as increased expression of enzymes and increased expression for other regulatory hormones.

240
Q

What are the main effects of glucocorticoids?

A
  1. Prevention of hypoglycemia/catabolism (lipolysis, proteolysis, and gluconeogenesis) 2. Supress immune response
241
Q

What are the 3 main targets of glucocorticoids?

A

Adipose, muscle, and liver

242
Q

What hormones is cortisol permissive for?

A

Glucagon and epinephrine

243
Q

What are the 3 generic responses to stress that Selye found>

A
  1. Adrenal hypertophy 2. Atrophy of thymus/lymph nodes 3. GI ulcers
244
Q

How long is the half life of epinephrine?

A

2 minutes

245
Q

What does the adrenal medulla act like?

A

Sympathetic post-ganglionic neurons

246
Q

What are the metabolic effects of epinephrine?

A

Dec insulin and inc glucagon, lipolysis, glycogenolysis in muscle, and glycogenolysis and gluconeogenesis in liver

247
Q

How are glucagon and epinephrine and cortisol similar and different?

A

Have similar metabolic effects, but cortisol and epinephrine have receptors expressed on a broader range of target cells

248
Q

What is primary hypercortisolism?

A

Cortisol-secreting adrenal hormones that are not regulated by ACTH

249
Q

What is secondary hypercortisolism/Cushing’s Syndrome?

A

Pituitary tumour that over-secretes ACTH

250
Q

What is iatrogenic hypercortisolism?

A

Secondary to cortisol therapy for other conditions

251
Q

What is hypocortisolism/Addison’s disease?

A

Primaray adrenal insufficiency, often immune problem that attacks cells in adrenal gland. Caused by mutations in key enzymes such as Hydroxylase 21

252
Q

What is ACTH synthesized from?

A

Pro-opiomelanocortin (POMC)

253
Q

What is alpha MSH used for?

A

Melanin synthesis, immune response, decreased food intake

254
Q

What other effects does CRH have?

A

Effects on food intake and mood disorders

255
Q

What cells of the thyroid gland secrete thyroid hormone?

A

Follicular cells

256
Q

What is the colloid?

A

the glycoprotein matrix in the thryoid gland

257
Q

What does the thyroid gland secrete?

A

Thyroid hormones and calitonin

258
Q

What is thyroid hormone made from?

A

Tyrosin and iodine

259
Q

What type of hormone mechanism is thyroid hormone similar to?

A

More like steroids…binds to nuclear receptor

260
Q

How does thyroid hormones travel in the blood?

A

Bound to thyroid-binding globulin because it is lipophilic

261
Q

What is hte main circulating form of thyroid hormone?

A

T4

262
Q

What is the most active form of thyroid hormone?

A

T3

263
Q

How is T4 converted to T3 at target cell?

A

Deiodinases remove an iodine

264
Q

Steps in thyroid hormone synthesis?

A
  1. Na+/I= symporter brings I- into the cell 2. Pendrin transporter moves I- into colloid 3. Follicular cell makes enzymes and thyroglobulin for colloid 4. Thyroid peroxidase adds idoine to tyrosine to make T3 and T4 5. Thyroglobulin is taken back into cell in vesicles with the iodines attached 6. Intracellular enzymes separate T3 and T4 from thyroglobulin 7. Free T3 and T4 enter circulation
265
Q

What is thyroid hormone essential for?

A

Normal growth and development, expecially the nervous system

266
Q

Wha tis the main function of thyroid hormone?

A

Provide substrates for oxidative metabolism…increase O2 consumption and generation of heat (thermogenesis) in most tissues and increase activity of Na+/K+ ATPase and interact with other hormones to modulate carbohydrate, protein, and lipid metabolism

267
Q

Symptoms of hyperthyroidism?

A

Increased O2 consumption, increased heat production (intolerant of heat), muscle weakness (protein catabolism), and neurological and cardiac effects

268
Q

What is the most common cause of thyroid pathologies?

A

Graves disease. Autoantibodies that resemble TSH overstimulate thyroid gland (not subject to negative feedback regulation)

269
Q

What are the sympthoms of hypothyroidism?

