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BIO 203 > QUIZ 5 > Flashcards

QUIZ 5 Flashcards

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1
Q

Chemical energy

A
  • fuel for cellular work
  • ingested organic molecules are broken down and potential energy of their covalent bonds is converted to ATP
  • energy cant be created or destroyed
  • different amounts of ATP are derived from different food molecules
  • one calorie= energy required to raise 1 ml of water 1 C
  • food calories are kilocalories
  • lipids (triglyceride) -> 120 ATP/steric acid -> 9kCal/gram
  • carbs -> 30 ATP/glucose -> 4kCal/gram
  • proteins -> 30 ATP/amino acid -> 4kCal/gram
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2
Q

organic precursors

A

organic raw materials for biosynthesis (carbon skeleton)

–digest proteins down to amino acids and use to make our own nutrients

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3
Q

essential nutrients

A

substances animals cannot synthesize

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4
Q

dietary water

A

water ingestion/production of metabolic water

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5
Q

dietary needs

A
  • repackage energy in covalent bonds in food into ATP

- ATP energy currency -> work

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6
Q

lipids

A
  • most common lipid we digest is tryglyceride -> 3 fatty acids and one glycerol
  • glycerol covalently linked to carboxyl group of fatty acid
  • molecule that dissolved in a nonpolar solvent
  • ex. cholesterol
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7
Q

unsaturated

A
  • double bond present
  • there could be H there
  • presents a kink
  • liquid at room temp
  • oleic acid
  • cis double bond
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8
Q

ester linkages

A
  • joins glycerol to carboxyl group of fatty acid

- middle fatty acid can rotate

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9
Q

phospholipid

A
  • glycerol attached to two fatty acids and one phosphate group
  • bilayer
  • phosphate it on exterior (hypdrophilic)
  • fatty acids on interior (hydrophobic)
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10
Q

saturated fats

A
  • straight (no kink)
  • H bonds all around
  • solid at room temp
  • stearic acid
  • can be more a risk for cardiovascular disease
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11
Q

steroids

A
  • lipid related molecules whose structure includes four linked carbon rings
  • cholesterol is primary source of steroids in human body
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12
Q

chemical energy: carbohydrates

A
  • monosaccharides (fructose, glucose)
  • disaccharides (sucrose)
  • polysaccharides
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13
Q

alpha glycosidic linkages

A
  • digestable
  • same side
  • ex. glycogen, starch
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14
Q

beta glycosidic linkages

A
  • non digestable
  • alternating -> allows for hydrogen bonds between neighboring chains -> cross bridges
  • ex. chitin, cellulose (1-4 linkage of beta glucose)
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15
Q

sucrose

A
  • fructose + glucose = sucrose
  • alpha glycosidic linkage
  • table sugar
  • digestable
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16
Q

dextrose

A
  • term for glucose
  • in 0 calorie sweeteners
  • its actually 4 calories
  • agonist binds to receptors -> sweet taste response
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17
Q

starch

A
  • alpha 1-4 linkage of alpha glucose -> amylose -> linear chain
  • alpha 1-6 linkages -> branched -> amylopectin
  • polymer
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18
Q

glycogen

A
  • highly branched

- polymer

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19
Q

polymers

A
  • stores glucose (monomers) as polymers
  • if you tried to store monomers it creates too much osmotic pressure created by many individual monomers
  • pack more as polymers
  • glycogen & starch
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20
Q

proteins

A
  • chains of amino acids
  • central carbon
  • amino group
  • hydrogen
  • carboxylic acid group
  • side chain (R)
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21
Q

peptide bonds

A
  • links amino acids

- formed by ribosomes

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22
Q

dehydration synthesis

A
  • produces water
  • links two structures by removing water
  • forms polypeptide
  • directional
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23
Q

primary strucutre

A

-linear sequence of amino acids

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24
Q

secondary structure

A
  • folds in characteristic ways
  • beta pleated sheets- antiparallel or parallel, amine hydrogen and carboxylic oxygen form H bonds
  • alpha helix- carbonyl oxygen interacts with H of amine group (hydrogen bonds) -> 3.6 amino acids per turn
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25
Q

tertiary structure

A
  • interactions between R groups
  • chaperones help fold correctly
  • once they been denaturation does not refold into protein
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26
Q

quaternary structure

A
  • hemoglobin

- more than one polypeptide interaction

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27
Q

denaturation

A
  • hydrochloric acid in stomach denatures proteins for digestion
  • H ions denatures
  • enzymes then have excess to cleave bonds
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28
Q

Essential nutrients

A
  • substances the body is unable to synthesize from organic precursors
  • essential amino acids
  • essential fatty acids
  • vitamins
  • minerals
  • malnutrition- state of insufficiency of an essential nutrient
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29
Q

essential nutrients: amino acids

A
  1. methionine
  2. valine
  3. threonine
  4. phenylalanine
  5. leucine
  6. isoleucine
  7. tryptophan
  8. lysine
    - histidine (required for newborns)
    - 1-6 found in corn and other grains
    - 2-8 found in beans and other legumes
    - meat & fish fulfill these
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30
Q

essential nutrients: fatty acids

A
  1. alpha-linolenic acid
  2. linoleic acid
    - omega 3 fatty acid
    - omega 6 fatty acid
    - require through diet
    - ex. olive oil
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31
Q

essential nutrients: vitamins

A

-organic molecules required in small amounts
Fat soluble (accumulate in body):
-A: visual pigments, gene regulation
-D: allows dietary calcium to be absorbed
-E: antioxidant
-K: blood clotting
Water soluble (easily eliminated in urine):
-B complex: coenzymes -> many, deficiency can cause diseases
-C: antioxidant- connective tissue synthesis -> scurvy

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32
Q

antioxidants

A
  • protect against the oxidative effects of O2

- vitamin E and C

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33
Q

essential nutrients: minerals

A
  • inorganic substance needed in small amounts
  • calcium: 2nd messenger muscle contraction
  • sodium, potassium, chloride
  • iodine: thyroid hormone
  • iron: hemoglobin (O2 transport)
  • Mn, Co, Cu, Ni, Zn, S: enzyme cofactors
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34
Q

digestion occurs in specialized compartments

A
  • intracellular digestion: specialized organelles: vacuoles

- extracellular digestion: gastrovascular cavities, alimentary canals

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35
Q

intracellular digestion

A
  • vacuoles
  • unicellular
  • brings food (bacteria) in through oral groove
  • cytosome- specialized for endocytosis-> consumes food
  • pendocytosis- taking in liquid
  • food vacuole forms and is digested
  • absorbs essentials
  • exocytosis of waste through anal pore
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36
Q

gastrovascular cavities

A
  • single opening to the outside used for both ingestion and elimination
  • ex. hydra, flatworms (planarians)
  • allows animal to consume larger prey than could be ingested and digested intracellularly
  • cellular specialization- cells for secretion of acid, enzyme, and hormones; cells for absorption of nutrients
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37
Q

hydra

A
  • gastrovascular cavities
  • 10mm
  • anchored by basal disc
  • no anus
  • cnidarians
  • tentacles (stingers)- neurotoxins paralyze animal
  • gas exchange occurs in the same cavities
  • nutritive cells
  • flagella creates current
  • gland cells- digestive enzymes
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38
Q

alimentary canals

A
  • two openings to the outside, one for ingestion (mouth) and one for elimination (anus)
  • tube extends between openings
  • food generally moves through the tube in one direction (with some exception- vomit)
  • specialized regions within tube for digestion and absorption in a stepwise fashion
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39
Q

alimentary canal: birds

A
  • lack teeth
  • esophagus leads to crop
  • crop- used for food storage
  • moves to glandular stomach- chemical digestion
  • move to gizzard- muscular organ that mechanically digests
  • food can move backward from gizzard to stomach for more chemical digestion
  • moves to intestine then anus
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40
Q

alimentary canals: humans

A

-esophagus to stomach

-

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41
Q

sphincters

A

-control movement through GI tract
-upper and lower esophageal
-lower sphincter- prevents stomach acid backflow -> defect -> heart burn
-anal sphincter
-pyloric sphincter
Alimentary canal:
-oral cavity (mouth)
-esophagus
-stomach
-small and large intestine
Accessory organs:
-salivary glands
-liver
-gallbladder
-pancreas

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42
Q

layout of alimentary system

A
  • Ingestion/digestion- oral cavity -> pharynx -> esophagus
  • storage/grinding digestion- crop -> stomach -> gizzard
  • digestion/absorption- intestine
  • elimination- anus
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43
Q

oral cavity

A
  • ingestion
  • mechanical digestion
  • teeth, tongue, muscles, jaw
  • carnivores- sharp teeth
  • omnivores- molars
  • food is ground into smaller particles to provide greater surface area for digestive enzymes
  • initial chemical digestion of carbohydrates -> salivary amylase
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44
Q

oral cavity: saliva

A
  • salivary glands- exocrine glands
  • produced by salivary glands:
    1. parotid gland
    2. sublingual gland
    3. submandibular gland
  • hypotonic solution
  • triggered by presence or anticipation of food
  • functions:
  • lubricates mouth and food to facilitate swallowing: mucins (glycoproteins)
  • begins carbohydrate digestion- salivary amylase breaks starches into smaller polysaccharides
  • protects from invading microbes- immunoglobulins, enzymes, resident microbes
  • balance: ion and buffers
  • taste molecules need to be dissolved in saliva in order to taste
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45
Q

parotid gland

A
  • salivary exocrine gland

- rich in enzymes like amylase

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46
Q

sublingual gland

A
  • salivary exocrine gland
  • rich in mucins
  • lubricates food to swallow
  • glycosylated proteins that are viscous
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47
Q

submandibular gland

A
  • salivary exocrine gland

- mixed, with both enzymes and mucins

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48
Q

salivary gland

A
  • Na/K ATPase pump -> creates gradient for sodium reabsorption
    1. Acinar cells secrete extracellular fluid with proteins enzymes -> isotonic to ECF
  • aquaporins are present here and water follows solute into duct
    2. in the duct of the gland NaCl is reabsorbed and HCO3 & K are secreted -> hypoosmotic to blood plasma
  • no aquaporins in duct
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49
Q

oral cavity: tongue

A
  • dissolved molecules enter the taste pore
  • several cells inside the taste pore allow to detect taste
  • must be dissolved in saliva
  • sweet, salt, bitter, sour, umami
  • type 1 support cells- may sense salt
  • receptor cells (type 2)- detect sweet, umami, and bitter
  • presynaptic cell (type 3)- detects sour
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50
Q

umami

A
  • savory
  • meat
  • amino acid glutamate stimulates receptors for detection of umami
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51
Q

bitter

A
  • avoidance mechanism

- toxins are bitter

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52
Q

receptor cells (type 2)

