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BIOL 1080 > Rest of Bio > Flashcards

Rest of Bio Flashcards

1
Q

What is the cardiac cycle?

A

Contraction of atria (AKA atrial systole), followed by contraction of ventricles (ventricular systole), followed by a rest (diastole) when neither chamber is contracting

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2
Q

What is the contraction called?

A

Systole (arterial BP –120–/80)

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3
Q

Relaxation is called?

A

Diastole (arterial 120/–80–)

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4
Q

What is diastolic arterial pressure called?

A

AFTERLOAD the pressure against which the heart must work to eject blood during systole (systolic pressure)

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5
Q

What do neural and endocrine signals control?

A

Strength and rate of heart contractions

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6
Q

What does sympathetic innervation (norepinephrine) do on heart rate

A

Increases

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7
Q

What does parasympathetic innervation (acetylcholine) do on heart rate?

A

Decreases

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8
Q

What does epinephrine do on each contraction?

A

Increases the strength

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9
Q

What happens from rest to exercise?

A
  • Heart rate can increase to nearly 200 bpm
  • Cardiac outpuut INCREASES from 5-25L/min
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10
Q

What is electrical signal propopaged by?

A
  • Nodes
    SA (sinoatrial) node (hearts natural pacemaker: electrical impulses are generated here
    AV (atrioventricular) node
  • Nerves
    Bundle of His
    Bundle branches
    Purkinge fibres
  • Intercalated disks (gap functions)
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11
Q

What does cardiac muscle consists of?

A

Individual cardiomyocytes connected by intercalated disks (gap junctions) to work together as a single functional organ

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12
Q

What are some examples of miscommunication of the heart?

A

Results in some kind of arrhythmia

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13
Q

What does abnormal sinoatrial (SA) node firing result in?

A

Result in tachycardia, bradycardia, tachy is fast, brady is slow

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14
Q

What do blocks do?

A
  • eg at the AV node, vary in terms of blockage
  • Can slow down or prevent signal propogation from atria to ventricles
  • Ventricles can contract independently (bundle of His, 40 bpm)
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15
Q

Why are fibrillations more serious?

A

Occuring when cells depolarize independently

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16
Q

What is atrial fibrillation?

A

Also called A-fib, is a quivering or irregular heartbeat (arrthymia)

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17
Q

What is atheroscelorisis?

A
  • Narrowing of arteries due to calcified fatty deposits (plaque) and thickening of the wall, triggered by damage to arterial wall (inflammation), can lead to heart attacks or stroke, when this occurs in the arteries of heart muscle, called coronary artery disease
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18
Q

What are factors of atherosclerosis?

A
  • Elevated blood lipids, hypertension, inflammatory mediators (C-reactive protein)
  • Diet (sodium, potassium, saturated/trans fat)
  • Smoking, physical inactivity, obesity/diabetes
  • Age, genetics
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19
Q

How do you treat coronary artery blockage?

A
  • Angioplasty (a catheter and balloon are threaded into the coronary atery to the point of blockages)
  • Bypass surgery (vein taken from arm or leg; one end attached above the blockage and the other below)
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20
Q

What is hypertrophy?

A

sign of being “overworked” heart muscle will respond and hypertrophy just like your skeletal muscle would repsond to weight-lifting

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21
Q

How does the heart reflect of athletes?

A

Mostly an increase in LV chamber (need to increase cardiac output)

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22
Q

How does the heart reflect of weightlifters?

A

Mostly increase in LV wall and septum thickness (need to overcome increased after load- the amount of pressure needed to eject blood during ventricular contraction

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23
Q

Why is enlargement of the heart bad?

A

Causes include high blood pressure and narrowing of aortic valve… heart must work harder to overcome these

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24
Q

Why is enlargement of the heart good?

A

Athletes heart- an appropriate adaptation, occurs in both athletes and weightlifters

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25
Q

Does BP vary with cardiac cycle?

