I. 9.1: ANATOMY AND FUNCTION OF THE URINARY SYSTEM
A. SELECTIVE RESORPTION
1. PCT – location where most of the resorption occurs (most of water
a) Not very regulated
2. DCT and other parts of nephron– where the remaining resorption takes place
B. SECRETION
Most takes place in DCT and collecting ducts (this is also where many drugs are elminated)
C. CONCENTRATION AND DILUTION
DCT and collecting ducts; regulated by ADH and aldosterone
1. ADH – produced by posterior pituitary:
a) ↑ with low BP/BV to open water channels in DCT and allowing most of the water to be resorbed
b) ↓ with high BP and high plasma volume, leaving urine dilute
2. Aldosterone – produced by the adrenal cortex:
a) ↑ with low BP; causes increased resorption of Na+ by the DCT
(1) This causes increased plasma osmolality, increased thirst and increased water retention
(2) Also stimulated by angiotensin II, low serum osmolality
b) ↓ with high BP/BV, more Na+ is lost through urine
D. LOOP OF HENLE AS A COUNTERCURRENT MULTIPLIER
1. Descending limb: permeable to water, but not ions (water exits, filtrate becomes more concentrated)
2. Thin ascending limb: not permeable to water, permeable to ions which are lost from high-concentrated filtrate
3. Thick ascending limb: not permeable; actively transports salt into the surrounding tissue, making it very salty, causing the medulla to pull water out of the DCT when ADH opens water channels
E. VASA RECTA ARE A COUNTERCURRENT EXCHANGER
1. Blood in the vasa recta has high concentration of blood cells and proteins, which further sucks water from the medulla, keeping the medulla very concentrated and salty
II. 9.2: RENAL REGULATION OF BP AND pH
A. BP
1. JG cells (in afferent arteriole) are baroreceptors that monitor BP
a) They secrete renin, which catalyzes angiotensinogen → angiotensin I (which then gets converted to angiotensin II by ACE in lungs)
b) Angiotensin II is a powerful vasoconstrictor, also stimulates release of aldosterone
2. Macula densa (in distal tubule) – chemoreceptors that monitor filtrate osmolality in DCT; when osmolality ↓, this indicates ↓ GFR
a) These cells then stimulate JG cells to produce renin and also directly cause vasodilation of the afferent arteriole
B. pH
1. ↑ pH causes kidney to secrete bicarb in urine(made with carbonic anhydrase)
2. ↓ pH causes kidney to secrete H+ in urine
3. Note: this process takes days; compare to respiratory acid-base regulation, which is fast
III. 9.3: ENDOCRINE ROLE IN THE KIDNEY
| HORMONE | SOURCE | TARGET AND EFFECT |
| Aldosterone | Adrenal cortex | DCT: causes Na+ resorption and K+ excretion via formation Na+/K+ ATPases basolaterally; end results is higher Na+ osmolarity in blood, increased BV (through ADH) |
| ADH | Posterior pituitary | Distal nephron: makes it permeable to water, so water is resorbed, urine is concentrated; works with aldosterone to increase BV |
| Calcitonin | C cells (thyroid) | Bone, gut, kidneys: causes ↑ Ca++ deposition in bones, ↓ absorption in gut, and ↑ excretion in kidneys |
OVERALL: ↓ Ca++ in serumPTHParathyroidBone, gut, kidneys: opposite of calcitonin
OVERALL: ↑ Ca++ in serumEPOKidneysMarrow: increased RBC synthesis
IV. 9.4: THE DIGESTIVE SYSTEM – AN OVERVIEW
A. ENZYME OVERVIEW
1. Pancreatic lipase: 1 triglyceride → 2 fatty acids + monoglyceride
2. Ptyalin and amylase: polysaccharide → disaccharides
3. Brush border enzymes: disaccharides → monosaccharides
4. Gastric acidity/pepsin: polypeptides → dipeptides and tripeptides
5. Brush border peptidases: dipeptides and tripeptides → AAs
B. STOMACH EXOCRINE:
1. Gastric glands (parietal cells/chief cells): secrete acid and pepsinogen
a) Chief cells – pepsinogen (the chief likes to drink pepsi)
b) Parietal cells – acid, intrinsic factor (if you get splashed with acid, you will intrinsically be a pariah)
c) Goblet cells: secrete mucus
V. 9.5: DIGESTIVE SYSTEM
A. MOUTH – 3 FUNCTIONS
1. Fragmentation – mastication
2. Lubrication – saliva
3. Some digestion (no protein digestion in mouth)
a) Ptyalin (salivary amylase) – breaks down some starches into disaccharides
b) Lingual lipase – some fat digestion
c) Lysozyme – bacterial cell wall breakdown
B. ESOPHAGUS
C. STOMACH – 3 FUNCTIONS
1. Partial digestion of food
a) Acid – HCl is secreted by parietal cells; this hydrolyzes some polypeptides and activates pepsinogen
(1) Parietal cells also secrete intrinsic factor, necessary for B12 absorption
b) Pepsin – secreted by chief cells as pepsinogen before it is activated by HCl; breaks down protein (chief cells are stimulated by histamine to release this)
c) Gastrin – hormone secreted by stomach wall in response to food in stomach; causes HCl secretion, pepsinogen secretion, and gastric motility
2. Regulated release of food into small intestine
a) Motility – forms chyme
b) Sphincters
3. Destruction of microorgansims
a) Low pH
D. SMALL INTESTINE
1. Anatomy – surface area most important
a) Villi
(1) Contain capillaries that absorb monosaccharides and AAs
(2) Contain lacteals that absorb cholymicrons (in lymphatics), then reach bloodstream through the thoracic duct
