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Physl 210 B > GI and Respiratory Physl > Flashcards

GI and Respiratory Physl Flashcards

1
Q

Functions of the GI tract?

A

Digestion
Absorption
Excretion
Host defense

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2
Q

Digestion

A

Physical breaking down of food consumed into absorbable nutrients for the body to use, through the use of GIT motility, pH changes, enzymes and detergents.

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3
Q

Absorbtion

A

Taking in nutrients consumed from the intestines to the blood of lymphatic system, for body to use.

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4
Q

Excretion

A

Removal of waste products that could not be absorbed by the body.

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5
Q

Host defense

A

GIT forms a barrier with outside environment and contains a highly developed immune system; GIT can inactivate harmful bacteria

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6
Q

Components of the GI tract

A

Mouth, pharynx, esophagus, stomach, small intestine (duodenum, jejenum, illeum), large intestine

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7
Q

Accessory organs

A

Pancrease, liver, gallbladder

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8
Q

GI tube structure

A

Top third of esophagus: skeletal muscle

Rest of GI tract: smooth muscle

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9
Q

Villi

A

Found in the intestinal tube
Project into the lumen
Below surface there is a crypt or invagination

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10
Q

Layers of the GIT

A

Mucosa
Submucosa
Muscaleris externa
Serosal layer

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11
Q

3 layers of the mucosa

A

Epithelium
Lamina propria
Muscalaris mucosa

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12
Q

Epithelium & its function

A

Layer of cells that lines all body cavities and surfaces
Function:
-selective uptake of nutrients, electrolytes, water
-prevent harmful substances from coming through

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13
Q

Apical surface

A

Faces the inside of the tube/lumen

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14
Q

Basolateral surface

A

Closest to the blood surface, away from the lumen

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15
Q

How is SA increased?

A

Presence of villi, microvilli, and crypts

Folds

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16
Q

Where do epithelial cells come from?

A

From stem cells within the crypt that differentiate into a variety of cells

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17
Q

2 pathways that chemicals use to cross the epitherlial layer?

A

Paracellular pathway

Transcellular pathway

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18
Q

Paracellular pathway

A

Chemicals move between cells across the tight junctions; only water and small ions can diffuse across

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19
Q

Transcellular pathway

A

Cross the cell by using transport proteins

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20
Q

Lamina propria

A

Consists of connective tissue, blood vessels, nerve fibers, lymphatic vessels, inflammatory cells

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21
Q

Muscularis mucosa

A

Thin layer of smooth muscle

May be involved in moving villi

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22
Q

Submucosa

A

Under mucosa layer

Contains blood vessels, lymphatic vessels, submucosal nerve plexus, connective tissue

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23
Q

Submucosal nerve plexus

A

Relays info to and from the mucosa

Influences secretion

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24
Q

Muscularis externa

A

Contains circular muscle, myenteric nerve plexus, longitudinal muscle

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25
Q

Circular muscle

A

Fibers are in a circular pattern to contract and relax in order to open/close the tube

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26
Q

Myenteric nerve plexus

A

Regulates the smooth muscle function of the GIT

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27
Q

Longitudinal muscle

A

Lengthens/shortens to control length of tube

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28
Q

Serosa

A

Connective tissue layer and forms connections between the intestine wall and abdominal wall

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29
Q

Portal circulation and its purpose?

A

Carries blood from intestinal tract to the liver

Important in removal of harmful substances, via the liver

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30
Q

Hepatic artery

A

Carries oxygenated blood from the heart to the GI organs and liver

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31
Q

Hepatic portal vein

A

Carries less oxygenated blood to the liver that has already been perfused by the GI tract organs

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32
Q

In series circulation vs in parallel

A

For in parallel, blood goes directly to the target organ, while in series, blood perfuses the organ/tissue after already perfusing a separate one prior to.
Liver predominantly has in series circulation, leading to blood high in nutrients but lower in oxygen.

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33
Q

What 2 factors regulate secretion and motility in the GI tract?

A

Volume and composition of what’s inside

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34
Q

Reflexes regulating secretion and motility in the GI tract are initiated by? (3)

A
  1. Distension of GI wall by volume of luminal contents
  2. Osmolarity of contents pH
  3. Concentration of specific contents like monosaccharides, fatty acids, peptides, amino acids
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35
Q

Reflexes are propogated by which receptors?

A

Mechanoreceptors- activated by pressure, stretch
Osmoreceptors- activated by change in osmolarity
Chemoreceptors- activated by chemicals

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36
Q

Enteric/intrinsic regulation

A

Occurs completely within the GI
Involves the myenteric and submucosal plexi.
Critical for involuntary functions like digestion
Can function independently of the CNS

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37
Q

Extrinsic regulation

A

Occurs outside the GI walls, in the ANS

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38
Q

Sympathetic GI responses

A
  • small volume of thick saliva

- peristalsis and secretion inhibited

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39
Q

Parasympathetic GI responses

A
  • large volume of watery saliva
  • increases peristalsis and secretion
  • stimulates bile release
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40
Q

Long reflex

A

Extrinsic pathway. CNS is stimulated by smell of food for example and eventually GI tract is stimulated to break down food.

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41
Q

Short reflex

A

Intrinsic pathway. Same response is geenrated in Gi tract without any input from CNS. Simply due to food consumption and receptors detecting it, causing a response.

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42
Q

4 types of chemical messenger regulation?

A

Endocrine
Neurocrine
Paracrine
Autocrine

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43
Q

Endocrine regulation

A

Hormone-secreting gland secretes a hormone into the blood, and then travels via blood to its target cells

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44
Q

Neurocrine regulation

A

Nerve cell produces an electrical signal which causes release of a NT that travels across a synapse to a post synaptic target cell (usually an effector, or nerve cell)

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45
Q

Paracrine regulation

A

Cell releases a paracrine substance which diffuses through ISF and acts on target cells nearby the release site.

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46
Q

Autocrine regulation

A

Cell releases autocrine substance which acts in the cell that released it

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47
Q

CCK is stimulated by?

A

Presence of fatty acids and amino acids

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48
Q

What doe CCK do?

A

Stimulated pancreas to increase digestive enzyme secretion, and stimulates gallbladder to contract in order to release bile acids for fat breakdown

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49
Q

Intestinal motility? How is it stimulated?

A

Causes contents to move along GI tract. Stimulated by contraction and relaxation of the 2 muscle layers

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50
Q

Peristalsis and how it works?

A

Main driving force for food moving down the GI tract.

Circular muscle contracts on oral side of bolus while longitudinal muscle relaxes, and vice versa.

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51
Q

Segmentation and its functions?

A

Contraction and relaxation of intestinal segments (little movement towards large intestine)
Allows mixing of contents
Causes delayed transit time, allowing more time to absorb nutrients

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52
Q

Pacemaker cells

A

Located in the smooth muscle of GIT and are constantly under spontaneous depolarization-repolarization cycles

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53
Q

Slow waves

A

Give the GIT the basic electrical rhythm
With an excitatory input, slow waves are depolarized over threshold and an action potential occurs leading to muscle contraction.

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54
Q

Frequency of contraction is dictated by?

A

Basic electrical rhythm

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55
Q

Force of contraction is dictated by?

A

Hormonal and neuronal input

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56
Q

3 phases of GI control?

A

Cephalic
Gastric
Intestinal

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57
Q

Cephalic phase and how its initiated? Reflexes?

A

Initiated by stimulation of receptors in the head through sight, smell, taste, chewing of food, emotional state.
Reflexes regulated by parasympathetic fibers that activate neurons in the neuronal plexuses.

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58
Q

Gastric phase and how its initiated? Reflexes?

A

Receptors in stomach are stimulated by stretching, distension, acidity, peptide, amino acids.
Short (gastrin) and long (ACH) neural reflexes.

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59
Q

Intestinal phase and how its initiated? Reflexes?

A

Receptors in intestine are stimulated by osmolarity, stretch, distention, digestive products.
Short and long neural reflexes and by CCK, secretin, GIP hormones.