A

Decreased O2 consumption, increased heat production (intolerant to cold), neurological effects, fatigue, effects on skin, nails, and hair

270
Q

Most common cause of hypotyroidism?

A

Iodine deficiency

271
Q

Control of growth depends on?

A

Growth hormone, plus many other direct and permissive roles such as insulin, thyroid hormones, sex steroids, adequate nutrition, absence of chronic stress, and genetics

272
Q

What are the effects of growth hormones can be either what or what?

A

Effects can be direct (target cells express GH receptor) or indirect (mediated by insulin like growth factors produced by the lover or the target cells themselves)

273
Q

Metabolic effects of growth hormone?

A

Carbohydrates = indirect effect leads to inc. in plasma glucose Fat = incr. lipolysis and beta oxidation Protein = inc. AA uptake, inc protein synthesis, dec oxidation of protein for energy

274
Q

With respect to CHOs and fat, the metabolic effect of growth hormone are?

A

Catabolic/”anti-insulin”

275
Q

In respect to prtein, the effects of growth hormone are?

A

Anabolic/”pro-insulin”

276
Q

Deficiency in growth hormones due to GH hyposecretion or GH receptor mutations causes?

A

Dwarfism (although GH issues are not a common cause)

277
Q

Excess growth hormones beforce closure of growth plates of long bones causes?

A

Giantism

278
Q

Excess growth hormones after closure of growth plates in long bones causes?

A

Acromegaly…elongated chin

279
Q

The EXOCRINE pancreas produces…

A

Digestive enzymes

280
Q

Insulin lowers plasma by…

A

promoting fat synthesis, enhancing cellular utilization of AA, increasing glucose transport into most cells, and enhancing cellular utilization and storage of glucose

281
Q

Why are insulin and glucagon released in response to AA in blood?

A

Co-release of glucagon and insulin following ingestion of a pure protein meal will prevent hypoglycemia

282
Q

Diabetics who require exogenous insulin usually inject it rather than taking it as a pill, why?

A

Insulin is a protein and will therefore be broken down by the digetive system before it goes to the tissues.

283
Q

Hypothalamic-Pituitary Axis for thyroid hormone?

A

TRH –> TSH –> Thyroid gland –> Thyroid Hormone (T3 and T4)

284
Q

Hypothalamic-Pituitary Axis for cortisol?

A

CRH –> ACTH –> adrenal cortex (zona fasculata) –> cortisol

285
Q

Hypothalamix-Pituitary Axis for insulin like growth factors?

A

GHRH –> GH –> Liver –> insulin like growth factors –> many tissues

286
Q

How is soft tissue growth assessed?

A

Assessed by weight…involves both hypertrophy and hyperplasia (proliferation of cells)

287
Q

What does soft tissue growth require?

A

Requires GH (IGFs), thyroid hormone, and insulin. GH synergistic with thyroid hormone for protein synthesis and nervous system development. Insulin permissive for many GH effects.

288
Q

How is bone growth assessed?

A

Assessed by height

289
Q

What does bone growth require?

A

Hormonal support, protein, and sufficient calcium.

290
Q

What is the ECM of bone made of?

A

Calcium-phosphate crystals precipitated on collagen-based lattice.

291
Q

What is bone growth influenced by?

A

Calcium homeostasis

292
Q

What is the purpose of compact bone?

A

Dense, used for support

293
Q

What is the purpose of spongy bone?

A

Trabecular, spongy bone, forms calcified lattice

294
Q

What is the diaphysis?

A

The shaft of a bone

295
Q

Steps in the growth of long bones

A
  1. Proliferating columns of chondrocytes at epiphyseal plate secrete collagen and other ECM components 2. Older chondrocytes degenerate, leaving spaces 3. Osteoblasts invade spaces, lay down Ca-PO4 matrix (hydroxypatite) on cartilage base 4. Osteoblasts revert to less active form (osteocytes)
296
Q

How are bones continually remodelled?