b) Peyer’s patches – areas of lymphocytes scattered throughout small intestine
c) Duodenum – first portion of the small intestine, part of digestion and first part of absorption occurs here
(1) Enzymes in duodenum:
(a) Enterokinase is secreted, activates tripsynogen → tripsyn (from pancreas)
(b) Brush border enzymes
(2) Hormones in duodenum:
(a) CCK – secreted in response to fat in duodenum; causes pancreas to secrete enzymes, GB to contract, and stomach to slow motility
(b) Secretin – secreted in reponse to acid in duodenum; causes pancreas to release bicarb and water, neutral or slightly basic outcome
(c) Enterogastrone – ↓ stomach emptying
d) Ileum and Jejunum– last portions of small intestine; absorption of the rest of the stuff
E. COLON
1. Absorbs water and minerals
2. Colonic bacteria produce vitamin K and keep colonization of harmful bacteria at bay
VI. 9.6: GI ACCESSORY ORGANS
A. EXOCRINE PANCREAS – controlled by CCK (stimulates enzymes) and secretin (stimulates bicarb)
1. Amylase – polysaccharides → disaccharides
2. Lipase – hydrolyzes triglycerides at the surface of micelles
3. Nucleases – hydrolyze DNA and RNA
4. Proteases – polypeptides → di and tripeptides
5. Trypsin – activates other pancreatic enzymes (carboxypeptidase, collagenase)
B. ENDOCRINE PANCREASE
1. α cells – secrete glucagon
2. β cells – secrete insulin
3. δ cells – secrete somatostatin
C. BLOOD SUGAR REGULATION
1. ↓ BGL → insulin only
2. ↑ BGL → glucagon, epinephrine, cortisol
D. LIVER AND GB
1. Bile – made of cholesterol and bile salts, emulsifies fat
2. Hepatic portal system – liver receives deoxygenated blood draining from stomach and intestines; takes out and processes nutrients
3. Nitrogenous waste – liver converts toxic ammonia to urea
4. Production of cholesterol – liver takes up the cholymicron remnants and makes cholesterol
5. Plasma proteins – clotting factors, albumin, globulin, fibrinogen are all made in liver
6. Detoxification – smooth ER of hepatocytes convert toxins into less toxic products
VII. 9.7: A DAY IN THE LIFE OF FOOD
A. CARBOHYDRATES
1. Mouth – ptyalin hydrolyzed some starches
2. Stomach – acid kill microorganisms, hydrolyzes some polysaccharides
3. Duodenum – amylase breaks down polysaccharides into disaccharides, brush border enzymes further break these down into monosaccharides
4. Absorption – large, hydrophilic monosaccharides are taken up by secondary active transport (goes with sodium ion flow); once the cells have high monosaccharide concentration, they flow out with facilitated diffusion into nearby capillaries
5. Storage – liver picks up these molecules and stores them for energy
B. PROTEINS
1. Mouth – chewing, but no digestion
2. Stomach – acid and pepsin hydrolyze peptide bonds
3. Duodenum – chyme is released into duodenum and stimulates release of CCK and secretin, which in turn causes GB to release bile and pancreas to release bicarb and other enzymes (trypsinogen is activated to trysin by enterokinase, which then activates other enzymes); these work on the tuna until all that is left are di- and tripeptides, which are hydrolyzed to AAs by brush border enzymes
4. Absorption – secondary active transport pulls cell in, the facilitated diffusion brings it out into capillaries
5. Storage – similar to carbohydrates
C. FATS
1. Mouth – a little lipase helps start digestion
2. Stomach – nothing really happens since they are hydrophobic and float above acid
3. Duodenum – fat stimulates CCK release → bile release, which emulsifies fat; CCK also stimulates pancreatic enzymes, which hydrolyze fat to monoglycerides and free fatty acids after it is broken up into micelles
4. Absorption – these freely diffuse into cells, where they are turned back into triglycerides, organized into cholymicrons, and travel via lacteals and the lymph system to finally reach the bloodstream
5. Storage – picked up by liver and adipose tissue (both have lipoprotein lipase), which breaks triglycerides back down into monoglycerides and free fatty acids
VIII. 9.8: VITAMINS
| Vitamin | Function |
| fat soluble | |
| A (retinol) | Visual pigment which changes conformation in response to light |
| D | Stimulates Ca++ absorption from the gut; helps control Ca++ deposition in the bone |
| E | Prevents oxidation of free fats |
| K | Necessary for formation of clotting factors |
| water soluble | |
| B1 (thiamine) | Needed for enzymatic decarboxylations |
| B2 (riboflavin) | Made into FAD, electron transporter |
| B3 (niacin) | Made into NAD+, electron transporter |
| B6 (pyridoxine) | A coenzyme involved in protein and AA metabolism |
| B12 (cobalamin) | A coenzyme involved in the reduction of nucleotides to deoxynucleotides |
| C (acsorbic acid) | Necessary for collagen formation |
| Biotin | Prosthetic group essential for the transport of CO2 groups |
| Folate | Enzyme cofactor used in the transport of methylene groups; synthesis of purines and thymine; required for development of normal fetal nervous system |