A

Yes

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26
Q

What does a systolic BP mean

A

Maximum pressure
- When the ventricles contract, sending blood in the arteries

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27
Q

Diastolic blood pressure mean?

A

Minimum pressure
- When the heart relaxes between beats- not zero due to elastic recoil of arterial wall

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28
Q

What does blood pressure categories mean?

A

Normal numbers less than 120 systolic, less than 80 diastolic

Elevated 120-129 systolic, and less then 80 diastolic

High BP (hypertension stage 1) 130-139 systolic, and 80-89 diastolic

High BP (hypertension stage 2) 140 or higher systolic and 90 or higher diastolic

Hypertensive crisis (consult with your doctor) higher then 180 systolic and higher then 120 diastolic

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29
Q

What does vasoconstriction mean?

A
  • Alpha-receptors are located on arteries
  • Norepinephrine and epinephrine bind to alpha 2 adrenergic receptors
  • Causes arteries to constrict (vasoconstriction)
  • This increases BP
  • Eg during excercise
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30
Q

What does vasodilation mean?

A
  • Blood vessels in skeletal muscles lack alpha-receptors
  • Norepinephrine and epinephrine bind to b2 adrenergic receptors found in arteries of skeletal muscle
  • This dialates vessels of the skeletal muscles (vasodilation) so they can receive increased blood flow
  • Eg also during excercise!
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31
Q

What happens to BP during aerobic (cardio) excercise?

A

Cardiac output increases 5x during excercise, up to 8 in athletes

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32
Q

Does BP increase dramatically during excercise?

A

Not really, why not?
- Distribution of blood does not increase proportionally- blood flow is diverted to where it is needed during excercise the working muscles
- Dialation of vessels to skeletal muscle and heart increases blood flow to the muscls (beta 2 receptors and local metabolites)
- Constriction of vessels to the gut and kidneys decreases blood flow to the organs (alpha receptors)
- Dialating vessels in muscle decreases resistance and have a lot of muscle mass
- So, BP does NOT increase dramatically during excercise

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33
Q

What is resistant excercise?

A

muscles against a force eg weightlifting, can cause dramatic increases in BP
-Why holding your breath increases inthoaratic pressure during the lift- called Valsalva maneuver

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34
Q

What does the GI track represent?

A
  • It “sees” not only our food, but potentionally toxic substances and infectious agents
  • Unique mechanisms to deal with this:
  • Sense and expel noxious substances (vomit, diarrhea)
  • Specialized populations of T cells localized to the intestinal mucosa
  • Eg Peyers patches
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35
Q

How does it go through the body GI?

A
  • Oral cavity (upper esophageal sphincter)
  • Esophagus (lower esophageal sphincter)
  • Stomach (pyloric sphincter)
  • Small intestine (ileocecal valve)
  • Colon (large intestine)
  • Anal sphincter
  • Rectum
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36
Q

How long is the GI track?

A
  • 28 ft long
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37
Q

Is there a highly variable transit time?

A

Total of 30-80 h
- 5-8 hrs in stomach and small intestine
- Rest of time in colon

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38
Q

What is microbiome?

A
  • Bacteria, etc
  • Protects against pathogenic microbes that enter/reside in the tract
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39
Q

What is the intrinsic (aka enteric) nervous sytem?

A

Control and coordinate all this functioning (eg opening and closing of sphincters)

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40
Q

What are the 4 basic processes?

A

Motility
- Peristalsis (contraction and relaxation of muscles throughout the digestive tract)

Secretion
- Saliva, mucous
- Antibodies (IgA)
- Digestive enzymes
- Bile
- Bicarbonate

Digestion

Absorption
- Water
- Nutrients

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41
Q

What is the celiac phase of digestion and absorption?

A
  • Chemical and mechanical digestion begins in the mouth
  • Chewing (mastification)
  • Secretions in response to sensory stimuli (sight, smell, taste) prepares the GI tract for food processing
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42
Q

What is salivary secretion under control of?