A

Carbonic anhydrase makes H+ and HCO3- from CO2 and H2O. HCO3- is antiported with CL- on the basolateral membrane. Cl- flows through channel on apicl membrane to area of bone resorption. H+ pumped out apical membrane via active transport. H+ and Cl- and enzymes dissolve bone in the area of bone resorption.

297
Q

Where is calcium found in the ECM?

A

Matrix of bones and teeth

298
Q

What is calcium’s purpose in the ECF?

A

NT release, secretion/exocytosis, cardiac/smooth muscle, and for the clotting cascade

299
Q

Where is calcium found intracellularly, and what is it used for?

A

Found in the cytosol, SR, and mitochondria. Used for muscle contraction and signalling pathways.

300
Q

What is another name for calcitrol?

A

Vitamin D3

301
Q

Where is the largest reservoir of calcium in the body?

A

Bone, but very little is ionized and available for exchange. This small pool is in equilibrium with Ca2+ in interstitial fluid.

302
Q

How much of ingested calcium is absorbed?

A

1/3

303
Q

How is calcium abosrobed?

A

By paracellular and transcellular routes. Transcellular = apical Ca2+ channels, basolateral Na+-Ca2+ exchangers and Ca2+-ATPases

304
Q

What accounts for Ca2+ output?

A

Primarily via the kidneys + urine. Freely filtered and most reabsorbed. Hormonally controlled reabsorption at distal nephron only (transcellular only, similar transporters to those in gut)

305
Q

What is PTH released in response to?

A

Drop in plasma calcium

306
Q

Where does PTH act?

A

Kidney, bone, intestine

307
Q

What is PTH’s action on the kidney?

A

Increase Ca2_ reabsoprtion (at the expense of PO4-)

308
Q

PTH effect at bone?

A

Increased osteoclast activity

309
Q

PTH effect at gut?

A

Increaed Ca2+ absorption (via vitamin D3)

310
Q

Endocrine control of Ca2+ homeostasis?

A

Endogenous precursors/Diet –> Vitamin D –> liver –> calcitriol –> kidney (PTH works here, too) –> calcitriol/active vitamin D3 –> bones, distal nephron, and intestine –> increased plasma Ca2+, negative feedback to PTH

311
Q

How is phosphate homestasis parallel to Ca2+ homepstasis?

A
  1. Absorbed in gut (enhanved by vitamon D3) 2. Filtered and reabsorbed in kidneys (excretion enhanced by PTH, reabsorption enhanced by D3)
312
Q

Although glucagon, epinephrine, and cortisol are similar in their effects on metabolism, what effect is unique to cortisol?

A

Suppression of the immune system

313
Q

A person with primary hypercortisolism would have///

A

Elevated cortisol and decreaed ACTH (primary = cortisol secreting tumour not under regulation of ACTH)

314
Q

Graves’ disease is caused by auto-antiobdies that act as TSH agonists, which are not affected by usual feedback loops. What will happen to the size of the thyroid gland?

A

It will increase

315
Q

A person with a mutation in the 21-hydroxylase enzyme would have ____ ACTH levels and _____ adrenals.

A

high, enlarged

316
Q

What determines the sex of a baby?

A

The the sex determining transciption factor on the sperm

317
Q

Steps in sexual differentiation

A
  1. Build generic gonads (weeks 3-6 of gestation, gonad is “indifferent”) 2. Differentiate gonads down either male of female pathways (clearly testes by 7 weeks, clearly ovaries by 8 weeks) 3. Build appropriate internal duct work for internal transport of gametes 4. Build appropriate external genitalia for receipt/delivery of male gametes.
318
Q

3 sets of kidneys built during development

A
  1. Pronephros 2. Mesonephros+mesonephric ducts (Wolffian…male) 3. Para-mesonephric duct (Mullerian, female)
319
Q

Hormone responsible for the regression of the Mullerian duct in males?

A

AMH (anti Mullerian hormone)

320
Q

Somatic cell types in female reproductive system?

A

Granulosa and theca cells

321
Q

Somatic cells in testis?

