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Bio > Bios 355 Exam 4 > Flashcards

Bios 355 Exam 4 Flashcards

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1
Q

Water balance

A

Total fluids > 40 L
25 L is cytoplasm
15 L is ECF
ECF > plasma is 3 L, interstitial fluid is 10 L, transfluid is 2 L
Transfluid > saliva, GI fluid, ocular fluid, pleural fluid
Gain > 2.1 L (food and water)
> 0.3 L (metabolic water)
Oxidative phosphorylation in mitochondria

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2
Q

ETS

A 
Final electron acceptor oxygen > forms H2O
Gain > 2.4 L/day 
Loss > evaporation across skin: 0.35 L
         > respiratory evap. 0.35 L
         > feces: 0.2 L
         > urine: 1.5 L 
Water gain must equal water loss
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3
Q

Osmotic sensors

A 
Located in the hypothalamus 
Increase OP sensor > increase AP freq. 
When sensor swells: physical change of cell alters the open probability of the channel 
\: decrease Na influx 
\: decrease AP freq.
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4
Q

Hypothalamic neurons

A

Axon lead to posterior pituitary
AP will cause the release of the hormone ADH (anti diuretic hormone) (vasopressure)
ADH released into blood when the osmotic sensors increase AP freq.

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5
Q

Role of ADH

A
  1. Target is cells of the collecting duct of the nephron
  2. Bond to ADH receptors on C.D.
    > activate increase cAMP
    > activate PKA
    > stimulate insertion of vesicles into plasma membrane
    Increase blood OP
    Increase ADH > increase aquaporin, osmotic rate, and water reabsorption
    Decrease urine vol.
    increase urine OP
    Decrease blood vol.
    Decrease blood OP
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6
Q

Drink a large vol. of water

A 
Decrease OP in blood/ECF
Decrease osmotic sensor AP freq. 
Decrease rate of release of ADH
Decrease aquaporin 
Decrease water reabsorption 
Increase urine vol. 
absence of ADH - collecting duct autonomically retrieves the aquaporin by endocytosis
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7
Q

Other mechanisms to cause the release of ADH

A
  1. Primary: osmotic sensors
  2. Vascular stretch receptors (baroreceptors)
    > send AP to hypothalamus
    Baroreceptors detect low vol. and pressure > stimulate hypothalamus > increase AP freq. > increase ADH release > water conservation and thirst
    Increase blood vol. > increase blood pressure
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8
Q

Kidney-cardiovascular connection

A

ADH > produced by posterior pituitary
Role: 1. Increase water permeability of C.D. (Insertion of aquaporin channels)
2. Increase thirst
Result: decrease ECF OP

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9
Q

Thirst (behavioral drive)

A

Promoted by: high ADH
Angiotensin (activated by kidney)
Increase water intake from outside
Increase blood vol. > increase blood pressure

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10
Q

Feed forward systems

A

Sensors in GI tract that signal what is coming
Water sensors > respond (increase AP freq.)
>signal brain > decrease sensation of thirst

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11
Q

Control blood Na
Control blood volume
Control blood pressure

A

NaCl is the dominant ECF solute

Change NaCl - change OP and volume

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12
Q

How is NaCl, volume and pressure regulated

A
  1. Nephron of kidney has specialized cells called the juxtaglomerular apparatus (JGA)
  2. JGA cells can release an enzyme called renin
    A) decrease afferent arteriole pressure
    B) sympathetic nervous stimulation of JGA
    C) macula densa can cause JGA to release renin when Na is low
  3. Renin is a protease - convert an inactive plasma protein called angiotensinogen > made by liver > angiotensinogen I (cleave 10 amino acids)
  4. Angiotensin I > angiotensin II (active)
    ACE: angiotensin converting enzyme
  5. Angiotensin II
    A) promotes peripheral vasoconstriction (increase resistance > increase pressure)
    B) stimulates cardiovascular control center in medulla to increase sympathetic activity > increase HR, increase SV, increase C.O., increase BP
    C) stimulates cells in the brain to promote behavioral changes and induce thirst > increase water intake, increase blood vol. > increase BP
    D) causes adrenal gland to produce and secrete the steroid hormone aldosterone
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13
Q