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60
Q

Hypothalamus role

A

Maintains homeostasis
Command centre for neural and endocrine control coordination
Control of behaviour

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61
Q

Feeding centre? Lesion causes what?

A

Located in the lateral region of hypothalamus
Activation of this centre increases hunger
Lesion causes weight loss

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62
Q

Satiety centre? Lesion causes what?

A

Located in the ventromedial region of hypothalamus
Activation makes you feel full
Lesion causes weight gain by overeating

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63
Q

Orexigenic factors and examples

A 
Increase appetite
Neuropeptide Y (secreted by hypothalamus)
Ghrelin (by stomach endocrine cells)
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64
Q

Anorexigenic factors and examples

A 
Decrease appetite
Leptin (by adipose tissue)
Insulin (by pancreas)
Peptide YY (by intestine)
Melanocortin (by hypothalamus)
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65
Q

How does ghrelin work?

A

Secreted by endocrine cells of stomach when body is in fasting state. Ghrelin is released in blood and travels to hypothalamus to stimulate release of neuropeptide Y to try to increase food intake.

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66
Q

Lack of leptin results in?

A

No appetite regulation, obesity

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67
Q

What 3 factors stimulate the thirst centre?

A
  1. Increased plasma osmolarity
  2. Decreased plasma volume
  3. Dry mouth or throat
  4. Prevention of over hydration
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68
Q

Increased plasma osmolarity

A

Stimulates osmoreceptors and the release of vasopressin or ADH to conserve water at kidney

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69
Q

Decreased plasma volume

A

Decrease in blood volume and pressure stimulates baroreceptors and will alter sympathetic and parasympathetic outflow to increase arterial pressure to normal levels

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70
Q

Intrarenal baroreceptors

A

When blood pressure in kidneys decreases, baroreceptors are stimulated and acitvation of the renin-angiotensin system occurs. This system produces angiotensin II affects hypothalamus and has been shown to to increase thirst in animals.

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71
Q

3 main pairs of salivary glands?

A

Parotid
Submandibular
Sublingual

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72
Q

Composition of saliva

A

Hypotonic and slightly alkaline.
Made of water, electrolytes (potassium and bicarbonate), digestive enzymes (lipase, amylase), glycoproteins (mucin), antimicrobial factors (lysozyme, lactoferrin)

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73
Q

Lysozyme

A

Breaks down bacterial cell walls

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74
Q

Lactoferrin

A

Prevents multiplication of bacteria by chelating iron

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75
Q

Functions of saliva (6)

A

Moistens/lubricates food to make it easier to swallow
Initiates digestion with digestive enzymes
Allows small bit of food to dissolve through taste buds
Prevents microbial colonization due to antibacterial factors
Aids in speech
Buffer- neutralizes acidic food or acid reflux

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76
Q

3 cell types that make up salivary glands?

A

Acinar cells
Ductal cells
Myopithelial cells

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77
Q

Acinar cells

A

Secrete initial saliva

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78
Q

Ductal cells

A

Create the alkaline hypotonic nature of saliva

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79
Q

Myoepithelial cells

A

Contain characteristics of both epithelial cells and smooth muscle cells

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80
Q

Saliva movement

A

Moves from the acinus to striated duct via myoepithelial cells contracting the acinus end, moving contents towards striated duct.

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81
Q

Tight junctions of acinar cells vs ductal cells

A

Acinar cells have leaky tight junctions, allowing for passage of water and small ions while ductal cells do not allow water to pass

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82
Q

Why is the primary secretion of saliva isotonic?

A

Because there is no limit on how much water and sodium pass through the leaky acinar tight junctions.

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83
Q

Parasympathetic pathway for regulation of salivary gland function..how is it stimulated? How can it be inhibited?

A

Dominant regulatory pathway
Stimulated by smell/taste of food, or pressure receptors in mouth, or during nausea
Can be inhibited by tiredness, fear, fatigue

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84
Q

Sympathetic pathway for regulation of salivary gland function..how is it stimulated?

A

Minor pathway
Increases saliva flow
Increases protein secretion from acinar cells and stimulates myoepithelial cells to contract to increase flow

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85
Q

Amylase

A

Enzyme found in saliva that breaks down starch

Can only break alpha-1,4 linkages

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86
Q

Plant starch is made up of?

A

Glucose polymers amylose and amylopectin

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87
Q

Amylose

A

Straight chain of glucose polymers with alpha-1,4 linkages

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88
Q

Amylopectin

A

Chain of glucose polymers with both alpha-1.4 and 1,6 linkages

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89
Q

Breakdown of amylose creates?

A

Maltose and maltotriose

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90
Q

Breakdown of amylopectin creates?

A

Maltose, maltotriose, and alpha limit dextrin due to the alpha 1,6-linkages not being broken

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91
Q

Lingual lipase

A

Breaks down fats , can remain active in stomach

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92
Q

When are amylase and lingual lipase especially important?

A

When there are conditions of reduced pancreatic activity (digestive enzyme secretion)

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93
Q

Xerostomia

A

Dry mouth

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94
Q

Conditions where saliva secretion is impaired?

A

Congenital
Schogrens disease- Autoimmune dieases where immune system attacks salivary glands
Drug side effects
Radiation therapy

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95
Q

Consequences of salivary gland impairment?

A 
Decreased oral pH
Tooth decay
Dry mouth
Esophageal erosions due to no saliva being able to neutralize stomach acid coming up esophagus
Difficulty chewing/swallowing food
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96
Q

Treatment for impaired salivary production?

A

Frequent sips of water

Fluoride treatment for bacteria

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97
Q

How is swallowing initiated?

A

Pressure receptors in the pharynx stimulated by presence of food or liquid entering pharynx

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98
Q

Pharynx

A

Tube at the back of esophagus common to food and air

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99
Q

Larynx

A

Between pharynx and trachea containing vocal chords; voicebox

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100
Q

Glottis

A

Area in larynx around vocal chords where air can pass

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101
Q

Epiglottis

A

Cartilage flap that closes to prevent food from entering lungs

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102
Q

Process of swallowing

A

Chew food
Food moves to back of throat
Soft palette elevates to prevent food from going up nose
Respiration inhibited by impulses from swallowing centre
Larynx raised, epiglottis closes and covers trachea
Food enters esophagus

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103
Q

Esophagus anatomy

A

Mucus is secreted

Stratified squamous epithelium

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104
Q

Stratified vs squamous

A 
Stratified= in layers
Squamous= flattened
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105
Q

Upper esophageal sphinctor

A

Ring of sketal muscle located below the pharynx

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106
Q

Lower esophageal sphinctor

A

Ring of smooth muscle located where the esophagus joins the stomach.

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107
Q

When are esophageal spinctors closed?

A

Always closed, except for when swallowing, vomiting, or burping,

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108
Q

Heart burn causes

A

Lower esophageal sphincter not closing properly
Big meal
Pregnancy

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109
Q

Stomach functions

A

Storage of food

Chemical and mechanical breakdown of food

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110
Q

Pepsinogen

A

Secreted by the stomach, and cleaved to form enzyme pepsin

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111
Q

Pepsin

A

Enzyme that initiates protein digestion in stomach

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112
Q

HCl

A

Secreted in stomach, and helps break down macromolecules in food.
Partial sterilization of food

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113
Q

Intrinsic factor

A

Secreted by stomach

Essential for absorption of vitamin B12 in iliem

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114
Q

Fundus and body & what do they secrete?

A

Both have a thin layer of smooth muscle

Mucus
HCl
Pepsinogen

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115
Q

Antrum and what does it secrete?