A

Sertoli and Leydig cells (express Sry)

322
Q

Wolffian derivatives in males?

A

Epididymis, vas deferens, and accessory sex glands

323
Q

Mullerian derivatives in females?

A

Fallopian tubes, uterus, cervix, upper vagina

324
Q

What is the most potent androgen?

A

Dihydrotestosterone (DHT)

325
Q

What hormone is needed or external genitalia development in men?

A

DHT

326
Q

What are largest cells in the body?

A

Oocytes (non motile)

327
Q

How do eggs move?

A

Must be transported via smooth muscle conrtraction or movement of cilia within reproductive tract

328
Q

What is the smallest cell in the body?

A

Spermatozoa (also only flagellated cells_

329
Q

Timeline of gamete formation in females?

A

Mitosis in stmel cells starts nad ends in fetal life. Enter meiosis, arrest in late prophase of meiosis I (in fetal life) Females are born with all the oocytes they will ever have. Resume meiosis when “selected” for ovulation, arrest (again) until fertilized)

330
Q

Timelone of gamete formation in males?

A

Beginning at puberty, mitosis in “stem” cells (spermatogonia) shortly followed by meiosis and differentiation into functional sperm. Males produce fresh gametes throughout life.

331
Q

The differentiation of gonads down either the male or female pathway is under the control of?

A

SRY, which is contained on the Y chromosome

332
Q

In order for male external genitalia to develop, what must be present?

A

DHT

333
Q

In order for the Wolffian duct to be retained, what must be present?

A

Testosterone

334
Q

The Mulleriam duct is made from what kidney?

A

Para-medonephric duct

335
Q

The Wolffian duct is made from what kidney?

A

Mesonephric ducts

336
Q

One primary spermatocyte yields how many sperm?

A

4 sperm

337
Q

One primary oocyte yields how many eggs?

A

1 (+ 2 polar bodies)

338
Q

Hypothalamic-Pituitary-Gonadal Axis?

A

Int. and Ext. environmental stimuli –> GnRH from hypothalamus –> LH and FSH from ant. pit –? LH acts on endocrine cells in gonads to produce steroid and peptide hormones –> FSH acts gonads for gamete production

339
Q

Main hormone product of testes?

A

Testosterone (peripheral conversion to DHT)

340
Q

Main hormone products of ovaries?

A

Estradiol (estrogen) and Progesterone (progestin)

341
Q

All gonasal steroids mediate what tpe of feedback at the hypothalamus and anterior pituitary?

A

Mediate negative feedback with the exception of estradiol under certain conditions

342
Q

What is the LH surge, and what does it do?

A

As a result of enhanced pituitary responsiveness to GnRH, LH secretion increases dramatically. Causes meiosis to resume in the developing follicle with the first meiotic division, which converts the primary oocyte into a secondary oocyte (egg) and a polar body

343
Q

How is GnRH usually released?

A

In pulses, with each pulse being followed by a pulse in LH/FSH

344
Q

What does the exposure to steady/non pulsatile levels of GnRH do?

A

Causes gonadotropin-releasing cells in the pituitary to shut down (down regulation or desensitization).

345
Q

Why is steady exposure to GnRH agonists used as a treatment for hormone-dependent cancers?

A

Constant levels of GnRH agonists = shut down GnRH release from ant. pit. = less FSH and LH = less androgens or estrogen = less cancer

346
Q

What causes the testicular migration into scrotal sac?

A

Testosterone

347
Q

Why are the testes outside the body?

A

Normal spermatogenesis requires temperatures 2-3 degrees less than body temperature

348
Q

What is the failure of the testes to descend called?

A

Crytorchidism

349
Q

What are the male accessory glands highly dependent on?

A

DHT support (if you don’t have DHT, won’t become a female, but accessory glands will be tiny)

350
Q

What provides the majority of the volume of semen?

A

The accessory sex glands (apprx 99%)

351
Q

Endocrine approaches of treating prostate cancer?