A
  • detect sweet, umami, and bitter
  • g-protein coupled receptor
  • binding -> gustducin -> influx of Ca -> release of ATP through channels -> paracrine signals and binds to primary sensory neuron or neighboring cells -> action potential fire
  • detects glutamate (umami)
  • release ATP when ligand binds to their g-protein couple receptor, acts in paracrine matter
  • ATP works as signal
  • ATP binds to primary sensory neurons -> stimulates nerve
  • ATP can also bind to neighboring cells
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53
Q

presynaptic cell (type 3)

A
  • forms synapse with primary sensory neurons
  • neurotransmitter is serotonin
  • channel that conducts H ions
  • senses H+ ions or decrease in pH -> H+ enters through channel -> H+ closes K channels -> decrease in K -> depolarization -> Ca influx -> serotonin released by exocytosis -> synapse with primary gustatory neurons
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54
Q

deglutition

A
  • swallowing
    1. tongue pushes bolus against soft palate (top) and back of mouth, triggers swallow reflex
  • back of throat (pharynx) has sensory pressure receptors -> sensory afferent neurons send signal to medulla oblongata -> swallow -> move down esophagus -> smooth muscles contract behind bolus -> peristalsis -> moves bolus into stomach
  • saliva keeps pieces of food together
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55
Q

spicy

A
  • binds to pain receptors

- somatosensory pathways

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56
Q

epiglottis

A
  • cartilage
  • as we swallow closes and blocks trachea
  • aspiration- food moves in airway
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57
Q

pharynx/esophasgus

A
  • conducts bolus of food to stomach by creating pressure gradients: bulk flow
  • in humans:
  • striated skeletal muscle at top of esophagus (voluntary)
  • smooth muscle in lower esophagus (involuntary peristalsis)
  • salivary amylase continues to digest starch and glycogen
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58
Q

peristaltic contraction

A
  • contracts behind to bolus
  • smooth muscle- involuntary
  • relaxed in front of bolus so it can be propelled forward
  • seconds after it happens again
  • controlled by enteric nervous system
  • rhythmic contractions
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59
Q

swallowing

A
  • starts out voluntary
  • once it hits the back of the throat (pharynx) there is feedback loop to the medulla
  • efference -> contraction of smooth muscle -> peristalsis in the esophagus (autonomic)
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60
Q

sphincters

A
  • opening from the esophagus -> lower esophageal sphincter

- exit of stomach -> pyloric sphincter

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61
Q

stomach

A
  • parietal cells secret hydrochloric acid -> denatures proteins and breaks apart extracellular matrix that holds tissues together
  • secretes a proenzyme- pepsinogen -> converted to pepsin
  • pepsin- cleaves peptide bonds
  • pH of 1 or 2
  • storage: large distensible organ -> we do not need to eat constantly -> small intestine not overwhelmed with food
  • initial chemical digestion of proteins (some lipids via gastric lipase) takes place
  • mechanical breakdown of food particles
  • absorption of small hydrophobic substance (ethanol) (not main site)
  • endocrine organ -> gastin
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62
Q

anatomy of the stomach

A
  • lower esophageal sphincter
  • fundus
  • body
  • antrum
  • pylorus- connects stomach to duodenum
  • pyloric sphincter
  • rugae- foldings increase the SA
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63
Q

surface of stomach

A
  • epithelium is folding inward in the invaginations -> mucosa
  • mucosa forms gastric glands
  • smooth muscle layer- submucosa
  • three layers of smooth muscle -> myenteric plexus
  • contractions mechanically breakdown food
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64
Q

gastric acid

A

hydrochloric acid

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65
Q

mucous surface cell and mucous neck cells

A
  • secretes alkaline mucous
  • protects stomach from its own acid
  • mucous neck cells are located in the neck of the gastric gland
  • alkaline comes from bicarbonate
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66
Q

parietal cells

A
  • secretes gastric acid (hydrochloric acid)
  • in the gastric gland
  • washed up into the lumen to denature proteins
  • also produces bicarbonate ion (base)
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67
Q

chief cells

A
  • produces pepsinogen (zymogen)- inactive enzyme
  • released into the lumen and onto the surface
  • due to low pH pepsinogen autocatalyzes itself -> forms pepsin (active)
  • pepsin- endopepdidase, cleaves peptide bonds
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68
Q

G cells

A
  • endocrine cells
  • produces gastrin
  • gastrin NOT released into lumen -> released into circulation
  • interstitial -> circulatory
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69
Q

stomach: protein digestion

A
  • acidic environment of stomach (pH 1-2)
  • disrupts extracellular matrix that binds cells together
  • denatures (unfold) proteins
  • creates more surface area on food particles -> more interactions between enzymes and substrates
  • kills some microbes (some protection)
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70
Q

secretion of hydrochloric acid

A
  • secreted by parietal cells
  • H+/K+ ATPase pump in the apical surface (lumen of stomach side)
  • not electrogenic (one for one)
  • carbonic anhydrase combines water, CO2, and carbonic acid -> H+ and bicarbonate (HCO3-) -> H+ moves across apical surface into lumen
  • biocarbonate moves across basolateral membrane (interstitial fluid side) in exchange for Cl -> Cl moves across apical surface into lumen
  • H+ and Cl form hydrochloric acid
  • bicarbonate moves into the capillaries by bulk flow -> gets incorporated into alkaline mucus
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71
Q

stomach acid (HCl)

A
  • secondary and tertiary structures are disrupted by H+ ions
  • H+ ions compete with hydrogen bonds -> denature secondary and tertiary structures
  • unravels
  • after they are denatured now peptide bonds are easier to cleave
  • dont usually refold (bc they need chaperones) but ribonucleases can help renature
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72
Q

pepsin

A
  • pepsinogen- inactive enzyme -> had 44 additional amino acids that maintain zymogen in an inactive form
  • pepsinogen (inactive) -> pepsin (active) after release from chief cells into the lumen of stomach
  • activated only where needed
  • low pH of lumen causes the catalytic conversion
  • HCl causes pepsinogen to unfold and autocatalytically cleave the inhibitory 44 amino acids -> pepsin
  • pepsin cleaves pepsinogen to generate more pepsin
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73
Q

stomach: gastric juice

A
  • aqueous mixture of pepsin and acid in the stomach lumen
  • effective at digesting proteins because:
  • acid denatures the proteins, exposing peptide bonds to pepsin
  • pepsin is one of few enzymes that is most effective at low pH (gastric lipase also functions optimally at low pH)
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74
Q

stomach: protection

A
  • alkaline mucus coats and protects the stomach epithelial cells from pepsin and HCl
  • mucus neck/surface cells -> alkaline mucus
  • bicarbonate (from parietal cells) is incorporated in the mucus
  • mucus- physical barrier
  • bicarbonate- chemical barrier that neutralizes acid -> if pepsin where to get to the bicarbonate layer activity would decrease due to higher pH (7)
  • epithelial cells constantly sloughed- mitosis generates enough new epithalial cells to replace lining about every 3 days -> sloughed off cells are digested with food
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75
Q

GERD

A
  • reflux of gastric juice into the esophagus can cause gastroesophageal reflux
  • common after big meal
  • acid and pepsin in direct contact with esophagus -> burns
  • heart burn
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76
Q

peptic ulcer disease

A
  • gastric juice can cause gastric and duodenal ulcers
  • mucus defenses are compromised (not enough)
  • pepsin and acid come in direct contact with living tissue of stomach
  • digests the stomach itself
  • common in duodenum (70%) because there is less protection there
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77
Q

omeprazol (prilosec)