A

Autonomic control (stimulated by sympathetic and parasympathetic nervous system)

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43
Q

What does salivary secretion do?

A
  • Softens and lubricates food
  • Provides enzymes: amylase and some lipase (but no protein digestion)
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44
Q

What is the Gastric phase of Digestion and Absorption?

A
  • Secretory cells of gastric mucosa- note the influence of the Parasympathetic Nervous System (rest and digest)
  • It increases intestinal and gland activity, and relaxes sphincter muscles in GI tract
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45
Q

What digests in the stomach?

A

Protein and fat, but not carbs

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46
Q

What happens in small intestine and acessory organs?

A

Pancreas: main contributor of digestive enzymes
- Enzymes are released from pancreas in inactive form eg trypsinogen
- Activated in small intestines by enterokinase in brush border of duodenum to form trypsin - for protein digestion

Gallbladder: stores bile (produced by liver)
- Fat digestion

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47
Q

Is there absorption in the small intestine?

A

Yes

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48
Q

What does small intestinal mucosa do?

A

Villi increase surface area to promote nutrients absoprtion

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49
Q

What secretions in the lumen of the small intestine upon opening of the pyloric sphincter and food (chyme) entering the upper duodenum

A
  1. Bicarbonate- from cells in the intestinal epithelium and in pancreatic seretions
  2. Digestive enzymes- from pancreas
  3. Bile acids (as bile fluid)- from liver/gallbladder
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50
Q

Digestive enzymes anchored on the luminar surface of small intestine epethilial cells

A
  1. Disaccharides
  2. Amino peptidases
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51
Q

What is maltose?

A

2 glucose

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52
Q

What is sucrose?

A

Fructose and glucose

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53
Q

What is lactose?

A

Galactose and glucose

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54
Q

What is starch?

A

Glucose + glucose and glucose

55
Q

What type of transport does glucose and galactose need?

A

Active meaning they require ATP

56
Q

What type of transport does fructose need?

A

Facilitated does not require ATP

57
Q

What does it mean for somone to have celiac disease?

A

Means they have a deficiency in lactase which breaks down lactose results in a lactose intolerance

58
Q

What does protein digestion require?

A

Sometimes require cotransport with something esle or transcytosis (in cell)

59
Q

How does Peptide and Amino Acid Tranpsort work?

A
  1. Proteins broken down into smaller peptides
  2. Epithelial cells screte peptidases to break down larger peptides into individual amino acids
  3. Transported throughout the body via the bloodstream in order to produce energy (in liver) or protein synthesis
60
Q

What does emulsifying fat do?

A

Making fat soluble with bile

61
Q

Fat is…

A

Nonpolar

62
Q

How does fat digestion work?

A
  • Starts in mouth and continues using lipase in stomach and small intestine
  • Chyme when eneters the duodenum and triggers release of bile (made in liver and stored in gallbladder)
  • Bile helps with emulsification
  • Bile salts are amphipathic, both hydrophobic and hydrophilic can help with water and the lipids is like a soap or detergent
63
Q

What helps to break triglycerides into mono?

A

Pancreatic lipase

64
Q

What does microvilli do to help with fats?

A

Help to transport fats into digestive system

65
Q

What can monoglycerides help to form?

A

Form micelles that help with vitamin and fat absorption

66
Q

What do chylomicrons help to do?

A
  • Help to transport triglycerides to body
  • Do not go into bloodstream originally because too large to go into lympatic system through the thoracic duct near the heart
67
Q

How are lipids absorbed?

A

As fatty acids and monoglycerides

68
Q

How are the fatty acids and monoglycerides reassembled?

A

Reassembled into triglcerides and packaged as cyclomicrons which are a type of lipoprotein

69
Q

Cyclomicrons are…

A

Too large to cross the capillary wall and are first absorbed into the lymphatic system, and will reneter circulation via thoracic duct near the heart

70
Q

What comes in from the ileum? (ileocecal valve)?