A

Has a thicker layer of smooth muscle

Mucus
Pepsinogen
Gastrin

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116
Q

Pyloric sphincter

A

Controls emptying of the stomach

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117
Q

Endocrine vs exocrine

A

Exorcrine chemical messenger requires passage through blood , while exocrine involves secretion into ducts and then directly onto epithelial surface

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118
Q

Mucus

A

Protects the stomach epithelium from digestive enzymes and acid

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119
Q

Gastrin

A

Important in stimulating HCl production and stomach motility

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120
Q

Histamine

A

Stimulates HCl production

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121
Q

Somatostatin

A

Inhibits HCl production

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122
Q

Mucous cell

A

Located at luminal end of gastric gland

Secretes mucous

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123
Q

Parietal cell

A

Located in fundus

Secretes intrinsic factor and HCl

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124
Q

Chief cell

A

Found in gastric glands

Secretes pepsinogen

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125
Q

Enteroendocrine cell/G cell

A

Found in gastric glands in antrum

Secrete gastrin

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126
Q

Enterochromaffin-like cell

A

Found in gastric glands

Secretes histamine

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127
Q

D cell

A

Found in gastric glands

Secretes somatostatin

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128
Q

Canaliculi

A

Increase SA of cells to maximize secretion

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129
Q

Na/K ATPase

A

Primary transport

3 Na out, 2 K into cell for every molecule of ATP

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130
Q

H/K ATPase

A

Primary transport
Pumps out a proton (H) into lumen
Cell becomes more basic

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131
Q

Carbonic anhydrase

A

Parietal cell gets rid of base by removing bicarbonate
Catalyzes formation of carbonic acid from h20 and co2
Carbonic acid dissociates into H and bicarbonate

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132
Q

Cl/HCO3 exchanger

A

HCO3 is pumped out in exchange for Cl ion

Secondary active transport

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133
Q

4 chemical messengers that regulate insertion of H/K ATPase into membrane?

A

Gastrin
Histamine
ACH
Somatostatin

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134
Q

Advantage of having inactive precursor?

A

Prevents autodigestion

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135
Q

3 phases of gastric secretion?

A

Cephalic phase
Gastric phase
Instestinal phase

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136
Q

Cephalic phase & how is acid secreted?

A

Brain is stimulated by sight, smell, or taste of food which provides excitatory stimulation via vagus nerve to the stomach
Vagal nuclei in brain cause parasympathetic nerve to release ACH at parietal cells and acid is secreted

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137
Q

Gastric phase & how is acid secreted?

A

Occurs when food reaches the stomach
Stimulated mainly by presence of food causing G cells to release gastrin into blood.
Gastrin interacts with parietal cell to increase acid production

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138
Q

Intestinal phase & how is acid secreted?

A

Occurs when partially broken down food from stomach enters SI
INHIBITORY phase due to presence of fat, acid, digestion products (slow digestion is wanted so phase is inhibitory)
Mediated by secretin and CCK, which have a negative influence on gastrin production

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139
Q

3 ways ACH can stimulate acid secretion at parietal cell?

A
  1. Stimulates ECL cells to release histamine
  2. Inhibits somatostatin production in D cells
  3. Stimulates G cells to produce gastrin
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140
Q

In what way does gastrin stimulate acid secretion at parietal cell?

A
  1. Stimulates ECL cells to release histamine
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141
Q

What happens once acid secretion is happening at a high rate?

A

ACH released from parasympathetic nerves and the stimulation is reduced as acid is produced and as you are eating.
Acid produced has an inhibitory effect on gastrin release from G cells

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142
Q

Somatostatin inhibits what?

A

Gastrin release from G cells

Histamine release from ECL cells

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143
Q

Peristaltic waves

A

Weak contractions in the stomach

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144
Q

Pyloric sphinctor & what happens when it closes?

A

Located between antrum of stomach and duodenum.

When it closes, some food is able to enter the duodenum, but most is retained in stomach for further digestion.

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145
Q

What determines strength of contraction?

A

Amount of stimulus

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146
Q

What determines the frequency of contraction?

A

Basic electrical rhythm

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147
Q

Causes of vomiting?

A

Psychogenic (you think of something like a food and its triggered)
Ear infection (motion sickness)
GI disturbances
Pressure in CNS
Chemoreceptors in GI tract and brain detect toxins

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148
Q

Where is the vomiting centre?

A

Medulla oblongata

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149
Q

What mechanisms happen when vomiting centre is stimulated?

A 
Increased saliva production
Breath held in mid-inspiration
Nausea
Glottis closes off trachea
Lower esophageal sphinctor and esophagus relax
Diaphragm and abdominal muscles contract
Reverse peristalsis
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150
Q

Consequences of vomiting

A

Dehydration
Electrolyte imbalance
Metabolic alkalosis-elevated pH of a tissue due to acid lost
Tooth enamel erosion from acid

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151
Q

Peptic ulcer

A

Erosion of GI tract mucousa

Can occur in stomach, esophagus or duodenum

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152
Q

Causes of ulcers?

A

Imbalance of aggressive factors (pepsin and acid) and protective factors (mucus and bicarbonate)
Infection from bacterium Helicobacter Pylori
Non-bacterial factors like smoking, excessive alcohol, drugs that reduce prostaglandin production

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153
Q

Ulcer treatment

A

Antibiotics
H/K pump inhibitors
Histamine receptor antagonists
Prostaglandin type drugs

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154
Q

Gastric bypass surgery

A

Stomach is divided into a smaller pouch which connects to SI, limiting how much food is absorbed. Used to weight loss

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155
Q

Is the stomach essential for life?

A

No, but complications can arise

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156
Q

Consequences of having stomach tied off or removed?

A

Intrinsic factor cannot be secreted without a stomach, so people must get vitamin B12 injections to prevent anemia.
Stomach is useful in reducing amount of bacteria that enters system
Sterilizes food

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157
Q

Exocrine pancreas and function

A

Secretes substances into ducts that drain onto spithelial surface
Important for digestion
Source of majority of enzymes needed for digestion of carbs, fats, proteins etc
Secretes bicarbonate into duodenum

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158
Q

Endocrine pancreas

A

Ductless gland
Secretion occurs over epithelial basolateral surface for diffusion into blood
Not important in digestion but important in producing hormones regulating the body

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159
Q

Sphincter of Oddi/hepatopancreatic sphincter

A

Common to the bile duct and main pancreatic duct

Regulates the release of pancreatic and liver contents into SI

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160
Q

Pancreatic islets

A

Produce insulin

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161
Q

Acinar vs ductal cells within pancreatic ducts

A

Acinar- produce and secrete digestive enzymes

Ductal- secrete bicarbonate

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162
Q

Pancreatic juices

A

Isotonic and alkaline due to bicarbonate

Contains digestive enzymes and proteolytic enzymes which are stores and secreted in inactive forms

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163
Q

CFTR

A

Cl channel
Cystic fibrosis transmembrane conductance regulator
Allows Cl to diffuse out of duct cell into lumen

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164
Q

Ductular cell secretion of HCO3 steps

A
  1. CFTR channels open and Cl diffuses into lumen
  2. Cl in lumen exchanged for HCO3 in cell (HCO3 movies out)
  3. Neutral pH maintained by exchange of H moving out for Na moving in (secondary active transport)
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165
Q

What happens after a meal?

A

Acid enters lumen of stomach

Base bicarbonate leaves via blood

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166
Q

“The tide”

A

Anything moving into blood

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167
Q

In the stomach what happens to acid and base?

A

Acid moves into stomach lumen. Base moves into the blood.

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168
Q

In the pancreas what happens to acid and base?

A

Base moves into lumen, acid moves into blood.

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169
Q

Why is the pancrease essential to digestion?

A

Source of major enzymes requried for digesting carbs, fats, proteins, etc

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170
Q

Proteases

A

Enzymes that digest proteins into peptides and amino acids

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171
Q

Amylolytic enzymes

A

Digest starches into sugars

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172
Q

Lipases

A

Digest triglycerides into monoglycerides and free fatty acids

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173
Q

Nucleases

A

Digest nucleic acids into free nucleotides

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174
Q

How are enzymes packaged and where are they stored?

A

Packaged by the pancreatic acinar cells as proenzymes in zymogen granules
Stored at the apical pole of the acinar cell

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175
Q

Zymogens

A

Inactive precursor molecules

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176
Q

Enterokinase

A

Cleaves a pro-protease called tripsinogen into the protease trypsin

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177
Q

4 major proteases secreted by pancreas?