A

GnRH agonists (shuts down HPG axis), 5alpha reductase inhibitors (don’t make DHT = atrophy of prostate), and androgen antagonists (androgens cannot bind )

352
Q

Order of the testes’ layers from interstitial to tubular sides?

A

Intersitiium, tubule wall, lumen

353
Q

Spermatogonia?

A

Mitotic germ cells

354
Q

Primary spermatocyte?

A

Has entered Meiosis I (23 homologous chromosomes)

355
Q

Secondary spermatocyte?

A

Has entered Meiosis II (homologous chromosomes split into sister chromatids)

356
Q

Spermatid?

A

Completed meiosis but has not yet undergone cell remodelling

357
Q

What forms the “blood-testes barrier?”

A

Basal lamina + cells associated with basal lamina + tight junctions between Sertoli cells….allows sperm through easily, but not large cells

358
Q

What is the acrosome?

A

Region at head of spermatozoan that contains enzymes to aid in fertilization

359
Q

Mature sperm waiting for ejaculation are found in?

A

Caudal epipididymis

360
Q

How long does it take from spermatogonium ot release into lumen of seminiferious tubule?

A

64 days

361
Q

How long does it take for spermatozoan to travel down epipidymis from lumen to out of body?

A

12 days

362
Q

Endocrine control of spermatogensis?

A

GnRH –> FSH and LH –> LH works on Leydig cells in interstitium to produce testosterone to be used on Sertoli cells and the body – FSH on Sertoli cells to synthesize paracrine molecules needed fro spermatogonia mitosis and spermatogenesis and production of androgen-binding protein and inhibin

363
Q

What does androgen binding protein do?

A

Secreted by Sertoli cells into seminiferous tubule lumen where it binds to testoerone to make it less lipophilic so that it cannot diffuse out of tubule lumen

364
Q

Primary sex characteristics due to effects of testicular androgens?

A

Development and maintenance of internal and external genitalia. Support of spermatogenesis

365
Q

Secondary sex characteristics due to effects of testicular androgens?

A

Protein synthesis/muscle growth

366
Q

Effects of testicular androgens?

A
  1. Primary sex characteristics 2. Secondary sexual characteristics 3. Behaviour
367
Q

DHT (versus testosterone) is responsible for…

A
  1. Differentiation of external genitalia during development 2. Development and support of accessory sex glands 3. Male pattern baldness, acne, facial hair
368
Q

What does metrium mean?

A

Uterus

369
Q

What is the endometrium?

A

Inner lining of uterus consisting of glandular epithelium and lamina propria

370
Q

Myometrium?

A

Smooth muscle of uterus

371
Q

Layers of uterus from superficial to deep?

A

Myometrium, endometrium, lumen of uterus

372
Q

What is the broad ligament?

A

Holds female reproductive parts in place

373
Q

What is the fimbriae?

A

Extension of the Fallopian tubes that wrap around ovary, making sure that when an egg is released, it will get picked up in the Fallopian Tube

374
Q

Layers of follicle from superficial to deep?

A

Surface epithelium, theca, basal lamina, granulosa cells, antrum

375
Q

Stages of follicular development?

A

Primary follicle, secondary follicle, mature follicle with oocyte, ruptured follicle, ovulated oocyte. Follicle becomes corpus luteum and then regresses if pregnancy doesn’t occur.

376
Q

What does the corpus luteum secrete?

A

Progesterone to get the uterus ready for pregnancy

377
Q

3 phases of ovarian cycle

A
  1. Follicular phase 2. Ovulation 3. Lutueal phase
378
Q

3 phases of uterine cycle

A

Menses, proliferative phase, secretory phase

379
Q

KNOW HOW UTERINE AND OVARIAN CYCLE ALIGN

A

The menses and proliferative phases of the uterine cycle correspond to the follicular phase and ovulation; the secretory uterine phase corresponds with the luteal phase

380
Q

What causes menses?

A

Luteal regression = drop in estrongen and progesterone = menses

381
Q

Source of estrogen in menstrual cycle?

A

Follicle

382
Q

Strongest regulator of uterine growth?