A
  • drug
  • blocks H+/K+ ATPase proton pump
  • covalently bonds to cystine residues in the pump -> disables
  • parietal cells no longer release acid into the lumen
  • raises pH of stomach
  • provides time for ulcer to heal itself
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78
Q

stomach: mechanical digestion

A
  • contents of stomach are mixed by contractions of smooth muscle in the stomach wall
  • mixture of contents is called acidic chyme
  • contractions slowly push the acid chyme through the pyloric sphincter into the small intestine
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79
Q

small intestine: functions

A
  • major organ of digestion and absorption
  • major site of enzymatic hydrolysis of macromolecules of food
  • major site for absorption of nutrients (mostly monomers) into blood
  • largest part of intestine (6 meters)
  • endocrine organ
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80
Q

small intestine: nutrient absorption

A
  • occur mainly in jejunum (and ileum)
  • 3 levels of organization increase SA (300m^2) and facilitate absorption:
  • plicae- large circular folds
  • villi- finger like projections
  • microvilli- epithelial cells on each villus have microscopic projections
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81
Q

anatomy of small intestine

A
  • smooth muscle
  • contracts in peristaltic motion
  • crypt- glandular evaginations -> exo/endocrine cells
  • circular muscle, longitudinal muscle
  • peyers patch- lymphoid tissue (immune system)
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82
Q

villus

A
  • rich blood supply (many capillary)
  • most food is absorbed here
  • increase SA
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83
Q

lacteals

A
  • part of lymphatic system

- within the villus

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84
Q

goblet cells

A

secrete mucus on villus

-mucus for lubrication rather than protection

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85
Q

crypts

A
  • have exo/endocrine
  • envagination
  • most fluid secretion occur here
  • stem cells in crypts produce new epithelial cells to replace dead or damaged
  • secrete ions and water (exocrine)
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86
Q

enterocyte

A

-transport nutrients and ions

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87
Q

microvilli

A
  • make up brush border

- increase SA

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88
Q

duodenum

A
  • 23 cm long, posterior to pyloric sphincter
  • acid chyme from stomach is mixed with digestive juice from: pancreas, liver/gallbladder, secretory cells in intestine wall
  • chemical digestion
  • bile salt- molecule of cholesterol that is conjugated to an amino acid
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89
Q

jejunum

A
  • largest portion of small intestine
  • 3 meters
  • major site of chemical digestion and absorption
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90
Q

illeum

A
  • more absorption

- whats not absorbed by jejunum is absorbed here

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91
Q

bile

A
  • contains bile salts, bile pigments, and cholesterol
  • -cholesterol (hydrophobic) molecule conjugated into amino acid (hydrophilic) -> ampipathic molecule
  • secreted by liver cell; stored in gallbaldder
  • released into common bile duct -> into duodenum
  • bile salts (cholesterol + amino acid):
  • act as detergents -> coat fat droplets and keep them from clumping together (emulsifiers)
  • facilitate fat hydrolysis by lipases
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92
Q

pancreatic juice

A
  • exocrine pancreas secretes enzymes (zymogens) and bicarbonate
  • released into the lumen of duodenom
  • acinar cells from exocrine pancreas secrete zymogens and bicarbonate into pancreatic duct -> lumen of small intestine
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93
Q

exocrine pancreas

A
  • bicarbonate- neutralizes acidic chyme from stomach into duodenum (raises pH to 7-8)
  • peptidases- continue digestion of protein
  • nucleases- hydrolyze DNA to RNA
  • amylases- continue digestion of carbohydrates
  • lipases- digests fats
  • all are initially released into pancreatic duct, which joins the common bile duct and empties into duodenum
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94
Q

zymogens

A
  • secreted by exocrine pancreas
  • inactive as secreted
  • become activated in the lumen of duodenum
  • enzymes along the brush border called enteropeptidases activate zymogens by activating trypsin by cleaving precursor trypsinogen into trypsin
  • trypsin activates zymogens enzymes -> digests foods
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95
Q

beta cells of the pancreas release insulin into ducts that lead into the circulatory system

A
  • false
  • no ducts in the beta cells
  • exocytosis -> capillaries
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96
Q

bile salts as detergents and emulsify lipids

A
  • lipid are not soluble -> bc bile salts are amphipathic they can emulsify (solubilize) lipids
  • break up lipid droplet into smaller micelles
  • hydrophobic side of the bile salt faces the lipid droplet and the hydrophilic side (amino acid) faces aqueous environment
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97
Q

lipid micelles

A
  • contain triglycerides, phospholipids, monoglycerides, biglycerides
  • lipase and colipase (pancreatic enzymes) breaks down triglycerides into fatty acids and monoglycerides -> these can be absorbed into intestinal cells by diffusion across brush border
  • cholesterol is transported into cells by carrier proteins
  • triglycerides are resynthesized and combine with cholesterol and proteins in intestinal cells to form chylomicrons
  • diffuse by exocytosis on the basolateral surface
  • chylomicrons are removed by lymphatic system (too large for capillaries)
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98
Q

chylomicrons

A
  • allows us to circulate hydrophobic substances in aqueous environment of lymph and circulatory
  • large
  • lipoprotein
  • phospholipid monolayer around the hydrophobic substances -> hydrophilic transport
  • cholesterol + triglycerides + proteins = chylomicrons
  • exocytosis through basolateral surface of small intestine cell -> move into lymphatics -> lymph to vena cava -> right side of the heart
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99
Q

small intestine: absorption of sugars and amino acids

A
  • sugars and amino acids are absorbed through epithelial cells and into the blood stream
  • capillaries in alimentary canal -> hepatic portal vein -> liver (removes any non-nutrient we may have absorbed) -> vena cava -> right atrium
  • often secondary active transport, using gradients of Na established by Na/K ATPase pump
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100
Q

hepatic portal system

A
  • most substances absorbed by the intestine pass through the liver
  • liver serves as a filter that can enzymatically modify and break down many potentially harmful xenobiotic substance before they get into the systemic circulation
  • enzymatic products are eliminated from the body in bile
  • digestive tract arteries -> capillaries of stomach and intestines -> hepatic portal vein -> liver -> hepatic vein -> vena cava -> right atrium
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101
Q

lipids

A
  • bypass the liver
  • bc they are too big to move through capillaries through bulk flow
  • lyphatics -> vena cava -> heart
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102
Q

carbohydrate breakdown

A
  • pancreatic enzymes introduced in the duodenum breakdown polymers
  • amylase
  • polymers-> disaccharides -> monosaccharides
  • monosaccharides are absorbed
  • glucose or galactose enters with Na (Na gradient made on basolateral surface -> secondary transport) with SGLT at apical and leaves through GLUT2 at basolateral
  • fructose enters on GLUT5 at apical and exits at GLUT2 at basolateral
  • glucose is able to diffuse into capillaries by bulk flow -> liver -> vena cava -> heart
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103
Q

endopeptidase

A
  • digests internal peptide bonds in the middle
  • include pepsin in the stomach
  • trypsin and chymotrypsin in small intestine
  • cleaves into smaller peptides -> more free ends
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104
Q

exopeptidase

A
  • digest terminal peptide bonds to release amino acids -> free amino acids
  • free amino acids are what is being absorbed
  • some peptides larger than tripeptides can be absorbed by transcytosis
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105
Q

absorption of amino acids and peptides

A
  • proteins cleaved by endopeptidase and exopeptidase -> free amino acids
  • amino acids cotransport with Na (Na gradient formed on basolateral surface -> secondary transport)
  • move across basolateral surface and enter capillaries by bulk flow
  • di and tripeptides cotransport with H+
  • small peptides are carried intact across the cell by transcytosis
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106
Q

absorption of water and solute

A
  • on basolateral surface there is a Na/K ATPase pump -> establishes gradient
  • Na transport across the apical surface through sodium channels, symporters with Cl, antiporters with H+, antiporters with HCO3-, and symporters with organic solute (glucose, amino acids)
  • water follows solute -> water moves through the paracellular pathway
  • water moves from the lumen of small intestine through the intestinal cell into the ECF
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107
Q

small intestine has a large capacity for absorbing water

A
  • small intestine absorbs a lot of water (7.5L a day)

- drinking too much water can cause increased absorption diluting blood volume -> death

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108
Q

large intestine (colon)

A
  • connected to small intestine at a T shaped junction
  • one arm of the T is a pouch called the cecum
  • functions:
  • reabsorption of water- most water reabsorption occur in small intestine, excess water in colon can lead to diarrhea, insufficient water in colon can lead to constipation
  • microbial digestion and absorption of microbial products
  • elimination
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109
Q

regulation of digestion by hormones

A
  • stomach secretes gastrin, a peptide hormone
  • duodenum secretes two peptide hormones: secretin & cholecystokinin (CCK)
  • released basolaterally into circulation
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110
Q

gastrin

A
  • gastrin is produced by G cells
  • released basolaterally into circulation (hormone from stomach)
  • stimuli:
  • food (proteins in stomach) and vagus nerve activation
  • targets (binds to):
  • chief cells -> pepsinogen -> pepsin
  • parietal cells -> stomach acid (HCl)
  • response:
  • increased protein digestion
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111
Q

secretin

A
  • released basolaterally into circulation (hormone from duodenum)
  • stimuli: low pH in duodenum caused by acidic chyme
  • targets: pancreas -> stimulates the secretion of bicarbonate
  • response: raises pH duodenum for increased digestion and protects the duodenum from acidic chyme
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112
Q

cholecystokinin (CCK)

A
  • released basolaterally into circulation (hormone from duodenum)
  • stimuli:
  • amino acids and fatty acids in duodenum
  • targets:
  • pancreas -> stimulates release of digestive enzymes (proteases, lipases, amylase)
  • gallbladder -> bile is released into duodenum when gallbladder contracts
  • response:
  • increased digestion of fats and proteins
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113
Q

evolutionary adaptations

A
  • appendix- has lymphoid tissue, houses bacteria that could potentially repopulate our system
  • cecum- houses bacteria
  • herbivores/omnivores have longer alimentary canals than carnivores, relatively
  • long cecum is one ex. (in other animals cecum breaks down cellulose)
  • plant materials more difficult to digest than animal cells
  • longer tract provides: more time for digestion and more SA for digestion
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114
Q

ruminants

A
  • cow
  • eats plant -> rumen -> reticulum (backward flow) -> large material goes to oral cavity to be rechewed
  • smaller material is passed to the omasum -> abomasum -> intestine
  • rumen- large fermentation chamber -> anaerobic breakdown of carbohydrates (cellulose)
  • abomasum- digestion
  • omasum- absorption
  • bacteria is digesting cellulose
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115
Q

symbiotic organisms

A
  • microorganisms thrive in fermentation chamber in herbivores
  • mircoorganisms provide nutrients
  • digest cellulose into monosaccharides
  • secrete fatty acid
  • provide essential nutrients (vitamins)
  • are digested by hosts to provide a direct nutrient source
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116
Q

most chemical digestion of carbohydrates occurs in the stomach

A
  • false
  • stomach is mostly for proteins
  • further digestion of carbohydrates is in the small intestine (duodenum) by amylases
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117
Q

chief cells secrete pepsin

A
  • false
  • it secretes pepsinogen
  • zymogen
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118
Q

pepsinogen enzymatically cleaves peptide bonds in ingested (dietary) proteins

A
  • false

- zymogen -> inactive

119
Q

in response to reduction in pH (caused by acidic chyme), secretin is released into the lumen of the duodenum