A

Ileal chyme (a chemical and particle rich liquid)

71
Q

What is in ileal chyme?

A
  • Any unabsorbed nutrients
  • Hormones and chemical messengers
  • Soluble fibre (prebiotic)
  • Insoluble fibre (bulking agent)
  • Microbes (probiotics and other)
  • Cellular debris
  • Excretion products from the liver
72
Q

What is the major diff from large and small intestine?

A

Large does absorption of water and ions

73
Q

What happens in the large intestine?

A
  • Colonic epithelium absorbs water and simple ions like sodium, potassium, magensium and calcium
  • Resident microbes digest and absorb chemical they can (prebiotics) in a process called fermentation, make short-chain fatty acids as end-products of fermentation
  • The resident microbes produce some vitamins (vitamin K, some B vitamins) as a by-product of their metabolism, some of their end products can have hormone like activity
  • The resident microbes produce gases during their digestion and consumption of illeal chyme (CO2, methane, hydrogen sulfide)
  • Newly arriving live microbes (probiotic or other) seek to get a foothold in the microbial ecossytem and multiply
74
Q

What motivates you to eat?

A

Hedonic and homestatic hunger

75
Q

What is hedonic hunger?

A

Drive to eat to obtain pleasure in the absence of an energy deficit

76
Q

Why is hedonic hunger good and bad?

A

Good since prevents disordered eating, but bad because leads to an increased intake or uneccesary calories

77
Q

What is homeostatic hunger or eating?

A

Increased motivation to eat following depletion of energy stores

78
Q

What is normal eating?

A
  • Going to table hungry, and eating until you are satisifed
  • Being able to choose food you enjoy and eat it and truly get enough of it
  • Being able to give some thought to your food selection so you get nutritious food, but not being so wary and restricitive that you miss out on enjoyable food
  • Giving yourself permission to eat because you are happy, sad, or bored, or just because it feels good
  • Mostly 3 meals a day, or four or five, or it can be choosing to much along the way
  • Leaving cookies on the plate because you will let yourself have cookies again tomorrow
  • Is overreacting at times, and feeling stuffed and uncomfortable and undereating at time wishing you had more
  • Is trusting your body to make up for mistakes in eating
  • Takes up some of your time and attention, but keeps its place as only one important area of your life
  • Varies in reponse to hunger, your schedule, food and feelings
79
Q

What is energy defined as?

A

The capacity to do work

80
Q

What is ATP?

A

the medium of energy exchange; adenosine triphosphate, one adenosine to 3 phosphate

81
Q

What generates the most ATP?

A

Glucose and fatty acid metabolism relatively little with amino acids but still some

82
Q

Where is the most ATP?

A
  • Some from glycolysis and Krebs but mostly the ETC
83
Q

Whay does glycolysis, beta oxidation and Krebs cycle produce?

A

Reducing equivalents: molecules that transfer an electron in a redox rxn
- NADH and FADH2

84
Q

What do NADH and FADH2 supply?

A

Supply protons (H+) and electrons (e^-) to the ETC

85
Q

What does glycolysis do?

A

Convert glucose into pyruvate

86
Q

What is anerobic respiration?

A
  • Without O2 by
  • Phoshocreatine (PCr) degredation
  • About 9-10 seconds worth

PCr+ADP+H+–) ATP+Cr (creatine)

  • ATP is rebuilt by adding a phospahte to ADP
87
Q

What does glycolysis do in anerobic to produce what?

A

Produced ATP, lactate gets produced in aneorobic eg sprints

88
Q

What is fat?

A

Most energy is stored as triglycerides (a form of fat) in our adipocytes

89
Q

What are carbs stored as?