A

Trypsinogen
Chymotrypsinogen
Pro-elastase
Pro-carboxypeptidase A & B

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178
Q

Amylolytic enzymes? (1)

A

Pancreatic amylase

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179
Q

Lipolytic enzymes? (3)

A

Lipase
Phospholipase A2
Cholesterase

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180
Q

Trypsinogen: activated by? Active enzyme? Action? End products?

A

Enterokinase
Trypsin
Hydrolyzes peptide bonds
Peptides and amino acids

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181
Q

Chymotrypsinogen: activated by? Active enzyme? Action? End products?

A

Trypsin
Chymotripsin
Hydrolyzes peptide bonds
Peptides and amino acids

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182
Q

Pro-elastase: activated by? Active enzyme? Action? End products?

A

Trypsin
Elastase
Hydrolyzes peptide bonds
Peptides and amino acids

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183
Q

Pro-carboxypeptidase A&B: activated by? Active enzyme? Action? End products?

A

Trypsin
Carboxypeptidase A&B
Hydrolyzes bonds at C-terminal
Peptides and amino acids

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184
Q

Pancretic amylase ? Action and end products?

A

Cleaves starches to sugars

Maltose, malitriose, alpha limit dextrins

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185
Q

Lipase? Action and end products?

A

Hydrolyzes triglycerides

Free fatty acids and 2-monoglycerides

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186
Q

Phospholipase A2: Inactive enzyme? Activated by? Action and end products?

A

Prephospholipase A2
Trypsin
Hydrolyzes phospholipids
Free fatty acids and lysophospholipids

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187
Q

Cholesterolesterase? Action and end products?

A

Hydrolyzes cholesterol esters

Free fatty acids and cholesterol

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188
Q

S-cells role

A

Produce secretin when acid enters duodenum from stomach

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189
Q

Secretin

A

Hormone that stimulates release of bicarbonate

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190
Q

I-cells role

A

Release CCK when fats and protein enter upper SI from stomach

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191
Q

CCK

A

Hormone that stimulates release of digestive hormones

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192
Q

Circulating secretin stimulates?

A

Pancreas and liver duct cells to increase bicarbonate secretion

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193
Q

Secretin and CCK bot inhibit what? What does this result in?

A

Both inhibit gastric secretion, which results in slowed stomach motility and reduced acid secretion

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194
Q

Which channel is mutated in cystic fibrosis?

A

The Cl channel involved in HCO3 secretion

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195
Q

Cystic fibrosis

A

Defective Cl channel
Enzymes do not get flushed from the ducts and never reach the intestine
Retained proteolytic enzymes can result in autodigestion
Patients must recieve supplements of digestive enzymes and antacids

196
Q

People with cystic fibrosis can still produce what?

A

Digestive enzymes

197
Q

Gallbladder

A

Sac located under liver

198
Q

Bile ducts

A

Run from the liver and join to form the common hepatic duct which then joins with the common bile duct

199
Q

Hepatic lobule and structure

A

Functional unit of the liver

Has a hexagonal structure and central vein running through centre and a portal triad in each corner

200
Q

Portal triad structure

A

Consists of a hepatic artery, hepatic portal vein, and a bile duct

201
Q

Hepatocytes

A

Epithelial cells of the liver that form canalicular networks

Produce and secrete bile acids

202
Q

Canalicular networks

A

Tube like structures that join together until they form bile ducts

203
Q

Bile components produced by hepatocytes are put into what?

A

Canalicular networks, and then flow towards bile ducts

204
Q

Blood flow occurs where?

A

Other side of the hepatocyte

205
Q

Major functions of the liver?

A

Detoxifying blood
Formation and secretion of bile
Metabolizing and storing nutrients
Producing circulating proteins

206
Q

Bile

A

Breaks down fat

207
Q

6 components of bile

A 
Bile acids
Cholesterol
Salts
Phospholipids
Bile pigments
Trace metals
208
Q

Bile acids

A

Made from cholesterol

Emulsification of fats

209
Q

What enzyme does bile work with to digest fat?

A

Pancreatic lipase

210
Q

Emulsification

A

Large fat droplets being made smaller

211
Q

What does emulsification require?

A

Mechanical disruption

Emulsifying agent to keep droplets from re-agreggating

212
Q

2 things in bile that help with emulsification?

A

Amphipathic bile acids and phospholipids

213
Q

Micelle and function?

A

Polar heads facing outside while non polar tails facing inside in a circular formation
Allows easier absorbtion, increased SA for more absorption

214
Q

Bile duct cells

A

Add bicarbonate, water and other salts to the bile

215
Q

Basic steps of bile acid recycling

A
  1. Bile acids released by liver/gallbladder into duodenum (from hepatocyte to bile)
  2. Reabsorbed in SI into portal circulation
  3. Transported back into hepatocytes from blood
216
Q

Bile acids are synthesized where?

A

In hepatocytes

217
Q

How are bile acids transported across apical surface?

A

Primary active transport in canalicular networks

218
Q

How are bile acids absorbed across epithelial cells in SI?

A

Na dependant secondary active transport pathway

219
Q

How is bile moved to blood?

A

Facilitated

220
Q

How is bile acids in blood moved into hepatocytes

A

Secondary active transporter

221
Q

How can foods high in fiber reduce cholesterol?

A

These foods bind to bile acids and are excreted in feces, preventing reabsorption of bile acids

222
Q

How do bile salts regulate hepatobiliary secretion?

A

As more bile salts are absorbed by iliem and returned to liver, more will be secreted into bile

223
Q

How does secretin regulate hepatobiliary secretion?

A

Increases bicarbonate secretion in bile ducts and in pancreas, stimulated by acid in duodenum

224
Q

How does CCK regulate hepatobiliary secretion?

A

Production stimulated by digested fats and proteins in upper SI. Increases contraction of gallbladder and relaxes spincter of Oddi causing bile release into duodenum.

225
Q

Cause of gallstones?

A

Excess cholesterol.

If concentration of bile becomes too high relative to bile acids, cholesterol will precipitate out

226
Q

Pigment stones?

A

Amount of bile pigments are increased due to excess RBC breakdown. Bile forms precipitates with Ca.

227
Q

Gallstones consequences?

A

Obstruction or infection of gallbladder, pancreas, or liver

Pain, nausea, jaundice, insufficient absorption of fats, and fat soluble vitamins

228
Q

Gallstones treatment options?

A

Cholecystectomy (removal of gallbladder)
Removal of stones
Drugs to dissolve stones

229
Q

Duodenum functions

A

Mixing of pancreatic digestive enzymes and bile with food
Absorption of nutrients
Release of CCK and secretin

230
Q

Jejenum functions?

A

Digestion and absorption continued

231
Q

Ileum functions?

A

Absorption of bile acids and vitamin B12

232
Q

Folds of Kerckring?

A

Circular folds…essentially the whole intestine is folded on itself

233
Q

4 epithelial cell types derived from stem cells?

A

Paneth
Endocrine
Absorptive/enterocytes
Goblet

234
Q

Paneth cells

A

Secrete antibacterial peptides

235
Q

Endocrine cells

A

Hormone producing cells (S and I cells)

236
Q

Goblet cells

A

Secretion of mucus

237
Q

Absorptive/enterocytes

A

Contain microvilli at apical surface of cell

238
Q

Brush border

A

Microvilli covering villi of SI; major absorptive surface

239
Q

Brush border enzyme

A

Anchored to the brush border with catalytic activity in the lumen

240
Q

Only form of carbohydrates that can be absorbed is?

A

Monosaccharides

241
Q

Sucrose

A

Glucose+fructose

Broken down by sucrase

242
Q

Lactose

A

Glucose+galactose

Broken down by lactase

243
Q

Monosaccharides that can be absorbed by GIT?

A

Glucose,fructose,galactose

244
Q

How do glucose and galactose move from lumen of SI to enterocytes?

A

Use Na dependent glucose transporter (secondary active transport)
Uses the Na gradient to drive uptake of sugar into enterocyte
Na gradient generated by Na/K ATPase

245
Q

How are glucose and galactose transported across the basolateral surface of enterocyte?