A
  • false

- secretin is a hormone

120
Q

structure of a long bone (femur or humerus)

A
  • bone is living tissue (connective tissue) -> organ
  • trabecular bone and compact bone consist of living cells (osteocytes, osteoblasts, and osteoclasts) embedded in a mineralized Ca organic matrix (collagen and hydroxyapatite)
  • bone is an organ composed on multiple tissues:
  • bone and cartilage tissue
  • red marrow and blood (connective tissue)
  • blood vessels (endothelial tissue)
  • yellow marrow (adipose tissue, a type of connective tissue)
121
Q

osteoblasts

A
  • secrete proteins (collagen and proteoglycan)
  • create the matrix of bone
  • cells that take calcium from plasma and use it to build bone
  • growth and remodeling
122
Q

diaphysis

A

shaft

123
Q

epiphysis

A

-ends of the bone

124
Q

metaphysis

A

-includes the epiphyseal plate and scar

125
Q

epiphyseal plate

A
  • site of bone growth after birth
  • growth plate
  • made of cartilage from chondrocytes
  • linear growth
  • after puberty (no more growth hormone) osteoblasts create calcium phosphate crystals (hydroxyapatite) to replace cartilage)
126
Q

trabecular bone

A
  • aka spongy bone
  • aka cancellous bone
  • where red bone marrow is
  • found in epiphyses
  • trabeculae- distribute the force placed on the bone -> can remodel
  • present prior to puberty and after
127
Q

articulate surface

A

-forms joint with other bone

128
Q

chondrocytes

A
  • cartilage cells that secrete extracellular matrix scaffold for bone to grow on
  • associated with the ends of the bones that form joints (articular surface)
129
Q

osteoclasts

A
  • cells that resorb bone
  • these cells remove calcium from bone and deposit it in plasma
  • secrete enzymes and acids that deplete the cell matrix
  • multinucelated -> result from diffusion of macrophage stem cells
130
Q

osteocytes

A
  • mature, inactive osteoblasts found in bones that have stopped lengthening
  • still alive
131
Q

cartilage

A
  • cartilage is a type of connective tissue
  • composed of chondrocytes that secrete a large amount of collagen and heavily glycosylated proteins -> proteoglycans
  • collagen and proteoglycans makeup extracellular matrix and semi-rigid structural properties characteristic of cartilage
  • semi-rigid -> ear
132
Q

bone tissue

A
  • type of connective tissue
  • composed of osteoblasts, osteocytes, and osteoclasts
  • cells are embedded in extracellular matrix composed mostly of collagen and proteoglycans
  • extracellular matrix of bone is rigid due to mineralization with hydroxyapatite (calcium based mineral) -> key difference between cartilage and bone
133
Q

lacunae

A

-osteoblasts get trapped in here and become osteocytes

134
Q

bone growth

A
  • bones start out as cartilage in fetus
  • cartilage replaced by bone
  • growth continues at the ends of long bones in epiphyseal plates until end of puberty
  • epiphyseal closure occurs when bones stop growing
  • bone growth may be restarted after injury
135
Q

development of embryonic cartilage and bone

A
  • step 1- mesenchymal cells differentiate into chondrocytes -> chondrocytes at the center of the growing cartilage model secrete extracellular matrix (proteoglycan and collagen) -> forms a semi-rigid structure -> chondrocytes enlarge and begin to secrete phosphate salts and calcium -> cartilage begins to calcify -> chondrocytes die as the matrix calcifies
  • step 2- mesenchymal cells differentiate into osteoblasts -> osteoblasts cover the shaft of the cartilage in a thin layer of bone -> cells in the middle start to undergo apoptosis -> cavity forms
  • step 3- blood vessels penetrate the cartilage -> vascularization -> new osteoblasts form a primary ossification center -> mesenchymal cells differentiate into osteoclasts -> breaks down matrix -> forms a marrow cavity new osteoblasts form a primary ossification center
  • step 4- bone of the shaft thickens and cavity enlarges -> cartilage near each epiphysis is replaced by shafts of bone
  • step 5- blood vessels invade the epiphyses and osteoblasts form secondary centers of ossification at the ends of the bones
136
Q

mesenchymal cells

A
  • immature stem cells
  • differentiate into chondrocytes and osteoblasts depending on stage of bone development
  • osteoclasts are not formed by mesenchymal cells -> they are derived from macrophage stem cells!
137
Q

growth of epiphyseal plate

A
  • chondrocytes are rapidly proliferating and laying down extracellular matrix at the top of the plate
  • extending the bone upwards bc more cells are being added
  • osteoblasts are laying down new bone at the other end (trailing end) -> ossified
  • this process is driven by growth hormone
138
Q

why doesnt growth just happen at the ends of bones

A
  • bc joints need to be able to fit together

- this would affect bone/joint function

139
Q

bone remodeling

A
  • for life
  • osteoblasts secrete collagen and proteoglycans and calcium and phosphate minerals (hydroxyapatite)
  • hydroxyapatite binds to collagen and proteoglycans and form calcified bone matrix (rigid bone)
  • osteoclasts secrete acids (hydrochloric) and enzymes -> dissolves, breaks down and solubilizes bone matrix
140
Q

exercise

A
  • affects the balance of osteoblast to osteoclast
  • more exercise -> more osteoblast function -> denser bones
  • less exercise -> more osteoclast function -> less dense bones
141
Q

calcium balance in body

A
  • input from: diet
  • output to: urine (major) or feces (minor)
  • regulation by: parathyroid hormone (PTH), calcitriol (vitamin D3), and calcitonin (minor role)
  • calcium is absorbed in small intestine
  • 99% of Ca in bone
  • .9% in cells
  • .1% in ECF
  • calcium it taken from bones (resivior) and given to cells and ECF -> osteoporosis
  • PTH recovers Ca from kidney so its not excreted as urine
142
Q

blood

A
  • connective tissue
  • composed of cells, platelets, and fluid extracellular matrix (plasma)
  • extracellular matrix is fluid in blood (rigid in bone)
  • similar to interstitial fluid except plasma contains many proteins like albumins
  • plasma is 92% water weight
143
Q

components of blood

A
  • 42% RBC
  • <1% WBC
  • 58% plasma
  • PLASMA:
  • water, proteins, other molecules
  • composition varies (ex. hormone levels fluctuate)
  • CELLS:
  • erythrocytes
  • leukocytes
  • PLATELETS:
  • fragments of megakaryocytes (large cells)
  • no nucleus
  • have mitochondria, smooth endoplasmic reticulum, and vesicles (granules) filled with cytokines and other signaling molecules
144
Q

white blood cells

A
  • immune function
  • 4-11 x 10^3 cells per microliter
  • lymphocytes
  • monocytes- phagocytes, develop into macrophages and dendritic cells
  • neutrophils
  • eusinophils
  • basophils
  • mast cells
  • macrophages, dendritic cells, and neutrophils are key cells that can do phagocytosis
145
Q

platelets

A
  • secrete factors
  • fragments of megakaryocytes (large cells) -> platelets are not cells they are fragments of cells
  • no nucleus
  • carry out basic cellular function
  • composition varies -> not constant
  • composed of water, ions, organic molecules, trace elements, vitamins, gases
  • albumins- protein that contributes to plasma colloid osmotic pressure: carriers for various substances
  • have mitochondria, smooth endoplasmic reticulum, and vesicles (granules) filled with cytokines and other signaling molecules
146
Q

hematopoiesis

A
  • red blood cell formation
  • occur in red bone marrow
  • red bone marrow is in the epiphyses
  • in children its everywhere
  • in adults is mostly just ends of long bones, pelvic gurdle, spinal column, ribs, clavicle, scapula and skull bones
147
Q

yellow bone marrow

A
  • found in diaphysis

- mostly adipose tissue

148
Q

red bone marrow

A
  • forms in the spaces between the mineralized bone
  • contains pluripotent stem cells -> can develop into many but not all cell types
  • blood cells develop in red bone marrow in a process called hematopoiesis- the cells then move into circulation
  • differentiation- the process of activating a select set of genes to produce gene products found in only a specific cell type
  • found everywhere in children
  • found in ends of long bones, pelvic gurdle, spinal column, ribs, clavicle, scapula and skull bones for adults
149
Q

pluripotent hematopoietic stem cell

A
  • can become lymphocyte stem cell -> lymphocyte
  • can become uncommitted stem cell -> committed progenitor cells -> can become either eosinophil, basophil, monocyte, neutrophil, megakaryocyte (into platelet), or erythrocyte
  • refer to diagram in notes
150
Q

red bone marrow continues

A
  • highly vascularized
  • consists of blood cells in different stages of development and support tissue (stroma)
  • cells move in between endothelial cells into circulation
151
Q

lymphocytes

A
  • involved in specific immune responses
  • T cells
  • B cells
  • natural killer cells
152
Q

monocytes

A
  • large phagocytic cells

- can differentiate into macrophages (phagocytic) and dendritic cells (phagocytic)

153
Q

neutrophils

A

-neutral dye, granules, phagocytic

154
Q

eosinophils

A

-acidic dye, granules phagocyte

155
Q

basophils

A

basic dye, granules

156
Q

red blood cells

A
  • function- gas transport
  • appearance- round, red, biconcave, no nucleus
  • count- 4-6 x 10^6 cells per micoliter
157
Q

platelets

A
  • function- blood clotting
  • appearance- small fragments of cells
  • no nucleus
  • have granules
  • mitochondria
  • smooth endoplasmic reticulum
  • count- 1.5-4.5 x 10^5 cells per microliter
  • initially they are smooth -> when they are activated they become rough and stick
  • become activated when they are needed to clot
158
Q

blood clot (thrombus)