A
  • Glycogen in liver (about 150g): most concentrated as liver only about 2 kg
  • Glycogen in muscle (about 350 g): about 40% body mass in muscle most in muscle!
  • Only about 30 g of glucose is found in blood
90
Q

Where are proteins stored?

A
  • Represtens a large energy source
  • 40% of body mass is muscle
  • Obviously protected, but also will be used in starvation or caloric restriction
91
Q

What are the pros and cons of using carbs are fuel?

A
  • Aerobically, can generate ATP slightly faster than from fat
  • Can also generate ATP anerobically (3x faster than aerobic)
  • BUT holds a lot of water ie “heavier”, less energy dense than fat
92
Q

What are the pros and cons of using fat as fuel?

A
  • Doesnt hold water, more than twice as energy dense as carbs
  • Represents our most abundant energy reserve
  • BUT CANT provide energy anerobically (must have oxygen)
93
Q

What happens in the first 3-4 hours after a meal?

A
  • Absoptive state
  • Energy (macronutrients) are stored (ANABOLISM)
  • Excess nutrients taken up will be stored (ie anabolic state)
  • Glcogen (carb) stored in liver and muscle
  • Triglycerides (fat) stored in adipose tissue, liver and muscle
94
Q

Excess calories in the form of glucose or amino acids get converted to…

A

Fat

95
Q

What happens in the post absorptive state?

A
  • Fasting
  • Stored macronutritens are mobilized for energy (catabolism)
  • Glucose is spared for nervous sytem
96
Q

What is glucogenesis?

A

Making glucose from non-carb precursors (occurs in liver mainly but also kidneys) part of catabolism or post absorptive state

97
Q

What is glycogenesis?

A

Breaking down glycogen into glucose

98
Q

What is normal fasting blood glucose?

A

4-5.5 mmol/L (very narrow range)

99
Q

How does fasting blood glucose compare with free fatty acids?

A

Free fatty acids: vary from 0.2-2 mmol/L (10-fold range)

100
Q

Fasting hyperglycaemia?

A

High Glucose is greater then 7 mmol/L

101
Q

Fasting hypoglycemia?

A

Low Glucose is less then 3.5 mmol/L

102
Q

Why is blood glucose maintained so tightly?

A
  • Many cells require glucose (eg neural tissue, kidney)
  • Maintain osmotic balance (optimal concentrations of electrolytes and non-electrolytes are maintained)
  • Hyperglycemia can cause glycosyltation of amino acids in kidneyd, peripheral nerves, lens of the eye, causing damage
103
Q

What happens when blood gluocse is elevated via insulin?

A
  • Could be after a meal
  • Increase in insulin, increase in glucose uptake in cells, increase in glycogen synthesis, and decrease in glyocogenolysis and glucogenesis (lower the lysis as it converts and dont want to convert anymore)
104
Q

What happens when blood glucose is low via glucagon?

A
  • Induced by fasting
  • Plasma glucose decreases
  • Glucagon secretion increases, playing biggest hormonal role
  • Gluconogenesis and glycogenesis increases, and lipolysis (increase in breakdown of fatty acids) and plasma fatty acids (using fat from adipose tissue so not relying on glucose as much) increase, as well as plasma glucose increases negative feedback with plasma glucose, wants more glucagon to keep high
  • Also decreases insulin ie glucagon to insulin ration increases
105
Q

What is so important about changes in insulin and glucagon?

A
  • Reciprocal changes, not. just the changes in one of these hormones
106
Q

What does prolonged lower intensity rely on?

A
  • Eg marathon
  • Relies on plasma-derived substrates, particularly free fatty acids but also some blood glucose
  • As you increase excercise intensity, there is an increased need to mobilize energy stores (subtrates) within the muscle itself- glycogen and triglycerides (more complex)
107
Q

What is used predominantly in high intensity excercise?

A

Muscle glycogen

108
Q

What fuel does prolonged, low intensity excercise eg walking, slow jog require?