Aldosterone

A

Steroid
Enter the cells of the distal tubule (contain receptor for aldosterone)
Aldosterone binds receptor
Complex is then imported into the nucleus
Behaves as a transcription factor
Cause the transcription factor of Na transporters (Na channels, Na/K exchangers, NaK-ATPase)
Distal tubule will then start reabsorbing more NaCl
> increase NaCl
> increase osmosis
> increase fluid reabsorption
> increase blood vol.
> increase blood pressure

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14
Q

Other factors that can induce aldosterone release

A 
1. Increase in ECF K conc. 
    > stimulate the adrenal cortex to release aldosterone 
    > make more Na/K exchangers 
            > reabsorb Na but secrete K
2. Renin-angiotensin coupling
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15
Q

Regulatory response to high blood pressure

A

Pressure is measured at baroreceptors
Pressure is measured in atrial stretch receptors
Increase pressure in atria > produce and release atrial natriuretic factor (ANF)

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16
Q

What does ANF do?

A 
A) cause vasodilation 
B) decrease NaCl transport and fluid reabsorption 
> Distal tubule 
     Decrease NaCl
     Decrease fluid reabsorption 
     Increase urine vol.
     Decrease blood vol. 
> GI tract 
     Decrease NaCl
     Decrease fluid absorption 
     Decrease fluid entering body 
C) ANF stimulates mesangial cells of glomerulus 
   > decrease slit resistance 
   > increase GFR
   > increase urine production (decrease blood vol.) 
D) ANF decrease sympathetic activity at the cardiovascular control center in medulla (decrease C.O., and BP)
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17
Q

ANF

A 
Decrease NaCl transport 
Decrease fluid reabsorption 
Decrease blood vol.
Decrease blood pressure 
Vasodilator 
  > decrease resistance flow 
  > decrease pressure 
Decrease sympathetic activity 
Decrease slit resistance at the glomerulus 
   > increase GFR
   > increase urine production 
   > decrease blood pressure
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18
Q

Adrenomedulin

A

Peptide
Produced by adrenal gland, kidney, cardiac tissue
Increase K conductance > hyper polarize
A) decrease sympathetic AP freq. (short term response)
B) decrease aldosterone secretion
(Long term response)

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19
Q

Control acid-base balance

A 
pH has a dramatic influence on protein structure > therefore, must maintain pH within narrow limits 
1. Fixed acids 
   > amino acids 
   > fatty acids 
   > nucleic acids    
   > citric acids 
2. CO2 production 
CO2 + H2O <> H2CO3 <> H + HCO3
Increase CO2 > increase H (decrease pH)
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20
Q

Mechanisms to combat changes in pH

A 
1. pH buffers 
   > very fast 
   > low overall capacity 
2. Ventilatory compensation 
   > fast (respiratory compensations) 
3. Renal excretion 
   > very high capacity 
   > slower 
1 and 2 provide time to allow renal system to physically excrete protons (H)
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21
Q

Buffers

A

Proteins
Phosphate
HCO3
Bind or release protons (H) depending on pH

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22
Q

Respiratory compensation

A

Changes in ventilation rate drives by changes in pH

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23
Q

Respiratory compensation for metabolic acidosis

A 
> lactic acid 
  > keto acids 
Increase ventilation 
Decrease PCO2 
Decrease H (proton conc.)
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24
Q

Respiratory compensation for metabolic alkalosis

A 
Vomiting
Increase pH
Ventilation decrease 
  > increase PCO2 
  > increase H (proton conc., decrease pH)
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25
Q