A
  1. vessel constriction- blood loss -> constriction
  2. platelets arrive -> platelet adhesion -> platelet activation -> platelet aggregation
  3. formation of cross linked fibrin -> stabilizes the clot/platelet plug
  4. restriction of the clot forming process to the area of vessel damage -> spreading of clots is lethal!
    - note: no physiological mechanism to stop bleeding large arteries -> surgery
159
Q

platelet adhesion, activation, and aggregation

A
  • vessel wall is intact -> no collagen is exposed
  • collagen wall of blood vessel is exposed to platelets at site of vessel damage
  • platelet receptors in membranes bind to collagen -> activates -> platelets become rough -> platelets release several signaling molecules/factors that activate other platelets -> adhere to each other and the wall of the vessel -> loose platelet plug forms
  • collagen acts as ligand
160
Q

coagulation cascade

A
  • overlaps platelets activation
  • tissue factor exposed triggers coagulation cascade
  • cross linked fibrin -> reinforces platelet plug
  • stabilizes platelet plug
  • each step is amplification -> fast
  • Ca cofactor
161
Q

tissue factor

A
  • exposed tissue factor triggers coagulation cascade
  • transmembrane protein (not an enzyme) found in smooth muscle membrane
  • normally smooth muscle membrane is protected by endothelial cells
  • intact endothelium in tissue factors releases factors that inhibit platelet formation
  • during injury factor 7 (zymogen- inactive) comes in contact with tissue factor it activates -> conformation change -> factor 7 becomes enzyme
  • factor 7 converts many factor 10’s into active factor 10’s
  • active factor 10 cleaves prothrombin into thrombin
  • thrombin cleaves fibrinogen into fibrin monomers
  • active factor 13 cross links fibrin with Ca -> cross linked fibrin polymer
162
Q

positive feedback

A
  • active 10 will generate more active 7 -> active 10 is able to generate more active 7
  • thrombin will generate more active 9 which converts inactive 10 to active 10
  • positive feedbacks forms bursts of active 10
163
Q

conversion of fibrinogen into fibrin, subsequent fibrinolysis

A
  • tissue plasminogen activator (tPA) converts plasminogen (precursor to zymogen) into plasmin
  • plasmin- enzyme that breaks down fibrin fragments -> dissolved blood clot
164
Q

tissue plasminogen activator (tPA)

A
  • important drug
  • dissolved clot to prevent brain damage
  • stroke
165
Q

immunuology

A

-the study of the physiological defenses by which the body (the host) recognizes “self” from “non-self” (foreign matter)

166
Q

pathogens

A

microbes that could potentially cause disease

-some microbe are good

167
Q

abnormal self cells

A
  • cancerous cells-acquired mutations that allow to invade immune system
  • virally-infected cells- recognize host cells
  • old or dead cells- eliminate dead cells
168
Q

transplanted tissues or organs

A

-drugs suppress the immune system during transplant

169
Q

first layer of immune defense

A
  • barriers
  • physical- skin, mucosae, mucus, and other secretions
  • mechanical- flushing mechanisms such as cilia
  • chemical- enzymes and antibodies, pH
170
Q

second layer of immune defense

A
  • innate immune response: rapid, nonspecific, no memory, already present
  • cells:
  • macrophages
  • neutrophils
  • natural killer (NK) cells
  • dendritic cells
  • eosinophils
171
Q

second layer of immune defense

A
  • innate immune response: rapid, nonspecific, no memory
  • cells:
  • macrophages
  • neutrophils
  • natural killer (NK) cells
  • dendritic cells
  • eosinophils
  • Chemicals:
  • complement- system of peptides -> cascade
  • interferons- peptides that are released from host cells that have become infected
172
Q

third layer

A
  • adaptive immune response: slow, specific, has memory
  • cell mediated responses:
  • B lymphocytes
  • plasma cells
  • T lymphocytes
  • cytotoxic T cells
  • helper T cells

-antibody -mediated responses

173
Q

pathogens: viruses

A
  • viruses are not cellular life forms
  • viruses replicate inside host cells (ribosomes)
  • an infected host cell can release 1000s of viral particles
  • immune system must recognize and kill infected host cells
  • cytotoxic T lymphocytes are the main defense against viruses that have infected host cells
  • viral antigens are displayed via MHC 1 on infected cells
  • virus infected host cells release interferons (a peptide)
174
Q

influenza virus

A

-envelop surrounds nucelic acid

175
Q

antigens

A
  • small peptides

- displayed on surface of cells

176
Q

interferons

A
  • peptide signaling molecules
  • cytokines
  • released by virus infected host cells
  • signal to neighboring host cells to prevent them from also becoming a virus factory
177
Q

pathogens: bacteria

A
  • are cellular life forms
  • replicate rapidly on their own (need nutrients)
  • upon infection, replicate outside of host cells, in the hosts tissues
  • high mutation rate
  • release variety of toxins that kill host cells
  • release enzymes that break down host macromolecules -> cells disintegrate
  • release peptides that form pore in our cells -> rapid diffusion -> bacteria uses that cells nutrients
  • immune system must recognize and eliminate bacterial cells
178
Q

epithelium

A
  • protective barrier of skin and mucous membranes is the bodys first line of defense
  • GI tract
  • prevents microbes from getting into tissues
179
Q

gladnular secretions

A
  • trap and disable pathogens
  • secretions include:
  • mucus- catches microbes so it can be spit out or swallowed -> stomach kills microbes with pH
  • antibodies
  • enzymes
180
Q

stomach acidity

A

-the low pH of the stomach helps destroy swallows pathogens

181
Q

mechanical removal

A
  • pathogens can be physically removed
  • mucociliary escalator- cells that line our airways secrete mucus
  • tears- lysozymes in tears
  • coughing, sneezing
  • GI motility
182
Q

phagocytic cells

A
  • dendritic cells
  • neutrophils
  • macrophages
183
Q

antigen-presenting cells (APCs)

A
  • dendritic cells
  • macrophages
  • present antigens on surface by way of MAC 2 molecules
184
Q

primary lymphoid tissue

A
  • immune cells develop and mature into primary lymphoid tissue
  • where cells are born
  • *red bone marrow
  • *thymus- where T cells mature
185
Q

lymphatic pathway: pluripotent hematopioetic stem cell

A
  • becomes lymphocyte stem cells
  • cells are born in red bone marrow
  • in the thymus T lymphocytes mature (T cells)
  • B lymphocytes and NK cells develop
186
Q

adaptive immune response

A
  • T cells

- B cells

187
Q

B lymphocytes

A
  • develop into plasma cells

- plasma cells produce antibodies

188
Q

monocytes

A
  • develop into macrophage

- dendritic cells

189
Q

mast cells

A
  • packed with granules that contain histamine

- histamine causes inflammation

190
Q

thymus gland

A
  • in thoracic cavity beneath the sternum and above heart
  • important for development of T cells
  • eliminates T cells that recognize “self” as foreign
  • when it fails to eliminate T cells that recognize “self” as foreign -> autoimmune disease (B cells persist -> type 1 diabetes)
  • produces peptides: thymosin, thymopoietin, thymulin
191
Q

secondary lymphoid tissue

A
  • immune cells interact and response to pathogens in secondary lymphoid tissue
  • located in places where they can intercept pathogens to keep them from entering general circulation
  • encapsulated lymphoid tissue:
  • spleen
  • lymph nodes
  • diffuse lymphoid tissues:
  • GALT (gut-associated lymphoid tissue)
  • tonsils
192
Q

spleen

A
  • has macrophages that engulf foreign particles within circulation
  • removes old or dead RBC
  • secondary lymphoid tissue
193
Q

lymph nodes

A
  • throughout body
  • during injury bacteria enters interstitial fluid -> swept into vesicles
  • lymph nodes intercept these pathogens with macrophages
  • secondary lymphoid tissue
194
Q

GALT (gut-associated lymphoid tissue) and tonsils

A

-diffuse lymphoid tissue (secondary) -> adaptive immune system
-not encapsulated
-B cells and plasma cells (producing anitbodies) -> recognize foreign invaders
GALT:
-largest immune organ
-intestine
-bc intestine has thin surface for absorption it also allows for bacteria to diffuse in

195
Q

innate immune defenses

A
  • several strategies used to eliminate microbes or prevent them from reproducing or spreading within body
    1. phagocytes
    2. natural killer (NK) cells
    3. antimicrobial proteins- complement & interferons
    4. inflammation
    5. fever
196
Q

natural killer cells

A
  • release molecules that will kill an infected host cells
  • NK cells get very close to infected host cell and release chemicals to kill
  • induces programmed cell death
  • tumor cells
  • virus infected cells
197
Q

how do phagocytic cells know which cells are foreign?