A
  • Mainly blood glucose and fatty acids; some muscle triglycerides and glycogen
109
Q

What fuel foes moderate to high intensity eg cycling, jogging/running at 60 to 90% of VO2 max

A
  • Mainly muscle glycogen and triglycerides; blood glucose and fatty acids
110
Q

What fuel foes very high intensity eg sprinting, weightlifting ie large anerobic component require?

A
  • Muscle glycogen, phosopcreatine (PCr)
111
Q

Why do we age?

A

In our genes; genetic variation in “longevity” genes may influence lifespan

112
Q

How is DNA systhesized?

A

5’ to 7’

113
Q

Why do we age? Is it due to Genetic variation?

A
  • SIngle nucleotide polymorphisms (SNPs)
  • Each SNP represents a difference in a single DNA building block (nucleotide)
  • 10 million SNPs within the human pop
  • 1 every 300 nucelotides will contain SNP’s
  • Most frequent source for polymorphic changes
  • Not the only source for genetic variation
  • But represents major source that distinguishes one individual from another
  • Most is same
114
Q

What can infleunce genes?

A
  • Lifestyle (stress, nutrition etc) can influence health and/or performance
  • Caffeine for example has varying effects on people based on how fast one can metabolise it
115
Q

Are SNPs in a single CHS dense?

A

Yes

116
Q

Is there a lot of genetic variation due to SNPs

A

Yes

117
Q

What is HapMap Project?

A

Database that catalogues the 10 million SNPs identified in the human genome

118
Q

What is aging associated with?

A

Increase in inflammatory cytokines that contribute to age-related disorders such as Alzheimers, cardiovascular disease, arthritis

119
Q

What is aging associated with? What type of correlation…

A

Negative correlation as one increases other one decreases as BMI increases, cytokine decreases

120
Q

What is an inflammatory cytokine?

A

Interleukin-6 (IL-6), plasma levels positively correlated with greater mortality (higher IL-6, so does mortality)

121
Q

What SNP is the promoter of IL-6?

A

Associated with higher IL-6 and an increased mortality rate

122
Q

What is a polymorphism?

A

a DNA sequence variation that is common in the population (one SNP)

123
Q

What is a promoter?

A

Is a region of DNA that initiates transcription of a particular gene

124
Q

What another reason for why we age?

A
  • Mitochondria contains genes too
  • eg components of the ETC
  • Damage to mitochondiral genome occurs 10x more frequently than the nuclear genome
  • Due to generation of reactive oxygen species (ROS)
  • Highly reactive chemical species containing oxygen
    examples of peroxides, superoxide, hydroxyl radical, and singlet oxygen
125
Q

What is DNA polymerase gamma?

A

Replicates and proof reads/repairs mitochondrial DNA

126
Q

What happens if there is an error in replication?

A

More frequent as we age, accumulating mutations in mitochondrial DNA accelerates aging

127
Q

What happens with againg and mitochondrial DNA?

A

With aging, DNA polymerase gamma corrects errors less effectively

128
Q

Mitochondrial DNA replication is…

A

Error prone

129
Q

Is there a link between mitochondrial DNA mutations and againg phenotype?

A

Yes

130
Q

Can excercise reduce the effects of aging?

A

PolG mice didnt have that gene to help correct: lack mitochondrial DNA error correction and show increased mitochondrial DNA mutations and overall advanced aging
- Reduces DNA mutations, brings weight and muscle weight back to almost normal levels

131
Q

Aging is inevitable but…

A

Healthy aging can be influenced by lifestyle choices

132
Q

How does caloric restriction help?

A

20% to 40% reduction in daily energy intake, but without malnutrition
- Extended healthy lifespan in rats
- No conclusive evidence in humans

133
Q

How does excercise compare to drugs that are used to improve ability of muscle to respond to insulin? What is the orginization called?

A

Excercise is medicine, prediabetes reversable blood sugar high

134
Q
A

BIOL 1080 (4 decks)

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