Renal compensation

A 
Proximal tubule  
Decrease pH in urine 
Amino acid deamination 
  > release ammonia (NH3) 
  > very toxic 
Liver NH3 converted into urea 
NH3 + H > NH4 (when pH decreases)
NH3 > permeable (can exit urine)
NH4 > charged 
         > impermeable 
         > trapped in urine
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26
Q

Distal tubule

Type A intercalated cells

A 
Secrete protons (H) into urine 
Decrease pH in urine 
Increase pH in blood
H into urine
HCO3 into blood
Cl into cell 
HCl into urine
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27
Q

Type B intercalated cell

A 
Secrete HCO3 into urine and H into blood 
Increase pH in urine 
Decrease pH in blood 
HCO3 into urine 
Cl from urine into cell
H into blood
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28
Q

Intercalated cells of distal tubule

A

Responsible for fine tuning blood pH
Bring either secreted excess H into the urine (type A)
Or secrete excess HCO3 into the urine (type B)

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29
Q

Regulation of calcium

A

C-cells of the thyroid
Chief cells of the parathyroid
Above monitor Ca conc.

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30
Q

Calcium decreases in the blood

A

parathyroid releases PTH
Result: 1. PTH stimulates osteoclasts
Osteoclasts involved in bone remodeling, demineralization, release Ca into blood
2. Inhibit osteoblasts
> bone producing cells
> decrease rate of Ca deposition in the bone
3. Stimulates urinary Ca reabsorption (transport) > increase Ca reabsorption in the nephron
4. Stimulates production of calcitriol by the kidneys

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31
Q

Calcitriol

A

Steroid
Promotes transcription of Ca transporters
A) nephron
B) GI tract (increase uptake of Ca and overall body Ca)

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32
Q

Calcium increases in blood

A

Stimulate thyroid to release calcitonin
Result: 1. Inhibit osteoclasts
2. Inhibit or reduce Ca transport in the nephron distal tubule
Increase urinary Ca excretion

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33
Q

Digestion

A 
Mouth 
Pharynx 
Epiglottis 
Esophagus > esophageal sphincter 
Stomach > pyloric sphincter 
Small intestine > duodenum, jejunum, ileum
Large intestine > colon, rectum
Anal sphincter (15 ft long)
Accessory organs 
 > secrete into GI tract 
A) salivary glands 
B) pancreas 
C) liver
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34
Q

Layers of GI tract

A

Mucosa
Sub mucosa
Musculature
Serosa

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35
Q

Mucosa

A 
Inner lining 
Lots of invaginations 
Increase surface are 
Increase transport rate 
Cells have micro villi
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36
Q

Submucosa

A

Connective tissue
Blood vessels
Lymph vessels
Enteric nerves (unique to GI tract)

37
Q

Musculature

A 
Layers of SM
Circular SM (changes radius) 
Longitudinal SM (changes length) 
Myenteric plexus controls and coordinates the motor activity of the muscularis externa
38
Q

Serosa

A

Connective tissue
Holds the macrostructure in place
Continuation of the peritoneal that lines the abdominal cavity

39
Q

Motility (movement)

A 
How do you control the GI SM
A) enteric nerves 
B) GI hormones 
C) local paracrine factors 
D) stretch activated (mechanically gated ion channels)
40
Q

Peristaltic contractions

A

Progress wave of SM contractions

Move food forward

41
Q

Segmental contractions

A

Mixing
Kneading
Back and forth contractions
Controlled by enteric nerves

42
Q

Route through GI tract

A
  1. Physically > mastication (chewing), essentially breaking in down into smaller pieces (⬆️ surface area)
  2. Saliva > moisten, lubricates,water, antibodies, mucus, salts, amylase
  3. Swallowing reflex > trigger reflex by pushing the food bolus against the soft palate
  4. Pressure on the esophagus side of the esophageal sphincter cause the sphincter to relax, if sphincter does not close properly can lead to heart burn
  5. Enters stomach, segmental and peristaltic contractions > push chyme against pyloric sphincter
  6. Empty stomach slowly
  7. SI SM becomes activated, segmental followed by peristaltic contractions
  8. Continued until rectum > stored, wait for defication
43
Q