A
  • they express pattern recognition receptors (PRRs) on their cell membranes
  • PRRs specifically bind to pathogen-associated molecular patterns (PAMPs) -> classes of molecules that are the surface of the bacteria (ligand)
  • binding leads to phagocytosis and destruction of the microbe
198
Q

PAMPs and PRRs

A
  • PAMPs (pathogen-associated molecular patterns) are conserved molecular structures (molecular motifs) produced by microorganisms, but not by host cells
  • PAMPs can be though of as a molecular signature pattern for pathogens
  • ex. of PAMP is lipopolysaccharide (LPS)- component of cell walls of many bacteria
  • represent potential targets for the immune systems of host animals
  • recognized by PRRs (pattern recognition receptors on host cells (phagocytes)
  • PRRs evolved as a mechanisms to rapidly detect foreign invaders based on the presence of conserved molecular motifs
199
Q

mechanism for recognition for NK cells

A
  • normal host cells (with a nucleus) have major histocompatibility complex 1 (MHC 1) molecules on their surface; NKCs are blocked from attacking these cells -> dominant inhibition on
  • some viruses and tumors cause MHC 1 proteins to be down regulated -> infected host cells and tumor cells lack MHC 1 molecules and become targets for NK cells
  • perforin forms a channel in the target cell membrane -> granzyme initiate apoptosis (programmed cell death)
  • respond within first hour of an infection
  • release cytokines that activate other parts of immune system
200
Q

MHC 1

A

-major histocompatibility class 1
-all cells that have a nucleus express MHC 1
-

201
Q

cytokine

A
  • a family of peptide messengers released by one cell that affect the growth and activity of another cell
  • cytokines are made on demand, unlike peptide hormones, which are made in advance and stored in vesicles (insulin)
  • act locally
  • peptide signaling molecule
202
Q

antimicrobial proteins

A
  • complement proteins
  • interferons
  • control infection by:
  • directly killing microbial cells
  • inducing apoptosis in infected cells
  • aiding the adaptive immune system
203
Q

antimicrobial proteins: complement

A
  • a family of about 30 proteins that are activated in a cascade
  • made in advance
  • initially secreted in inactive forms
  • initiation of the activation cascade can occur by several mechanisms -> classical pathway
  • classical pathway is initiated when complement protein C1 bind to an antibody-antigen complex (an antibody bound to surface of a bacterium)
  • central complement protein is called C3
  • function of complement proteins:
  • acts as Opsonins
  • assemble into membrane attack complexes (MACs) -> pores
  • act as chemotaxins (attract other immune cells)
  • activate mast cells
204
Q

complement cascade- classical pathway

A
  • bacterium invades tissues -> into circulatory system
  • bacterium is coated in antibody
  • C1 binds to the antibodies -> activates C1
  • activation of hydrolase (an enzyme) that cleaves C3 protein into C3a and C3b
  • C3a- binds to mast cells which releases histamine -> causes inflammation
  • C3b- function as Opsonin
205
Q

C3a

A
  • binds to mast cells to release histamine
  • histamine causes inflammation
  • local capillaries dilate and become more permeable to cells and fluid -> leakage and fluid and cells into interstitial fluid
206
Q

Opsonin

A
  • chemicals (usually proteins) that bind to a microbe and promote phagocytosis
  • bacteria coated with antibodies -> antibody is acting as opsonin
  • tags bacteria
  • ex. C3b
  • C3b is not an antibody itself
207
Q

bacterial hiding antibodies

A
  • bacteria will hide antibodies behind a carbohydrate coat
  • this is where C3b comes into play
  • C3b is still able to be recognized by phagocytic cells
208
Q

C3b

A
  • functions as an opsonin
  • activates other complement proteins -> C9
  • C9- forms an aqueous pore in cell membrane
209
Q

complement cascade: Membrane attack complex (MAC)

A
  • a group of complement proteins (C9 and others) insert into the bacterial cell wall and form pores that cause cell lysis
  • C9 and other complement proteins insert themselves into membranes of pathogen -> create pores
  • water and ions enter the pathogen though pores -> pathogen swells and lyses
  • macrophages clean the debris
210
Q

antimicrobial proteins: interferons

A
  • proteins released by one virally infected host cell that prevent viral replication in neighboring host cells (interferons interfere with viral replication)
  • virus enters host cell -> synthesis of viral nucleic acid & proteins -> assembly of new viral particles -> release of viral particles -> viral invasion of another host cell -> repeat
  • group of about 20 cytokines that are produced by host cells
  • primarily used against virus but also against other pathogens and host cells that are tumorigenic
  • can also activate NKCs and macrophages
  • used for drug therapy
211
Q

interferon mechanism

A
  • interferons are produced by host cells
  • triggered by viral DNA
  • turn on host genes that express interferons in response to viral DNA
  • interferons are released by exocytosis
  • bind to cell surface receptor -> signaling cascade -> influences gene expression
  • proteins that are expressed interfere with viral replication by shutting down translation
  • prevents neighboring cells from doing viral replication
212
Q

interferon drug therapy

A
  • interferons beta-1a and beta-1b are used in a management of multiple sclerosis -> autoimmune disorder characterized by loss of myelin in neurons of brain and spinal cord
  • interferon therapy is also used along with other drugs as treatment for certain cancers
213
Q

inflammation

A
  • local redness, heat, swelling, and pain
  • chemical signals cause capillaries to become more permeable to:
  • plasma proteins -> causes water to move into tissues down osmotic gradient (swelling)
  • phagocytic cells-> neutrophils and monocytes leave the capillaries and enter the tissue in a process called extravasation (aka diapedesis)
  • major signal is histamine released from mast cells
214
Q

inflammation ex

A
  • splinter -> brings in bacteria
  • resident cells (cells already present in the tissue) like macrophages and mast cells work
  • mast cell release histamine which binds to receptors on endothelial cells of capillaries -> increase permeability
  • allows other immune cells to diffuse through and join the fight -> extravasation
  • mast cells also secrete chemotaxins which also attracts cells to join the fight
215
Q

overall reaction

A
  • bacteria enters ECF (interstitial fluid)
  • complement proteins become activated as bacteria is coated -> complement cascade
  • C3a activates mast cells which secrete histamine which increases inflammation -> additional cells help fight (extravasation)
  • phagocytes eat up debris
216
Q

inflammation: mast cells and histamine

A
  • inflammation is a component of normal immune response to invading pathogens
  • allergy is an inappropriate inflammatory response to nonpathogenic antigen such as pollen
  • initial immune steps that occur during the first exposure to an allergen are equivalent to the normal primary immune response to an antigen
  • after initial exposure, antibodies are generated against the allergen and bind to surface of mast cells
  • exposure after this results in an exaggerated inflammatory response characterized by the excessive release of histamine
  • drugs known as antihistamines block g protein receptors for histamine and help relieve some symptoms of allergic attack (histamine H1 receptor blockers)
  • normal immune pathway put into hyperdrive
217
Q

overall review

A
  • breach in the barrier -> bacteria enters ECF
  • replication of bacteria
  • compliment proteins are activated as bacteria is coated with antibodies (first line of defense) -> compliment C1 binds -> active C3a -> mast cells secrete chemotaxins and histamine -> increases permeability and attracts additional cells to be recruited at the site (extravasation)
  • macrophages engulf bacteria directly
  • opsonins (C3B protein) are created and coat the bacteria -> phagocytic cells recognize -> engulf
218
Q

fever: pyrogens

A
  • exogenous and endogenous
  • endogenous ex.- interleukin IL-1 (IL-1), *IL-6, and tumor necrosis factor (TNF)
  • exogenous ex.- components of the cell walls of bacteria (*lipopolysaccharide)
  • exogenous pyrogens can stimulate endogenous pyrogen production, or may act directly on the hypothalamus
  • initially act on a specific region of the anterior hypothalamus that lacks a blood brain barrier -> leads to synthesis of prostaglandin E2
  • pathogens replicate optimally at temperatures below 37C -> this is why fever inhibits reproduction (some immune cells work better at higher temp too)
  • fever can be associated with an increase in innate immune activity (phagocytosis) and increased microbial destruction/elimination
  • drugs such as aspirin reduce fever by blocking the production of prostaglandins
219
Q

prostaglandin E2

A
  • lipid signaling molecule which acts in the pre-optic nucleus of the hypothalamus to increase the temperature set point
  • synthesized after pyrogens act on specific region of anterior hypothalamus
220
Q

both macrophages and neutrophils are components of the innate immune response to a pathogen

A

true

221
Q

summary: host response to pathogen

A
  • lesion -> bacteria enters -> replicates
  • resident cells (macrophages & mast cells) release pro-inflammatory chemical signals (histamine)
  • histamine binds to receptors on endothelial cells -> capillary wall becomes more permeable -> more resident cells are recruited -> swelling -> increases blood flow to the site (red color) -> mast cells release more histamine
  • monocytes/neutrophils are joining the fight by engulfing
  • scar tissue and barriers are forming to prevent further bacteria
  • ALL bacteria must be engulfed
222
Q

inflammation

A

local redness, swelling, heat, pain due to increased capillary permeability to plasma proteins and movement of water from plasma to the interstitial compartment

223
Q

pus

A
  • yellowish
  • viscous fluid
  • forms as cells in the area (neutrophils) begin to die
  • plasma membrane of neutrophils breaks down and forms pus
224
Q

necrotizing fasciitis

A
  • flesh eating bacteria
  • antibiotics dont work
  • failure of innate immune system
  • vibrio vulnificus
  • bacteria is releasing enzymes and peptides that form pores in the cells of his skin/tissues
  • breaks down collagen and proteoglycan that forms the extracellular matrix
  • cells lyse and burst
  • IV drugs dont work bc the bacteria is breaking down the RBCs (drugs cant work bc they arent properly circulating in the blood)
  • rapid
  • not enough immune cells were recruited to the site to combat the bacteria
225
Q

antibacterial drugs

A
  • in the past bacterial infections were way more deadly
  • now that we have medication death rates have dropped
  • alexander fleming introduced these drugs in 1928
  • derived through microbes
  • bacteria can adapt to these drugs
226
Q

antigen presenting cells (APCs)

A
  • dendritic cells
  • macrophages
  • present foreign antigens to the adaptive immune system
227
Q

antibody mediated response

A

humoral response

  • refers to soluble factors (antibodies) that are present in blood plasma
  • specific recognition
228
Q

2 divisions of the adaptive immune system

A
  • cell mediated immunity: immune cells use contact with pathogens/abnormal cells and subsequent contact-dependent signaling processes to neutralize them (t and b cells)
  • humoral immunity: antibody mediated responses
229
Q