A

Use a Facilitated glucose transporter GLUT

246
Q

How does fructose move into the enterocyte?

A

Using a facilitated carrier GLUT5

247
Q

How is fructose transported across the basolateral surface of enterocyte?

A

Using facilitated glucose transporter GLUT2

248
Q

Carboxypeptidase

A

Pancreatic protease

249
Q

Aminopeptidase

A

Brush border enzyme

250
Q

Small peptides can be taken up by?

A

Secondary active transport coupled to H

251
Q

Large fat droplets are mostly composed of?

A

Triglycerides

252
Q

Pancreatic lipase can only act on? Why?

A

The surface of fat droplets because it is water soluble.

253
Q

What must happen in order for pancreatic lipase to act?

A

Fat droplets must be broken down into smaller ones

254
Q

What prevents re-aggregation?

A

Bile acids and phospholipids that bind to the outside of the smaller droplets

255
Q

As micelles break down they release what?

A

Fatty acids and monoglycerides

256
Q

Once epithelial cells absorb fatty acids and monoglycerides, what happens?

A

They are processed by the ER and converted back into triglycerides.
This is to maintain the diffusion gradient of the lumen of the SI to the epithelial cell, so that fatty acids and monoglycerides can be absorbed into the enterocyte via diffusion.

257
Q

Chylomicrons

A

Extracellular fat droplets absorbed by lacteals

258
Q

Lacteal

A

Lymphatic vessel in the intestinal villi

259
Q

Ferritin

A

Protein iron complex that acts as a storage form of iron

260
Q

When body stores of iron are high what happens?

A

Increased production of ferritin, so increased binding of ferritin in epithelial cells, and reduction of amount of iron released into blood

261
Q

What happens when there is a need for iron but the stores are depleted?

A

Decreased production of ferritin, so decreased retention in enterocyte, and more will be absorbed in blood rather than stored.

262
Q

Iron toxicities

A

Genetic defects in absorption control pathways
Poisoning
Excessive intake of supplements

263
Q

Iron deficiency anemia & causes?

A

Reduced number or size of RBC

Caused by not enough iron in diet, blood loss, poor iron absorption, intestinal diseases

264
Q

Why is fluid crucial in intestine?

A

Allows for contacts of food and digestive enzymes
Prevents damage of epithelium
Allows diffusion of digested nutrients to absorption site

265
Q

Where is the most fluid absorbed?

A

Small intestine

266
Q

Gradient direction for absorption vs secretion?

A

Inward direction for absorption, outward for secretion

267
Q

3 important electrolytes for water absorption?

A

Chloride, bicarbonate, sodium

268
Q

Absorption predominantly depends on ?

A

Na gradient

269
Q

Absorption of water in SI?

A

Na gradient of Na/K ATPase end up moving glucose into cell
Glucose and Na are brought in via SGLT and pumped out by Na/K ATPase
Cl follows Na and water follows them

270
Q

Secretion predominantly depends on?

A

Cl gradients

271
Q

Secretion of water in SI?

A

NKCC1 allows accumulation of Cl in enterocyte based on inwardly directed Na gradient
CFTR opens allowing Cl to enter intestinal lumen
Na follows Cl, and water will follow, being secreted into the lumen

272
Q

MMC and purpose?

A

Migrating myoelectric complex; referring to peristaltic activity.
Purpose is to move undigested material from SI to LI and prevents bacteria from staying in the SI

273
Q

Regulation of MMC?

A

Hormone motilin initiates MMC. Motilin release is inhibited when you eat to allow for segmentation

274
Q

Lactose intolerance

A

Cannot completely digest lactose. Results in decreased water absorption, gas, diarrhea

275
Q

Lactose intolerance solutions?

A

Take a lactase pill with meal, or drink lactose free milk pre treated w lactase

276
Q

Cholera

A

Caused by consuming bacteria Vibria Cholera in contaminated food or water. Causes vomiting and diarrhea

277
Q

What does the bacteria in cholera produce?

A

Toxin that increases production of cAMP
This causes Cl channel to open allowing large amounts of Cl into intestinal lumen, and water follows and is lost as diarrhea

278
Q

Cholera treatment?

A

Consume clean water with salts and glucose to replace fluids

279
Q

Ileocecal valve. When is it open/closed?

A 
Between cecum (appendix) and illeum
Open after a meal when ileum contracts, closed when LI is distended. Retains LI contents
280
Q

Colon functions?

A

Reabsorption of water
Reservoir for waste and undigested products prior to defecation
Absorb products of bacterial metabolism

281
Q

Internal vs external anal spinctors?

A

Internal- smooth muscle, involuntary

External- skeletal muscle, voluntary

282
Q

Important difference between SI and LI? Results in?

A

LI has no villi while SI does. Results in lower SA in LI.

283
Q

Absorptive cells in LI compared to SI?

A

Do not contain brush border enzymes in LI

284
Q

Process of defecation?

A

Rectum distends and activates mechanoreceptors
Rectum contracts, internal anal sphinctor relaxes while external contracts initially
Then vice versa occurs and feces voided

285
Q

7 functions of the respiratory system?

A 
Provides oxygen to tissues
Eliminates CO2
Filters and protects from microbial infections
Helps regulate blood pH 
Phonation (speech formation)
Olfaction
Blood reservoir
286
Q

Alveoli

A

Fundamental units of the respiratory system and contain lots of capillaries

287
Q

Pharynx is split into what 2 components?

A

Nasopharynx and laryngopharynx

288
Q

What happens to allow phonation?

A

Air travels through vocal cords in larynx

289
Q

Air passage pathway

A

Larynx, trachea, 2 primary bronchi, lungs

290
Q

Trachea and primary bronchi can characterized by what?

A

Semi-cartileginous C shaped ring and smooth muscle in back.

Protects and promotes elasticity

291
Q

Bronchi

A

Same cartilage sturctures as primary bronchi but not C shaped, rather plate shaped

292
Q

2 divisions of the tracheobronchial tree

A

Conducting zone and respiration zone

293
Q

Conducting zone, and what does it consist of?

A

Anatomically dead space where there are no alveoli so no gas exchange occurs.
Consists of the trachea, primary bronchi, bronchioles and terminal bronchioles

294
Q

Respiratory zone, and what does it consist of?

A

Further down and contains the alveoli where gas is exchanged.
Contains respiratory bronchioles, alveolar ducts, alveolar sacs

295
Q

Terminal bronchioles

A

Smallest airways WITHOUT alveoli

296
Q

Respiratory bronchioles

A

Occasional alveoli

297
Q

Alveoli sacs

A

Contain large number of alveoli

298
Q

Type I alveoli

A

Flat cell, lined with fluid containing surfactant.

These cells do NOT divide

299
Q

Type II alveoli and its functions

A

Not frequently found.
Produce surfactant
Can act as progenitor cells, so they can replicate into type I alveoli cells which cannot be replaced on their own

300
Q

Surfactant importance

A

Important for respiratory function

301
Q

How do O and CO2 diffuse through the respiratory membrane?

A

O diffuses from alveoli to blood stream

CO2 diffuses from blood to alveoli

302
Q

Pnueumocyte

A

Referring to either type I or II alveolar cells

303
Q

Ventilation

A

Movement of gas from atmosphere to alveoli by bulk flow

304
Q

Movement of gas is due to what?

A

Changes in pressure and volume; promotes movement of gas from area of high to low pressure

305
Q

5 steps of respiration

A

Ventilation
Exchange of O and CO2 between alveoli and blood by diffusion
Transport of O and CO2 through pulmonary and systemic circulation by bulk flow
Exchange of O and CO2 between blood in tissue capillaries and cells in tissues by diffusion
CO2 produced and O used by cells

306
Q

How is airflow produced?

A

Motor neurons innervate respiratory muscles by CNS stimulation.
Respiratory muscles contract
Thoracic volume, thoracic pressure, and intrapulmanory pressures change with contaction and relaxation, allowing for gas movement in/out

307
Q

3 categories of muscles involved in respiration?