Amylase

A

Breaks glycosidic bonds that form polymers
Breaks down carbs
Keep mouth clean

44
Q

Chemical digestion

A 
Starts in stomach > gastric glands that produce hormones, histamines, acid, digestive enzymes 
Protection > mucus bicarbonate 
Parietal cells > produce HCL
Chief cells > make pesinogen
Enterochromatin cells > histamines 
Endocrine cells > hormone (gastrin) 
D-cells 
G-cells
Mucus cells > binds water
45
Q

Digestion

A

Pancreas > stimulated by CCK to release enzymes
Reach intestine > trypsinogen to trypsin by enteropeptides
Trypsin activates all other enzymes
Trypsin and chymotrypsin are both endopeptidase
Carboxypeptidase > pancreas
Aminopeptidase > intestine

46
Q

Gastric glands

A

Mucus cells > produce the protective barrier that lines the stomach, constantly replenished
Parietal cells > produce HCl
Chief cells > make and release digestive enzymes, pepsinogen, and gastric lipase
Release contents by exocytosis
K and Cl move out along with water by osmosis
KCl helps power HCl, trade K for H

47
Q

Activating gastric gland

A

Parasympathetic innervation (Ach) > stimulates muscorinic cholinergic receptors
Reflex stimulation > sight, smell, taste, anticipation
Feed forward response
G-cells of the gastric gland > release gastrin
Further stomach activation
SM churning action
Activate the enzymes by low pH
Pepsinogen to pepsin
Endopeptidase breaks a peptide bond in the middle of the chain

48
Q

Pepsin

A

Cleave glycine-lysine linkages
Very common in collagen
Designed to break connective tissue

49
Q

CCK

A

Produced by endocrine cells in small intestine
Stimulates the pancreas
Promotes the secretion of digestive enzymes (made in acinar cells)

50
Q

Enzymes

A 
Trypsinogen 
Chymotrypsinogen 
Pro-carboxypeptidase 
Phospholipase 
Lipases target triglycerides/fat
Amylase targets carbs 
Nuclease breaks polymer bonds, DNA/RNA
Enzymes are inactive in the pancreas
51
Q

Inactive enzymes

A

Zymogens
High activity in beginning
Activate decreases as you progress (self degradation)

52
Q

Small intestine

A

Receiving chyme from stomach
Decreases pH > cause release of secretin > cause the pancreas to produce an alkaline fluid to neutralize the acid
Increase proteins
Increase carbs > release CCK > cause pancreas to release digestive enzymes

53
Q

CCK

A
  1. Release digestive enzymes
  2. Inhibits gastrin secretion (slow the rate of chyme entry into SI)
  3. Stimulates gall bladder (contracts and push bile into SI)
  4. Stimulates intestinal SM peristalsis (contractions)
  5. Acts on the CNS > decrease hunger
54
Q

Mucous surface cell
Substance secreted:
Function of secretion:

A

Mucus

Physical barrier between lumen and epithelium

55
Q

Mucous neck cell
Substance secreted
Function of secretion

A

Bicarbonate

Buffers gastric acid to prevent damage to epithelium

56
Q

Parietal cells
Substance secreted
Function of secretion

A

Gastric acid (HCl) and intrinsic factor
HCl: activates pepsin; kills bacteria
IF: complexes with vitamin B12 to permit absorption

57
Q

Enterochromaffin-like cell
Substance secreted
Function of secretion

A

Histamine

Stimulates gastric acid secretion

58
Q

Chief cells
Substance secreted
Function of substance
Activation of enzymes

A

Pepsin(ogen) and gastric lipase
Pepsin: digest proteins
GL: digest fats
Ach and acid secretion

59
Q

D cells
Substance secreted
Function of substance

A

Somatostatin

Inhibits gastric acid secretion

60
Q

G cells
Substance secreted
Function of substance

A

Gastrin

Stimulates gastric acid secretion

61
Q

Gastric lipase

A

Breaks down triglycerides (fats)