Step 1. encounter and recognize: adaptive immune

A
  • B cells
  • Helper T (TH) cells
  • cytotoxic T (TC) cells
  • encounter and recognize antigens (foreign molecule)
  • antigens are acting as ligands
  • bind with specific receptor proteins
230
Q

antigen

A
  • small foreign fragment of a protein, lipid or carbohydrate that triggers an immune response (usually protein bc of diversity)
  • only a small sequence needs to recognized
  • each adaptive immune cells can only recognize ONE potential antigen
  • healthy animals do not gave adaptive immune cells specific to self antigens (leads to autoimmune diseases)
  • many adaptive immune cells will never encounter an antigen they recognize (most arnt used)
  • have specific receptors that recognize foreign molecules
  • specific!
  • ex. 8-16 amino acids in a folded protein, thousands of potential antigens in a given protein, millions in a microbial cell
231
Q

PRR vs antigens

A
  • PRR recognize broad molecular patterns/motifs

- antigens recognize specific foreign molecules

232
Q

Step 2. activate: adaptive immune

A
  • T and B cells (lymphocytes) become activated after interacting with an antigen
  • lymphocytes respond to contact-dependent signaling by proliferating and changing patterns of gene expression
  • activated B cells proliferate -> become specialized to secrete antibodies
  • activated helper T cells release cytokines in order to help the overall response
233
Q

antibodies

A
  • soluble form of B cell receptors
  • specific to antigen
  • act as opsonins
  • trigger mast cell degranulation
  • activate complement
  • activate B cells
  • stable and can circulate for very long in the plasma
  • do not have enzymatic activity
  • neutralize toxins
234
Q

Step 3. Attack: adaptive immune

A
  • lymphocytes kill microbes or abnormal cells
  • cytotoxic T cells directly attack cells with exposed foreign antigens on their surface (virus and cancer cells)
  • antibodies that are produced by B cells are attacking by clumping antigens, inactivating bacterial toxins, acting as opsonins, triggering mast cell degranulation, activating compliment cascades, activating B cells
235
Q

lymphocytes

A

-B and T cells

236
Q

Step 4. Remember: adaptive immune

A
  • second response to a particular antigen is faster and more robust than the first response
  • memory
  • long term memory cells
  • 1st expose may take up to a week
  • 2nd exposure is rapid
237
Q

B cell receptors (BCRs)

A
  • expressed on surface of B cells
  • encoded by two genes that undergo rearrangement during development
  • huge amount of BCRs (10 billion)
  • secreted B cell receptors are antibodies
  • can bind soluble proteins directly (toxins)
  • consists of two identical heavy chains and two identical light chains linked by several disulfide bridges (stable)
  • not an antibody bc it has a transmembrane domain (membrane anchored antibody)
  • transmembrane and cytosolic domains initiate signaling cascade in response to antigen binding
  • alternative splicing of the initial RNA molecule splices out the transmembrane domain -> creates an antibody
  • bivalent- two antigen binding sites per antibody
  • *specificity stems from gene rearrangment in the variable region
  • constant regions are constant within a class
238
Q

T cell receptors (TCRs)

A
  • expressed on surface of T cells
  • encoded by two genes that undergo rearrangement during development
  • huge amount of BCRs (10 billion)
239
Q

B cell activation

A
  • antigen binds to B cell receptor
  • high specificity and high affinity interaction
  • 2nd messenger signaling pathways lead to changes in gene expression and other cellular processes
  • clonal expansion occurs- B cell divides to produce multiple identical cells with the same BCR (proliferation (OD MITOSIS))
  • some B cells become memory cells while others become plasma cells
240
Q

memory cells

A
  • long lived

- respond rapidly to nexr exposure to the same antigen

241
Q

plasma cells

A
  • short lived
  • each plasma cell secretes antibodies that recognize a specific antigen
  • differentiated B cells that secrete antibodies
  • antibodies are just soluble forms of the B cell receptor
  • a lot of endoplasmic reticulum present on these cells to ramp up production of antibodies (proteins)
242
Q

clonal expansion

A

B cell divides to produce multiple identical cells with the same BCR

  • proliferation
  • mitosis rapid
  • amplification
243
Q

B cells attack with antibodies

A

Antibody functions:

  1. antigen clumping- two bacteria become linked together making it easier to engulfed by a macrophage
  2. inactivation of bacterial toxins- simple binding to toxins can disable/neutralize them
  3. act as opsonins to tag antigens for phagocytosis- encapsulated bacteria is coated with antibodies which bind to phagocyte receptors (recognition) triggering phagocytosis
  4. trigger degranulation of mast cells- binding of pathogens releases granules which are packed with histamine -> kills pathogen by lysing
  5. activates compliment cascades- signals mast cells to degranulate
  6. activate B lymphocytes- proliferation of plasma and memory cells -> secretion of antibody
244
Q

T cell receptors TCRs

A
  • consists of one alpha chain and one beta chain linked by a disulfide bridge
  • monovalent! -> one antigen binding cells
  • two chains
  • variable region for gene rearangement
  • cannot bind soluble molecules directly (needs help) -> coreceptors
245
Q

T cell-antigen interactions

A
  • T cell interactions require:
  • antigen specific for a T cells TCR
  • correct MHC (Class 1 or 2)
  • other membrane proteins (CD8 or CD4) -> coreceptors
  • these extra proteins and helpers avoid T cells from self reactive -> safe guard
246
Q

antigen presentation

A
  • foreign proteins are digested inside a host cell
  • resulting peptide fragments (antigens) are displayed on the surface of the host cell by host membrane proteins called major histocompatibility complex proteins (MHCs)
  • process called antigen presentation
  • MHC proteins are essential for adaptive immune system to recognize foreign molecules
  • MHC proteins are subdivided into two groups: class 1 and class 2
247
Q

Class 1 MHC

A
  • expressed on the surface of all nucleated cells (bc all nucleated cells have the potential to become a viral factory or can have mutation)
  • interacts with cytotoxic T cells
  • requires CD8 co-receptor on cytotoxic T cells (helps with specificity of targeting)
  • causes destruction of infected or abnormal self cells
  • mistakes in this process can be very bad
248
Q

class 2 MHC

A
  • expressed on the surface of antigen presenting cells (macrophages, dendritic cells, and B cells)
  • interacts with helper T cells
  • requires CD4 co-receptor on helper T cells
  • causes enhancement of both B cell and cytotoxic T cell activity
249
Q

how are viral host cells being recognized as bad

A
  • viral proteins are being made
  • host enzymes break it down into viral protein fragments (antigens)
  • these associate with MHC class 1
  • undergo exocytosis and are being displayed on the surface
  • cytotoxic T cell comes and recognizes this foreign peptide
  • coreceptor CD8 interacts with MHC1 -> forms a tight junction that is super specific
  • protein-protein interaction
  • cell releases perforin and granzymes that kill the host cell
250
Q

antigen-presenting cells APCs

A
  • bridge between the innate and adaptive immune response -> macrophages (innate) are attracting adaptive immune (helper t cell)
  • macrophages, dendritic cells, and B cells are primary APCs
  • phagocytic cells that engulf pathogens and enzymatically break down the pathogens proteins to small peptide fragments (antigens) (no reason to kill the host cell)
  • antigens are displayed on the surface of the APC via MHC class 2 receptors
  • helper T cells interact with APCs that display (or present) antigen via MHC2 receptors
  • CD4 co receptor binds to MHC class 2 verifies the interaction
  • binding activates the T cell inducing it to secrete cytokines such as interleukin 2 which stimulates other immune cells -> cause them to proliferate and differentiate
251
Q

b cells

A

phagocytic

252
Q

class 1 MHC molecules are present on the surface of dendritic cells but not mast cells

A

false

  • this is true for class 2
  • class 1 can be found on dendritic and mast cells
  • class 1 MHC molecules are present on the surface on dendritic cells, but not RBCs (no nucleus) -> true
253
Q

adaptive immune response to pathogen include cell mediated immunity and humoral immunity

A

true

254
Q

T cell activation

A
  • antigen is presented to T cell on an MHC
  • antigen binds to T cell receptor -> high specificity and affinity interaction between MHC, antigen, TCR, and co receptors
  • 2nd messenger signaling pathways lead to changes in gene expression and other cellular processes
  • clonal expansion- t cell divides to produce multiple identical cells with the same TCR
  • cytokine production- t cells secrete cytokines that activate other innate and adaptive immune cells -> interleukin-1, interluekin-2, and tumor necrosis factor (TNF)
255
Q

interluekin-2

A
  • secreted by helper T cells in response to binding to class 2 MHC
  • stimulates other immune cells and cause them to proliferate
  • ex. increased proliferation of B cells -> differentiation -> plasma (antibodies) and memory cells
256
Q

MHC Class 1 and 2 work together

A
  • virus infected host -> displays viral peptides on surface -> class 1 MHC -> cytotoxic T cell recognizes
  • macrophage engulfs virus -> displays virus and MHC class 2 -> helper t cell binds -> secretes cytokines (interleukin-2)
  • interluekin-2 binds to receptors on the cytotoxic T cell and causes clonal expansion -> proliferation of cytotoxic t cells kills infected/abnormal host cells
257
Q

attack: cytotoxic t cells

A
  • virus infected host cells
  • display virus on surface
  • CD8 co receptor
  • class MHC 1
  • cytotoxic T cell recognizes and secretes perforin and granzymes (within same granule vesicle)
258
Q

perforin

A
  • peptide
  • initially inactive
  • in presence of calcium it will form a pore in the membrane of host cell
  • does not exist free in the plasma
  • cytotoxic cell is so close to the host cell the distance is short
  • causes unregulated flux of water, ions, small molecules, and enzymes -> swell
  • granzymes can enter through the pores -> cell death
  • produced by cytotoxic T cells (and NK cells) and is stored in inactive form in the same granules as granzymes
259
Q

granzymes

A
  • proteases (enzymes that break down proteins)
  • released by cytotoxic T cells (an NK cells) and stored in cytoplasmic granules (secretory vesicles)
  • enters host cells through pores made by perforin
  • initiate cell death pathways in host cell
  • controlled cell death
  • granzyme b initiates by activating caspases (enzymes that when activated control cell death)
  • programmed cell death is important bc lysing it would release so much dangerous debris -> collateral damage
260
Q