A

Pump muscles, airway muscles, accessory muscles

308
Q

Pump muscles

A

Make changes in pressure and volume at lung level

309
Q

Inspiratory vs expiratory pump muscles

A

Inspiratory- active during inspiration.

Expiratory- active during expiration

310
Q

Airway muscles

A

Keep airways open

311
Q

Accessory muscles

A

Facilitate respiration when there is an increased metabolic drive; ex used only when exercising pretty much

312
Q

Main inspiratory muscles?

A

Diaphragm
External intercostals
Parasternal intercostals

313
Q

Main expiratory muscles?

A

Internal intercostals

314
Q

Diaphragm, and what happens when it contracts?

A

Dome shaped structure, separates the lungs from the abdominal content.
When it contracts, it moves down, allowing rib cage to move up and out (widening) so overall INCREASE in thoracic volume

315
Q

External intercostals and their motion?

A

Help contract and lift rib cage

Bucket handle motion

316
Q

Parasternal intercostals and their motion?

A

Contract and pull sternum forward

Pump handle motion

317
Q

When are inspiratory muscles active?

A

All the time during inspiration

318
Q

When are expiratory muscles active?

A

Only during the expiratory phase of when you are MAKING AN EFFORT to breath out, so during stress, coughing, exercise. They do not contract during expiration at rest

319
Q

Internal intercostals

A

Used during forced expiration

Push rib cage down to reduce thoracic volume

320
Q

Inspiration at rest vs during deep breathing/exercising

A

At rest: diaphragm contracts expanding thoracic cavity
Deep breathing: stronger contraction of diaphragm, as well as recruitment of accessory muscles to allow further expansion of thoracic cavity

321
Q

Expiration at rest vs forced

A

At rest: abdominal and intercostal muscles are not active
Forced: abdominal muscles contract strongly causing diaphragm to move up and expel even more air
Internal intercostal muscles contract to move rib cage down

322
Q

What factors occur in someone with obstructive sleep apnea?

A

Depressed muscle tone of muscles in upper respiratory muscles
Reduction of openness in airway, resulting in snoring and large drops of O saturation in blood

323
Q

Why does sleep apnea occur?

A

Problem with neural control of breathing

Lack of excitatory drive which is needed to maintain tone

324
Q

Consequences of sleep apnea

A

Daytime fatigue
Changes in O saturation (resulting in cognitive impairment)
Cardiovascular risks

325
Q

How to treat sleep apnea?

A

No drug treatments but can administer a mask that delivers constant positive airway pressure and keeps upper aiways open.

326
Q

2 regions involved in filtering action?

A

Conducting zone (muco-ciliary escalator) and at the level of alveoli

327
Q

2 types of cells lining the surface of trachea. Function?

A

Goblet cells
Ciliated cells
Role is to entrap inert or biological particulates that were inhaled and remove them from airways.

328
Q

Ciliated cells

A

Have cilia on apical surface. Produce periciliary fluid

329
Q

Goblet cells

A

No cilia, produce mucus

330
Q

Periciliary fluid

A

Low density fluid produced by periciloary cells which allows cilia to move freely.

331
Q

SOL layer

A

Layer of perciliary fluid sitting on top of the ciliated cells

332
Q

Gel layer

A

Thick layer of mucus produced by goblet cells, distrubuted in patches

333
Q

What changes can affect the muco-ciliary layer?

A

Changes in thickness of the SOL or gel layers

334
Q

Smoking effect on goblet and ciliary cells?

A

Decreases ciliary cells activity, increase goblet cells

335
Q

What happens when silica or asbestos are inhaled? What condition can occur and why?

A

Macrophages recognize them as foreign objects and phagocytose them, but cannot digest them.
Silica and asbestos kill the macrophages and chemotactic factors are released.
Promotes fibroblasts into alveoli
Increases collagen which promotes lung stiffness, so pulmonary fibrosis can occur

336
Q

Spirometry

A

Test that determines the amount and rate of inspired and expired air

337
Q

Tidal volume

A

Volume of air breathed (in OR out) during one cycle

338
Q

Expiratory reserve volume

A

Amount of additional air that can be expired by forcibly exhaling to the max

339
Q

Inspiratory reserve volume

A

Amount of additional air that can be inspired by forcibly inhaling to the max

340
Q

Residual volume

A

Amount of air left in lungs after maximum expiration; cannot be expired even forcibly

341
Q

Vital capacity

A

Maximal volume of air that can be exhaled after maximal inspiration
VC= TV+IRV+ERV

342
Q

Inspiratory capacity and formula

A

Maximal volume of air that can be inhaled`

IC= TV+IRV

343
Q

Functional residual capacity and formula

A

Amount of air remaining in lungs after normal expiration

FRC= RV+ERV

344
Q

Total lung capacity

A

Amount of air in lungs after maximal inspiration

TLC= TV+IRV+FRC= VC+RV

345
Q

What cannot be measured by spirometry?

A

Residual volume

Also cannot measure any capacity with RV in the formula, therefore FRC and TLC cannot be measured using spirometry

346
Q

Total or minute ventilation

A

Amount of air exchanged within a minute or within a rate time

347
Q

How to calculate total or minute ventilation?

A

Respiratory frequency x tidal volume

348
Q

Alveolar ventilation

A

Amount of air moved into the alveoli per minute

349
Q

How to calculate alveolar ventilation?

A

Subtract the anatomical dead space volume from the tidal volume and multiply by the respiration frequency

350
Q

What kind of breathing is more effective in increasing alveolar ventilation? Why?

A

Deep breathing, as majority of the minute ventilation is dedicated for gas exchange

351
Q

FEV-1

A

Forced expiratory volume in one minute; how much of the vital capacity volume can be expelled in 1 min

352
Q

FVC

A

Forced vital capacity; same as vital capacity test

353
Q

3 factors looked at in spirometry tests

A
  1. FEV-1
  2. FVC
  3. Ratio of FEV-1/FVC
354
Q

Obstructive lung disease. Due to what? Obstructive pattern is common in patients with..?

A

Difficulty exhaling all the all from their lungs
Due to lung damage or narrowing of airways
Common in people with cyctic fibrosis, asthma

355
Q

Obstructive lung disease effect on FEV-1, FVC, and ratio?

A

FEV-1 reduced
FVC reduced or normal
Ratio reduced

356
Q

Restrictive lung disease. Due to what? Restrictive pattern is common in patients with..?

A

Difficulty filling lungs fully with air.
Lungs restricted from expanding due to condition causing lung stiffness.
Common in people with lung fibrosis, neuromuscular disease, scarring in lung tissue

357
Q

Restrictive lung disease effect on FEV-1, FVC, and ratio?

A

FEV-1 reduced (since amount of air inhaled is less than usual, amount exhaled will be less, even though one has the full ability to expel air )
FCV reduced
Ratio normal, but volume is less

358
Q

Helium dilution method?

A

Used to measure FRC

359
Q

Helium dilution method only measures what?

A

Communicating gas or ventilated lung volume

360
Q

2 classes of properties of mechanisms of ventilation?

A

Static and dynamic

361
Q

Static

A

Properties that are present when no air is flowing

362
Q

Dynamic

A

Properties that are present when the lungs are changing volume and air is flowing in/out

363
Q

Boyle’s law

A

At a contant temp, pressure and volume and inversely proportional
(increase in V=decrease in P)

364
Q

How does gas flow?

A

Bulk flow, from an area of high pressure to area of low pressure

365
Q

Pressure during inspiration

A

Thoracic cavity volume increases and pressure decreases, so air moves from an area of higher pressure (environment) to low pressure (alveoli)

366
Q

Pressure during expiration

A

Thoracic cavity volume decreases, so pressure increases so air moves from alveoli to environment (lower pressire)

367
Q

Visceral pleura

A

Covers surface of the lungs

368
Q

Parietal pleura

A

Attached to the inner surface of the thoracic cavity

369
Q

Interpleural fluid

A

Separates the visceral and parietal pleura, allowing them to slide around during inspiration

370
Q

Why do lungs have the tendency to collapse?

A

Elastic recoil

371
Q

What happens at equilibrium of lungs and chest wall?