Secreted by chief cells

62
Q

Pepsin

A 
Secreted by gastric gland 
Protein digestion 
Effective on collagen so digests meat 
Protease 
Cleaves glycine-lysine linkages
63
Q

Trypsin

A

Converts other pancreatic zymogens to their active forms
Protease
Pancreas

64
Q

Chymotrypsin

A

Protease

Pancreas

65
Q

Carboxypeptidase

A

Exopeptidase
Act on carboxy-terminal end
Pancreas

66
Q

Aminopeptidase

A

Exopeptidase
Acts on amino-terminal end of protein
Intestine

67
Q

Endopeptidase

A

Digest protein
Attacks peptide bonds in their interior of the amino acid chain and break long peptide chain
Pancreas

68
Q

Enteropeptidease

A

Concerts trypsinogen to trypsin

Pancreas

69
Q

Amylase

A

Digest starch to maltose
Made by pancreas
Breaks long glucose polymers into smaller glucose chains and disaccharide maltose

70
Q

Exopeptidase

A

Digest protein
Release single amino acids from peptides by chopping them off the ends, one at a time
Secreted by pancreas

71
Q

Lipase

A

Breaks down triglycerides

Removes two fatty acids

72
Q

Gastrin
Site of production
Target effects
Stimulus for release

A

G cells
Stomach
Stimulates gastric acid secretion and mucosal growth
Peptides and amino acids; neural reflexes

73
Q

Cholecystokinin (CCK)
Site of production
Target effect
Stimulus for release

A

Small intestine
Stimulates gallbladder contraction and pancreatic enzyme secretion and inhibits gastric emptying and acid secretion
Fatty acids and some amino acids

74
Q

Secretin
Site of production
Target effect
Stimulus for release

A

Small intestine
Stimulates HCO3 secretion, inhibits gastric emptying and acid secretion
Acid in small intestine

75
Q

Motilin
Site of production
Target effect
Stimulus for release

A

Small intestine
Stimulates migrating motor complex
Fasting

76
Q

Gastric inhibitory peptide (GIP)
Site of production
Target effect
Stimulus for release

A

Small intestine
Stimulates insulin release (feed forward) inhibits gastric emptying and acid secretion
Glucose, fatty acids, and amino acids in small intestine

77
Q

Glucagon-like-peptide-1 (GLP-1)
Site of production
Target effect
Stimulus for release

A

Small intestine
Stimulates insulin release, inhibits glucagon release and gastric function
Mixed meal that includes carbs or fats in lumen

78
Q

Basophils and mast cells
Abundance
Function
Classification

A

Rare
Release chemicals that mediates inflammation and allergic responses
Granulocytitic

79
Q

Eosinophils
Abundance
Function
Classification

A

1-3%
Destroy invaders, particularly antibody coated parasites
Cytotoxic and granulocytitic

80
Q

Neutrophils
Abundance
Function
Classification

A

50-70%
Ingest and destroy invaders
Phagocytitic

81
Q

Monocytes and macrophages
Abundance
Function
Classification

A

1-6%
Ingest and destroy invaders, antigen presenting
Antigen presenting
Phagocytitic

82
Q

Lymphocytes and plasma cells
Abundance
Function
Classification

A

20-35%
Specific responses to invaders, including antibody production
Antigen presenting and cytotoxic

83
Q

Dendritic cells
Abundance
Function
Classification

A

N/A
Recognize pathogens and activate other immune cells by antigen presenting
Antigen presenting

84
Q

IgG antibody

A

Found in plasma of adults

85
Q

IgA antibody

A

Found in external secretions (saliva, tears, interstitial and bronchial mucus, breast milk)

86
Q

IgE antibody

A

Attach to basophils and mast cells

87
Q

IgM antibody

A

Blood group antigens

88
Q

IgD antibody

A

Appear on the surface of B lymphocytes along with IgM antibodies

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