A

Estrogen

383
Q

The product of the SRY gene is…

A

a transciption factor that allows for the development of the testes

384
Q

In human males, mitotic divisions in germ cells…

A

begin at puberty and continue until late in life

385
Q

During meiosis, the chromosome number is halved as the result of…

A

as a result of the first meiotic division

386
Q

An XX individual with a mutation leading to loss of 21-hydroylase activity would be expected to have…

A

enlarged adrenal glands, ovaries (because she has no SRY), and masculinized/ambiguous genitalia (overproduction of weak adrenal androgens = masculine external genitalia)

387
Q

An XY individual with a mutation resulting in a non-dunctional androgen receptor would be expected to have…

A

testes (has SRY), female external genitalia (no androgen receptor = no DHT response to form penis)

388
Q

What is the most variable phase of the menstrual cycle?

A

The follicular phase

389
Q

What begins the follicular phase, and what does it trigger?

A

Begins with luteal regression, which triggers menses

390
Q

During the follicular phase, what is going on in the ovaries?

A

Follicles begin to grow, and the “selected” follicle grows the most. Follicles not selected to ovulate will degenerate/undergo atresia. Sustained exposure to high estrogen causes massive release of gonadotroponins…LH surge = ovulation. Maturing follicle secretes estrogen.

391
Q

During the folliclular phase, what is occurring in the uterus?

A

Part of the endometrial lining sheds due to steroid withdrawal (luteal regression), which is the beginning of menses. Rising estrogen (from maturing follicle) stimulates regrowth of lining…“proliferative phase”

392
Q

What does the luteal phase begin with?

A

Begins with LH surge, which triggers ovulation

393
Q

What does the LH sruge cause in oocytes?

A

Oocyte escapes ovary, completes Meiosis I in response to LH surge, arrests again in Meiosis 2

394
Q

During the luteal phase, what happens to the granulosa and theca of ovulatory follicle?

A

Transformed into luteal cells…solid, progesterone-secreting structure “luteinzation”

395
Q

What prevents the growth of large follicles during the luteal phase?

A

High ovarian steroids (progesertone especially, and some estrogen) suppress gonadotropins, preventing this growth

396
Q

In the absence of pregnancy, what causes luteal regression?

A

Occurs after approx. 12 days

397
Q

During the luteal phase, what is happening in the uterus?

A

Under the influence of progesterone and estrogen, the uterus continues to prepare for pregnancy “secretory phase”

398
Q

What triggers menses at the end of the luteal phase/beginning of follicular phase?

A

Steroid withdrawal/luteal regression

399
Q

The pathway sperm travels during fertilization?

A

Vagina, cervix, uterus, oviduct

400
Q

After the sperm arrives at the oocyte, what must occur?

A

Sperm penetrates through layer of granulosa cells and glycoprotein layer (zona pellucida) through assistance by enzymes released from acrosomal cap

401
Q

What does the fusion of the sperm membrane and the oocyte membrane cause?

A

Fusion of membranes acctivates oocyte, triggering completion of Meiosis 2, closely followed by syngamy with sperm and preparation for first mitotic division. Diploidy (23 pairs of chromosomes is re-established) Also triggers cortical granule reactions, an important mechanism for the prevention of polyspermy.

402
Q

What is cortical granule reaction?

A

After membrane fusion of egg and sperm, cortical granules in the peripheral cytoplasm of the egg release their contents into the space just outside the egg membrane. These chemicals rapidly alter the membrane and surrounding zona pellucida so that additional sperm cannot penetrate or bind.

403
Q

What is the zona pellucida?

A

A protective glycoprotein coat of the egg

404
Q

Steps in fertilization

A
  1. Membrane fusion of sperm and oocyte (cortical granule reaction) 2. Sperm nucleus moves into cytoplasm of egg 3. Oocyte completes second meiotic division 4. Union of sperm and eff nuclei to form diploid zygote nucleus (second polar body expelled)
405
Q

How long does it take for blastocyte (about 100 cels) to travel from the oviduct where it was fertilized to the uterus?