A

Inward elastic recoil of lungs balances out the outward elastic recoil of the chest wall

372
Q

How do lungs and chest wall interact?

A

Through the interpleural space between visceral and parietal pleurae.

373
Q

Intrapleural pressure

A

Pressure inside the pleura

374
Q

Alveolar pressure

A

Pressure inside the alveoli

375
Q

Transpulmonary pressure

A

Difference of the alveolar pressure minus the intrapleural pressure

376
Q

Intrapleural pressure is always what?

A

Negative (or subatomic) because of the opposing forces of elastic recoil

377
Q

What occurs when someon has a collapsed lung in terms of pressures?

A

The alveolar pressure and intrapleural pressure are equal

378
Q

Which pressure is static and determines lung volume?

A

Transpulmonary pressure

379
Q

Which pressure is dynamic and determines air flow?

A

Alveolar pressure

380
Q

Steps in inspiration

A

CNS sends excitatory signal to inspiratory muscles
Muscles contract and generate increase in thoracic volume
Increase in transpulmonary pressure
Increase in lung volume
Decrease in alveolar pressure
Air moves in

381
Q

Steps in expiration

A 
Relaxation of inspiratory muscles
Chest recoils (decrease volume)
Instrapleural pressure is back to normal so transpulmonary pressure is reduced
Increase in alveolar pressure
Air moves out
382
Q

Forces that affect resistance to air flow?

A

Inertia of respiratory system

Friction forces

383
Q

Different friction forces

A

Friction between different alveolar sacs
Friction between lung and chest wall
Resistance that airflow incurs when entering airway

384
Q

Laminar flow and where does it occur?

A

Subject invests little energy in airflow resistance

Occurs at small airways that are distal to terminal bronchioles

385
Q

Transitional airflow and where does it occur?

A

Takes extra energy to produce vortices, resistance increases.
Occurs at most of the bronchial tree

386
Q

Turbulant flow

A

No longer smooth and laminar

Found in larger airways such as trachea, larynx, pharynx

387
Q

How does Poiseuille’s Law relate to airflow resistance?

A

The smaller the radius of an airway, the more resistance

388
Q

Where is resistance lowest? Why is this?

A

In the small airways. In this case, this is due to them being arranged in parallel. So, when calculating resistance it is INVERSE of each resistance, resulting in minimal resistance.

389
Q

How to calculate resistance for airways arranged in parallel vs in series?

A

In parallel: sum of all the individual resistances

In series: inverse of each resistance

390
Q

How can small airways be occluded?

A

Contraction of smooth muscle
Edema (presence of fluids reduces space)
Mucus accumulation

391
Q

Lung compliance

A

Measure of the elastic property of lungs and how easily lungs expand

392
Q

Why is lung compliance considered to be a static and dynamic property?

A

Can be measured in the presence or absence of airflow

393
Q

How is lung compliance determined on graph?

A

Transpulmonary pressure on x axis and lung volume on y axis. Lung compliance is the slope!

394
Q

Pulmonary fibrosis: high or low lung compliance? Why?

A

Low. Patient has to make a big effort to breath in and increase transpulmonary pressure

395
Q

Emphysema: high or low lung compliance?

396
Q

Hysteresis

A

Difference in inflation and deflation compliance path

397
Q

Why does hysteresis exist?

A

Because there is more pressure needed to open an airways rather than keep an airway open

398
Q

Lung compliance is determined by?

A

Elastic components of lungs: elastin and collagen

Surface tension at the air-water interface within alveoli

399
Q

Where are elastin and collagen found?

A

In the walls of the alveoli, around blood vessels and bronchi

400
Q

Emphysema, what occurs?

A

Many large alveolar spaces, compared to a healthy dense network of alveoli.
Elastin is decreased so floppy lungs occur.
Increased compliance in which little pressure is needed to cause large changes in volume.

401
Q

Surface tension

A

Property that occurs at the interface between the surface and air in which attracting forces pull a liquid’s surface molecules together. Decreases lung compliance

402
Q

Role of surface tension in the lungs?

A

Type I alveolar cells come in contact with fluid that contains surfactant, and alveoli are lined with thin layer of fluid. Surface tension occurs at all fluid-air boundaries

403
Q

Effect of surface tension?

A

To cause the surface to maintain as small of an area as possible

404
Q

How does alveolar radius size affect amount of pressure needed to keep bubble inflated?

A

The smaller the radius, the more pressure needed to keep it open

405
Q

Composition of surfactant

A

Mixture of phospholipids
Hydrophilic head dips into the water
Hydrophobic tail sits in the alveolar air

406
Q

How does surfactant reduce surface tension? What does this result in?

A

Breaks strong attractive forces between water molecules at surface. Reduction in surface tension and increase in lung compliance making it easier to breath

407
Q

In smaller vs larger alveoli, surfactant is found…?

A

Closer together in smaller, farther apart in larger alveoli

408
Q

Functions of surfactant

A

Stabilizes alveoli

Reduces surface tension

409
Q

Why do premature babies have respiratory issues?

A

They don;t have enough surfactant in their lungs

410
Q

Ventilation is lower/higher in what parts of the lung?

A

Higher in the lower part , lower in the higher part

411
Q

How does gravity and posture affect ventilation?

A

Laying on your back, the highest ventilation is at the back of your lungs towards your back while the chest wall has less activity

412
Q

Where is pressure more negative/less negative at? Why?

A

Gravity affects the pressure and since lungs have weight, the weight increases pressures meaning pressure in the lower part of the lung increases (becoming less negative since it is already negative) while the top part of the lung has decreasing pressure, meaning it becomes more negative

413
Q

Dalton’s Law

A

Each gas has its own specific pressure and the total pressure of a mixed gas is calculated by the sum of the individual pressures

414
Q

Fick’s Law

A

The rate of transfer of a gas is proportional to the membrane SA, and depends on the diff in partial pressures of the 2 environments. Inversely proprotional to thickness of membrane.

415
Q

Diffusion constant

A

Amount of gas transferred between alveoli and blood per unit time.
Proportional to solubility of gas and inversely proportional to the square root of molecular weight.

416
Q

Henry’s Law

A

Amount of gas dissolved in a liquid is directly proportional to the partial pressure of gas in which the liquid is in equilibrium

417
Q

Concentration of gas molecules in a liquid is determined by?

A

Partial pressure and solubility

418
Q

Why is the PO2 in the air in alveoli lower than in atmosphere?

A

When air enters alveoli, lots is humidified resulting in increased PH20 and decreased PO2.

419
Q

Determinants of alveolar PO2? describe.

A

PO2 in atmosphere- depending on altitude, high altitudes have lower pressures so the PO2 is reduce PROPORTIONALLY (still same percentages)
Alveolar ventilation- increase in alveolar ventilation means increase in gas exchange
Metabolic rate- exercising results in lower PO2 since it needs O2
Lung perfusion- changes in cardiac output change the amount of blood passing through resp system, which alters alveolar PO2

420
Q

Determinants of alveolar PCO2?

A

PCO2 in atmosphere- when blood is in contact with respiratory membrane, large amount of CO2 diffuses to the alveoli, and alveolar PCO2 > atmospheric PCO2
Alveolar ventilation- decrease in alveolar ventilation means less exhalation of CO2 into atmosphere so PCO2 in alveoli > atmosphere
Metabolic rate- increase exercise increases CO2 production, so higher level of CO2 moving into alveoli to be exhaled
Lung perfusion

421
Q

Why do we need pulmonary circulation to be a low pressure system?

A

Because the respiratory membrane is fragile, and high BP could damage it.

422
Q

How is the respiratory system a high compliance system?

A

Thin walls allowing for small changes in pressure to result in large vessel expansion

423
Q

Ventilation/perfusion ratio

A

Balance between ventilation (bringing O into/removing CO2 from alveoli) and perfusion (removing O from alveoli and adding CO2)

424
Q

The greater the ventilation…?

A

The more similar PO2 and PCO2 will be similar to atmospheric pressures

425
Q

The greater the perfusion…?

