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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
Renal compensation
``` 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 ```
26
Distal tubule | Type A intercalated cells
``` 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 ```
27
Type B intercalated cell
``` 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 ```
28
Intercalated cells of distal tubule
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)
29
Regulation of calcium
C-cells of the thyroid Chief cells of the parathyroid Above monitor Ca conc.
30
Calcium decreases in the blood
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
31
Calcitriol
Steroid Promotes transcription of Ca transporters A) nephron B) GI tract (increase uptake of Ca and overall body Ca)
32
Calcium increases in blood
Stimulate thyroid to release calcitonin Result: 1. Inhibit osteoclasts 2. Inhibit or reduce Ca transport in the nephron distal tubule Increase urinary Ca excretion
33
Digestion
``` 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 ```
34
Layers of GI tract
Mucosa Sub mucosa Musculature Serosa
35
Mucosa
``` Inner lining Lots of invaginations Increase surface are Increase transport rate Cells have micro villi ```
36
Submucosa
Connective tissue Blood vessels Lymph vessels Enteric nerves (unique to GI tract)
37
Musculature
``` Layers of SM Circular SM (changes radius) Longitudinal SM (changes length) Myenteric plexus controls and coordinates the motor activity of the muscularis externa ```
38
Serosa
Connective tissue Holds the macrostructure in place Continuation of the peritoneal that lines the abdominal cavity
39
Motility (movement)
``` 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
Peristaltic contractions
Progress wave of SM contractions | Move food forward
41
Segmental contractions
Mixing Kneading Back and forth contractions Controlled by enteric nerves
42
Route through GI tract
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
Amylase
Breaks glycosidic bonds that form polymers Breaks down carbs Keep mouth clean
44
Chemical digestion
``` 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
Digestion
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
Gastric glands
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
Activating gastric gland
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
Pepsin
Cleave glycine-lysine linkages Very common in collagen Designed to break connective tissue
49
CCK
Produced by endocrine cells in small intestine Stimulates the pancreas Promotes the secretion of digestive enzymes (made in acinar cells)
50
Enzymes
``` 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
Inactive enzymes
Zymogens High activity in beginning Activate decreases as you progress (self degradation)
52
Small intestine
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
CCK
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
Mucous surface cell Substance secreted: Function of secretion:
Mucus | Physical barrier between lumen and epithelium
55
Mucous neck cell Substance secreted Function of secretion
Bicarbonate | Buffers gastric acid to prevent damage to epithelium
56
Parietal cells Substance secreted Function of secretion
Gastric acid (HCl) and intrinsic factor HCl: activates pepsin; kills bacteria IF: complexes with vitamin B12 to permit absorption
57
Enterochromaffin-like cell Substance secreted Function of secretion
Histamine | Stimulates gastric acid secretion
58
Chief cells Substance secreted Function of substance Activation of enzymes
Pepsin(ogen) and gastric lipase Pepsin: digest proteins GL: digest fats Ach and acid secretion
59
D cells Substance secreted Function of substance
Somatostatin | Inhibits gastric acid secretion
60
G cells Substance secreted Function of substance
Gastrin | Stimulates gastric acid secretion
61
Gastric lipase
Breaks down triglycerides (fats) | Secreted by chief cells
62
Pepsin
``` Secreted by gastric gland Protein digestion Effective on collagen so digests meat Protease Cleaves glycine-lysine linkages ```
63
Trypsin
Converts other pancreatic zymogens to their active forms Protease Pancreas
64
Chymotrypsin
Protease | Pancreas
65
Carboxypeptidase
Exopeptidase Act on carboxy-terminal end Pancreas
66
Aminopeptidase
Exopeptidase Acts on amino-terminal end of protein Intestine
67
Endopeptidase
Digest protein Attacks peptide bonds in their interior of the amino acid chain and break long peptide chain Pancreas
68
Enteropeptidease
Concerts trypsinogen to trypsin | Pancreas
69
Amylase
Digest starch to maltose Made by pancreas Breaks long glucose polymers into smaller glucose chains and disaccharide maltose
70
Exopeptidase
Digest protein Release single amino acids from peptides by chopping them off the ends, one at a time Secreted by pancreas
71
Lipase
Breaks down triglycerides | Removes two fatty acids
72
Gastrin Site of production Target effects Stimulus for release
G cells Stomach Stimulates gastric acid secretion and mucosal growth Peptides and amino acids; neural reflexes
73
Cholecystokinin (CCK) Site of production Target effect Stimulus for release
Small intestine Stimulates gallbladder contraction and pancreatic enzyme secretion and inhibits gastric emptying and acid secretion Fatty acids and some amino acids
74
Secretin Site of production Target effect Stimulus for release
Small intestine Stimulates HCO3 secretion, inhibits gastric emptying and acid secretion Acid in small intestine
75
Motilin Site of production Target effect Stimulus for release
Small intestine Stimulates migrating motor complex Fasting
76
Gastric inhibitory peptide (GIP) Site of production Target effect Stimulus for release
Small intestine Stimulates insulin release (feed forward) inhibits gastric emptying and acid secretion Glucose, fatty acids, and amino acids in small intestine
77
Glucagon-like-peptide-1 (GLP-1) Site of production Target effect Stimulus for release
Small intestine Stimulates insulin release, inhibits glucagon release and gastric function Mixed meal that includes carbs or fats in lumen
78
Basophils and mast cells Abundance Function Classification
Rare Release chemicals that mediates inflammation and allergic responses Granulocytitic
79
Eosinophils Abundance Function Classification
1-3% Destroy invaders, particularly antibody coated parasites Cytotoxic and granulocytitic
80
Neutrophils Abundance Function Classification
50-70% Ingest and destroy invaders Phagocytitic
81
Monocytes and macrophages Abundance Function Classification
1-6% Ingest and destroy invaders, antigen presenting Antigen presenting Phagocytitic
82
Lymphocytes and plasma cells Abundance Function Classification
20-35% Specific responses to invaders, including antibody production Antigen presenting and cytotoxic
83
Dendritic cells Abundance Function Classification
N/A Recognize pathogens and activate other immune cells by antigen presenting Antigen presenting
84
IgG antibody
Found in plasma of adults
85
IgA antibody
Found in external secretions (saliva, tears, interstitial and bronchial mucus, breast milk)
86
IgE antibody
Attach to basophils and mast cells
87
IgM antibody
Blood group antigens
88
IgD antibody
Appear on the surface of B lymphocytes along with IgM antibodies

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