necrosis

A
  • uncontrolled

- can cause collateral damage to surrounding cells

261
Q

adaptive immunity memory

A
  • primary immune response makes memory B cells, helper T cells and cytotoxic T cells that can persist for decades
  • subsequent exposure to an antigen causes a faster and more robust adaptive immune response
  • takes about 5 days for the body to even start making antibodies after first exposure
  • antibodies peak at 2 weeks
  • 2nd exposure sees antibodies right away exponentially at much higher levels
262
Q

vaccines: primary immune response

A
  • contain weakened or dead microbes or mixtures of molecules isolated from a microbe (lots of antigens)
  • microbes grown in a large quantities in cells or eggs (viruses_ or in vats (bacteria)
  • often contains adjuvants: immune response enhancing molecules (sometimes PAMPs)
  • cause a primary immune response, usually with little or no symptoms of microbial disease
  • no replication bc dead
  • often cause inflammatory response and fever
263
Q

immunosuppressants

A
  • cortisone, azathioprine

- *cyclosporine- isolated from a fungus found in a soil sample

264
Q

acute rejections

A
  • occurs after the first few months of transplant
  • mediated by T cells and B cells
  • can usually be prevented with immunosuppressants
265
Q

cyclosporine

A
  • blocks the expression of the gene that encodes interleukin-2 in T cells
  • in helper t cells ^
  • shows importance of interleukin-2 and helper t cells
266
Q

risks and limitation of immunosuppressants

A
  • infection
  • tumor formation, especially lymphomas
  • not a cure (must be taken for life)
  • reactivation of latent infection (TB)
267
Q

leading cause of death in america

A

-heart disease

268
Q

Heart disease: atherosclerosis in a coronary artery

A
  • caused by lack of exercise, poor diet
  • occlusion
  • build up of LDL cholesterol in artery of heart
  • blocks hearts blood supply
  • lack of blood flow causes ischemia- insufficient blood supply to a tissue -> tissues may die or have low function
  • waste products are not being removed
269
Q

major risk factors for heart disease

A
  • *high blood cholesterol (LDL cholesterol)
  • high blood pressure (hypertension)
  • diabetes
  • being overweight
  • being physically inactive
  • smoking
  • having a family history of heart disease
270
Q

cholecystokinin is a peptide hormone produced by cells of the stomach

A
  • false
  • produced by the duodenum (intestine) not stomach
  • CCK -> gallbladder -> smooth muscle contraction of gallbladder -> introduced bile into bile duct
  • CCK also initiates protein release in pancreas
271
Q

bile salts

A
  • from liver
  • detergents
  • ampipathic molecule
  • emulsifies fat droplets into micelles by coating them
272
Q

pancreatic lipase and colipase

A
  • break down triglycerides into monoglycerides and free fatty acids
  • monoglycerides and free fatty acids move out of micelles and into intestinal cells by diffusion (small enough)
  • cholesterol is transported into cells by carrier protein
  • triglycerides are resynthesized and combined with cholesterol and proteins in the intestinal cells to form chylomicrons
  • chylomicrons are removed by the lymphatic system
273
Q

chylomicrons

A
  • efficient way of transporting lipids in aqueous environment
  • triglycerides are resynthesized and combined with cholesterol and proteins to form chylomicrons
  • triglycerides are in the middle, phosphate head groups on outside -> efficient for transporting hydrophobic molecules
  • these chylomicrons are removed (exocytosis) by lymphatics (too big)
274
Q

lymphatics

A
  • chylomicrons that enter the lymphatic system are bypassing the liver
  • go to the right side of the heart and back into systemic circulation
  • it eventually ends up back in the liver where it repackages the chylomicrons as LDL cholesterol particles
  • increased pizza -> increased lipids -> higher your LDL cholesterol
275
Q

Low density lipoprotein (LDL) particle

A
  • triglycerides and cholesterol are transported in plasma as large, macromolecular complexes of lipid and protein known as lipoprotein particles
  • 45% cholesterol
  • 25% proteins (apolipoprotein B100 binds to lipids)
  • 21% phospholipids
  • 9% triglycerides
  • major risk factor for atherosclerosis
276
Q

development of artherosclerosis

A
  • LDL cholesterol accumulates in the wall of the artery
  • macrophages ingest cholesterol and become foam cells in the wall of the artery (innate)
  • over long period of time (decades) plaques form
277
Q

heart failure

A

-plaques and blocks limit the amount of blood flow
-heart adapts to the changes by enlarging
-walls become thinner and weaker (especially left ventricle) due to enlarge (cant pump out CO)
-

278
Q

pulmonary edema

A

-accumulation of LDL cholesterol in the walls of the left epicardial artery -> occlusion
-excess fluid accumulation in the lung tissues and air spaces, including the alveoli
-output from left ventricle is declining due to weakened heart muscle, right ventricle keeps pumping -> fluid backs up in the lungs -
> difficulty breathing
-bc left is enlarged they are pumping different volumes of blood (5 liters pumped on right side and only 2 pumped out)
-the extra 3 liters are pushed out into circulation at the level of pulmonary capillaries -> into lung interstitial environment (fused basement membrane) -> bc this layer in enlarging the diffusion distance is increasing -> less efficient diffusion of gases
-stiff lungs due to increased fluid as well
-difficulty breathing

279
Q
  • heart failure -> enlarged heart -> weak and thin walls -> CO drops -> MAP initially declines from 93 to 85 -> person feels light headed and lies down
  • with a MAP of 85 (drop in MAP) the kidneys will continue filtering blood at a normal rate (180L/day)
A

-true

-

280
Q
  • heart failure -> enlarged heart -> weak and thin walls -> CO drops -> MAP initially declines from 93 to 85 -> person feels light headed and lies down
  • with a MAP of 85 (drop in MAP) the levels of renin in the blood will increase significantly
A

-false

281
Q
  • heart failure -> enlarged heart -> weak and thin walls -> CO drops -> MAP initially declines from 93 to 85 -> person feels light headed and lies down
  • with MAP= 85 autoregulatory mechanisms would be sufficient to maintain a nearly constant GFR
A
  • true
  • if your using autoregulation to maintain GFR you dont need renin
  • myogenic -> reduced stretch -> relaxes -> increased flow an GFR
  • tubuloglomerular feedback -> reduced flow -> reduced paracrine factors -> relax -> increase flow and GFR
  • true for MAP of 80-180
282
Q

a normal health person is lying down and stands up suddenly. how person is vertical and heart must work against gravity to pump blood around circulatory system
-cardiac output falls from 5 to 3 -> the baroreceptor reflex will be initiated

A

-true

283
Q

a normal health person is lying down and stands up suddenly. how person is vertical and heart must work against gravity to pump blood around circulatory system

  • cardiac output falls from 5 to 3
  • sympathetic outflow will increase
  • heart rate and force of contraction will increase, leading to an increase in cardiac output
  • peripheral vascular resistance increases, due to vasoconstriction in vascular beds such as the skin and gastrointestinal tract
A
  • true
  • true
  • true
284
Q

a person with heart failure stands up suddenly. now person is ventricle and heart must work against gravity to pump blood around circulatory system

  • cardiac output falls from 5 to 2
  • with MAP 70, autoregulatory mechanisms will maintain GFR at 180 L/day
A
  • false
  • false because BP below 80 or above 180 is not controlled by autoregulatory mechanisms
  • GFR will drop
285
Q

a person with heart failure stands up suddenly. now person is ventricle and heart must work against gravity to pump blood around circulatory system

  • cardiac output falls from 5 to 2
  • with MAP 70, levels of circulating renin will increase
A
  • true
  • MAP below 80 renin increases
  • weakened heart -> MAP falls to 70 -> RAAS initiated -> different paracrine factors are released (prostaglandins) due to the dramatic drop in MAP -> act on granular cells -> release renin
286
Q

renin is a peptide hormone

A
  • false
  • its an enzyme
  • function in a pathway that produces a hormone
287
Q

vasopressin is a peptide hormone that is synthesized in the posterior pituitary

A
  • false
  • vasopressin is synthesized in the hypothalamus
  • released at the level of the posterior pituitary
288
Q

urine volume in heart failure patient decreases and blood volume increases

A
  • angiotensin 2 increases vasopressin and aldosterone release
  • vasopressin -> increase recovery of water
  • aldosterone -> increase sodium recovery
  • overall this is absorbing more water which increases blood volume and decreases urine
289
Q

nitroglycerin and furosemide (lasix)

A
  • nitroglycerin-given when difficulty breathing, goes into circulation, releases nitric oxide, vasodilator
  • furosemide-blocks ion uptake in the ascending loop of henle, increases urine volume by blocking reabsorption
  • blood volume decreases a little with increase in urine volume -> water is drawn from extracellular compartment (lung tissue) to maintain blood volume -> lungs clear of excess fluid -> person can breathe again
290
Q

heart failure development

A

-behavioral + genetic factors -> high LDL cholesterol -> risk of artherosclerosis -> over time -> coronary artery disease -> weakened LV heart muscle -> pulmonary edema -> difficulty breathing -> 911 -> furosemide and nitroglycerin -> increase in urine and vasodilation -> decreased workload on the heart -> lungs clear of fluid

291
Q

plaques

A
  • overtime the increase LDL cholesterol continues to accumulate
  • if the plaque ruptures -> VERY BAD!
  • rupture exposes tissue factor and collagen to the lumen of the blood vessel -> creates a clot -> blocks the artery -> cardio myocytes die -> lethal
292
Q

tissue factor binds to receptors on platelets

A
  • false

- tissue factor binds to tissue factor 7 -> initiates clotting cascade

293
Q

collagen is an extracellular matric protein that can function as a ligand and activate platelets

A

-true

294
Q

clot

A

-platelet plug + fibrin net -> stable

BIO 203 (5 decks)

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