A

4-5 days after fertilization

406
Q

How long after fertilization does it take for the blastocyte to implant in the uterus?

A

5-9 days

407
Q

What are the first differentiated cell types in mammalian embryo?

A

Inner cell mass versus trophectoderm

408
Q

What does the inner cell mass give rise to?

A

Embryo proper

409
Q

What does the trophectoderm give rise to?

A

All extra-embryonic membranes

410
Q

Order of extraembryonic membranes from superficial to deep

A

Placenta, chorion, amnion

411
Q

What carries oxygenated blood to fetus?

A

Umbilical VEIN

412
Q

What returns fetal blood to the placenta (de-oxygenated)?

A

Umbilical arteries

413
Q

How does maternal blood exchange oxygen and nutrients with fetal blood?

A

Through the maternal-fetal interface vis the chorionic villi contained in embryonic blood vessels.

414
Q

Does maternal and fetal blood mix?

A

NO!!

415
Q

What hormones does the placenta secrete?

A

Chorionic-gonadotropin, estrogen and progesterone, and placental lactogen

416
Q

What is hCG, and what does it do?

A

Chorionic gonadotropin. LH-like molecule produced by extra-embryonic tissues (chorion) that prevents luteal regression, which maintains progeststional environment by keeping progesterone levels high

417
Q

Where does the estrogen and progesterone during pregnancy come from?

A

the placenta, not the ovary

418
Q

What is hPL, and what does it do?

A

Placental lactogen. It is a protein related to GH and prolactin that modifies maternal intermediary metabolism to support fetal growth.

419
Q

Steps in parturition

A
  1. Cervical ripening/softening 2. Initiation of rhythmic uterine contactions 3. Delivery of the baby 4. Expulsion of placenta
420
Q

What controls parturition?

A

A sequential cascade of hormones that has considerable variation among species. Consistent finding, though, is positive feedback/neuroendocrine reflex involving oxytocin

421
Q

Positive feedback cycle of labour

A

Fetus drops lower in uterus –> stimulates oxytocin release –> causes uterine contractions –? push baby agaisnt cervix –> causing cervical stretch, and it begins again. Delivery of baby ends cycle.

422
Q

Where is oxytocin released from?

A

Posterior pituitary

423
Q

At puberty, what influences breat development in females?

A

Estrogen…growth and branching of ducts

424
Q

During pregnancy, what furthers the development of mammary glands?

A

Estrogen, GH, cortisol. Progesterone is needed for the final development step, which converts duct epithelium into a secretory epithelium. This process is similar to progesterone’s effect on the uterus, in which progesterone makes the endometrium into a secretory tissue during the luteal phase.

425
Q

During late pregnancy, what hormones cause the production of colostrum?

A

Progesterone and estrogen, and prolactin

426
Q

What does prolactin do throughout lactation?

A

Ongoing support of milk synthesis

427
Q

During lactation, what does oxytocin do?

A

Milk secretion (“let down reflex”)…contraction of myoepithelia cells of mammary gland

428
Q

What is luteinizaition?

A

Formation of the corpus luteum, following ovulation

429
Q

What indices completion of the first meiotic division in an oocyte?

A

LH surge. 2nd is due to fusion of sperm membrane to egg membrane

430
Q

A female taking an oral contraceptive of estrogen and progesterone would have…

A

low FSH and low LH

431
Q

If a male had a vasectomy, what would be an effect?

A

Ejaculate would not contain any sperm. However, testosterone would be be affected, and the ejaculate volume would not be affected.

432
Q

During the mid follicular phase of the cycle, the uterus is in what phase, and what are progesterone levels like?

A

Uterus is in the proliferative phase, and progesterone levels are low.

433
Q

What marks the transition from the follicular phase to the luteal phase?

A

Ovulation

434
Q

A man taking a 5-alpha reductase inhibitor to treat his male pattern baldness could expect the following side effects?

A

Shrinkage of prostate gland and lack of facial hair. (DHT affects accessory sex organs, facial hair, and causes baldness and acne).

Physiology 2 (16 decks)

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