A

The composition of alvelor air at the region of higher perfusion will be more similar to the mixed venous blood with a reduction in PO2 and increase in PO2

426
Q

High V/Q ratio is seen in what condition?

A

Collapsed lung or pleurisy

427
Q

What happens in a high V/Q ratio physiologically?

A

Blood flow is occluded

Very little gas exchange because theres no blood available

428
Q

What happens to PO2 and PCO2 in alveoli in a high V/Q ratio?

A

PO2 increases because there is no oxygen that passes to the lungs through vasculature
PCO2 decreases because there is no CO2 delivered and diffuses from capillary system to alveoli

429
Q

Alveolar dead volume

A

Region of lungs where there is a high V/Q ratio due to pathological condition. Region is over-ventilated and underperfused, therefore not contributing to gas exchange

430
Q

Anatomical dead volume

A

Differs from alveolar dead volume; it is the conducting zone

431
Q

Low V/Q ratio is seen in what condition?

A

Collapsed bronchi or bronchioles

432
Q

What happens in a low V/Q ratio physiologically?

A

Airflow is obstructed/occluded

No exchange of gas between alveolar air and atmosphere

433
Q

What happens to PO2 and PCO2 in alveoli in a low V/Q ratio?

A

Increased PCO2 and decrease in PO2

434
Q

Shunt

A

Portion of the venous blood that does not get oxygenated and is not available for gas exchange because of alveolar occlusion.

435
Q

V/Q ratio is lower where?

A

Bottom of the lungs

436
Q

PO2 and PO2 levels at top and bottom of lung if we have an ideal V/Q ratio?

A

At the bottom: slightly reduced PO2 and slightly increased PCO2
Top: reduced PCO2 and increased PO2

437
Q

Bronchiocontriction in an alveoli. What happens to the pressures?

A

Makes diameter of airway smaller leading to a reduction in ventilation
PCO2 is increased, PO2 decreased

438
Q

2 forms that O2 is carried in blood?

A

Dissolved in plasma

Bound to hemoglobin (98%)

439
Q

Hemoglobin structure

A

Protein made of 4 amino acid subunits called globins (2 alpha 2 beta) and 4 heme groups

440
Q

Heme group

A

Porphyrin ring structure in which an iron atom binds to oxygen

441
Q

What is an O2 dissociation curve?

A

Shows the interaction between hemoglobin and the arterial partial pressure of O2

442
Q

2 properties highlighted in an O2 dissociation curve?

A

Oxygen capacity- max amount of O2 that can be combined with hemoglobin
Hemoglobin saturation- percentage of the available hemoglobin sites that have O2 attached

443
Q

Factors that influence interaction between hemoglobin and O2?

A

Arterial PO2 (most important because as it changes, the saturation of hemoglobin changes)
pH
PCO2
Temp

444
Q

Cooperative binding

A

Occurs because we have deoxyhemoglobin (hemoglobin with no O bound to it)
Leads to sigmoidal shape of O2 dissociation curve

445
Q

Conformational changes in hemoglobin

A

After one O2 molecule binds, hemoglobin goes from a tense to relaxed state allow each consectuive O2 to bind more easily

446
Q

Anemia vs polycythemia Hb amounts?

A

Anemia- low Hb levels

Polycythemia- high Hb levels

447
Q

How does O2 in alveoli move to RBC?

A

Pressure gradient established since PO2 is higher in alveolar space than in plasma, so O2 moves into plasma
Another pressure gradient is established where O2 molecules move from plasma to RBC where they bind to Hb.

448
Q

How does O2 move from RBC to mitochondria in peripheral tissue?

A

Oxygen moves from RBC to plasma to interstitial fluid to space between cells to intracellular space to MIT

449
Q

There is more O2 unloading if…?

A

There is a lower PO2 in peripheral tissue

450
Q

What does a shift to the right of O2 dissociation curve mean?

A

For the same level of PO2, there will be a lower level of Hb saturation. It means that there is increased unloading of O2 since O2 affinity for Hb is reduced.

451
Q

Factors causing a shift right

A

Increased temp
Increased PCO2
Anything that increases metabolism causes increased unloading of O2

452
Q

Shift to left means?

A

Increased O2 affinity for Hb, less unloading

453
Q

DPG

A

Present in RBCs and is an end product of RBC metabolism

Shifts curve to the right

454
Q

Is CO2 or O2 more soluble ?

455
Q

3 ways CO2 is carried in blood?

A

Dissolved
Bicarbonate
Carbamino compounds

456
Q

Carbonic acid rxn

A

CO2+H2O—>carbonic acid

457
Q

Carbonic acid dissociates into?

A

H ions and bicarbonate

458
Q

Chloride shift ad function?

A

Bicarbonate exits RBCs and Cl anions enter

This functions to maintain the electrical neutrality in RBCs

459
Q

How is caraminohemoglobin formed?

A

CO2 interacts with the globin chain of hemoglobin

460
Q

CO2 has a higher affinity for…?

A

Deoxyhemoglobin (compared to oxyhemoglobin)

461
Q

What happens to the curve if PCO2 increases?

A

Shift to the right and a lower percentage of Hb is bound to O2

462
Q

H ions have a higher affinity for…?

A

Deoxyhemoglobin

463
Q

2 major effects of hemoglobin and H interacting?

A

Unloading of O2- at lower pH there is reduced Hb saturation of O2 and ore unloading; shift right
Hemoglobin buffers the change in pH at level of venous blood

464
Q

Respiratory acidosis

A

Hypoventilation (CO2 production > CO2 elimination)

Increased PCO2 and H ion concentration

465
Q

Respiratory alkalosis

A

Hyperventilation (CO2 production< elimination)

Decreased PCO2 and H ion concentration

466
Q

Metabolic acidosis

A

Increase in H ion concentration, independant of PCO2

467
Q

Metabolic alkalosis

A

Decrease in H ion conc, independent of PCO2

468
Q

3 regions in brain that control breathing?

A

Pontine, dorsal, and ventral respiratory groups

469
Q

Where is breathing initiated?

470
Q

Where is breathing modified?

A

By higher centers in CNS and inputs from central and peripheral chemoreceptors and mechanoreceptors in the lung and chest wall

471
Q

Why is ventral respiratory group the most important?

A

Contains the inspiratory and expiratory rhythm generator

472
Q

Pre Botzinger complex

A

Inspiratory rhythym generator

473
Q

Parafacial respiratory group

A

Groups of neurons within the ventral respiratory group

Important in active contraction of abdonimal muscles

474
Q

Where is rhythm of breathing initiated?

A

Ventral respiratory group in medulla

475
Q

Factors influencing rate of breathing?

A

Neuromodulary factors (neurotransmitters)
Suprapontine influences that are emotional
Sensory inputs

476
Q

Neuro respiratory pathway for inspiration

A

Pre Botzinger complex, inspiratory premotor neurons in VRG excited, excite phrenic and thoracic motor neurons, activate diaphragm and external intercostals

477
Q

Neuro respiratory pathway for active expiration

A

pFRG geenrates rhythm, expiratory pre motor neurons excited, activate thoracic and lumbar motor neurons, activate internal intercostals and abdominals

478
Q

2 peripheral chemoreceptors. What do they sense?

A

Carotid and aortic bodies. Sense changes in PO2, esecially hypoxia (decrease in PO2)

479
Q

2 cell populations in carotid bodies

A

Type I glomus cells

Type II sustentacular cells

480
Q

Type I glomus cells

A

Chemosensitive

Simialr to neurons and can genrate AP

481
Q

Primary stimulus for peripheral chemoreceptors?

A

Decrease in arterial PO2

482
Q

What happens in glomus cells when PO2 decreases?

A

Increased firing rate

483
Q

When do we see a strong increase in minute ventilation?

A

Only when theres a drastic drop in PO2 levels, like in lung diseases or high altitude

484
Q

Small increase in arterial PCO2 results in?

A

Very large changes in minute ventilation

485
Q

Central chemoreceptors

A

Close to ventral surface of medulla

Sense changes in PCO2

486
Q

Hypercapnia

A

Too much CO2 in blood

Physl 210 B (2 decks)

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