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regulate extracellular fluid volume & therefore BP
maintain ion balance
homeostasis of pH
cup-like sac at beginning of tubular nephron part where glomerulus filters. together with glomerulus is called renal corpuscle
glomerulus is inside, capillaries are permeable and some blood contents seep into tubules starting with bowman’s caprule - together renal corpuscle
filtered from blood, passes proximal tubule, descending and ascending limbs loop of henle, distal tubule and finally to collecting duct - as flow continuing exhange with blood - morefiltering and giving back to blood.
from proximal tubule down
always active tnspt - prox tubule, distal tubule and collecting duct: important in homeostatic of K+ and H+ (narrow range is importnant) (kd second line of pH modulation after respiratory), clearing metabolites of drugs, etc
includes OAT: organic anion transporter
amt filtered - reabsorbed + secreted = excreted
some things not filtered, some things filtered then reabsorbed, some things filtered and further secreted, etc.
throughout tubule starting in bowmans
transfer of soluable components like water and nitrigenous waste from blood to glomerulus and into bowmans capsule. 20% filtration fraction. NOT: cells, plasma proteins
hydrostatic pressure of blood dominant factor (push stuff out of glomerulus and into capsule) but opposed by osmotic pressure and pressure in tubular system
glomeruli filtration rate (GFR): measured to assess kd function
hydrostatic pressure of blood dominant factor (push stuff out of glomerulus and into capsule) but opposed by osmotic pressure stuff into blood, some fluid pressure of stuff in bowmans capsule already but will be lower
BP control IN kd (areterioles leading into nephron) is tighter than in overall body so blood pressure shouldn’t affect filtration. would have to be SEVERE blood pressure change (this causes kd damage)
surface area of glomerular capillaries and permeability between capillary and bowman’s capsule
throughout tubule starting in proximal tubule
lots of water (vast majority).
active or passive transport depending on what is transported and how
Na gradients drive chloride and water absorption. glucose too: active tnspt into. Na attracts negative anions. na+anions increases osmolarity and attract water.
water is ALWAYS passive. only EVER osmosis, down concentration gradient.
active (esp prox tubule): is driving force for reabsorption mof most other stuff.
can attract negative anions to sodium concentration - gradient attract water (b/c increased osmolarity)
channel/ passive tnspt going into cell out of tubule but into intersitial fluid active transport
gradient drives reab anions, water & glucose
tubule epithelium uptake glucose requires active transport - couples to passive tnspt of sodium (2ndary active tnspt), to get into intersititial fluid is passive glucose transport. normally little to no glucose present in urine HOWEVER uncontrolled diabetes mellitus. there is MAXIUMUM reabsorption limited by active transport into epithelium cells - if too much glucose some will get into urine.
transfer of hydrogen ions, creatinine and drugs from blood into collecting duct
happens in prox tubule, distal tubule & collecting duct: ALWAYS active transport
key for: balance of K+ and H+ (pH), metabolites of drugs/ foreign substances.
secretion organic anions
will trigger increase vaso constriction and cariac output. often trigger thirst (to increase volume), act on kd to conserve water/ minimize volume loss, opposite if high BP
more osmolarity in medulla. loop henle, descend more water into kd, ascending less so ions out of tubules. collecting duct fine adjustment, control permeability collecting duct to water and ions. mediated by hormones
gonads and adrenal cortex - adjust sodium reabsotpriton
low BP activate adrenals to release aldosterone to act on P cells
p cell (principle): influence gene transcription - increase expression protein channels/ pumps to overall Na/ K pump, reabsorption Na and secretion K
atrial natiuretic peptide and brain np: induced by increased blood volume. myocaridal stretch increase releases both types.
act on multi targets to oppose atII, vasopressin, aldosterone, decrease sodium reabsorption etc
. decrease sympathetic and therefore BP
recieve from proximal tubule, descending limb permeable to water but not ions/ salt so functions to concentrate, ascending permeable to ions/salt but NOT water
3 external layers: renal fascia (outermost), perirenal fat capsule, renal capsule (inner most layer)
cortex it outer region of kidney between renal capsule and medulla - glomeruli and proximal and distal tubules
medulla: innermost region, pyramid structures (renal pyramids seperated by renal columns that contain blood vessels) consisting of collecting tubes, Henle’s loop, vasa rectae, venulae rectae and medullary capillary plexus
Antidiuretic hormone (ADH), which is produced by the pituitary gland, controls the amount of water that is reabsorbed through the collecting ducts.
When blood is more concentrated (e.g. during dehydration), more ADH is secreted allowing more water to be reabsorbed by upregulating aquaporins on collecting duct
determined by serum creatinine. determined by decreased GFR. with failure there will be increased fluid in body (cause edema), increased acid, increased phosphate, later stage can be anemia and bone issues. imparts increased CVD risk
leads to waterloss/ dehydration - osmotic diuresis. the renal threshold of glucose (RTG) is how much can be in blood before begins to be excreted in urine (160-180 mg/dl)
protenuria causes edema! nephrotic syndrome when 3+ g albumin/ 24hrs (plus hyperlipidemia, hypoalbuminemia and edema). - indicates damage to Kd - protein should not be able to GET into urine
Albumin constitutes about half of the blood serum protein.
chemically diverse. adverse effects: hypovolemia, hypokalemia, hyperkalemia, metabolic alkalosis, acidosis & hyperuricemia
thiazide: effect distal tubule & inhibit Na/ chloride symporter-> water ret in urine
loop : cause high volume diuresis - inhibit sodium reabsorption
positive if urine is more dillute than plasma
fluid-deficient, sensed by osmoreceptors, -> increased secretion of ADH ->fluid retained and urine output to be reduced.
aldosterone A mineralocorticoid hormone, secreted by the adrenal cortex, that reg the balance of sodium and potassium in the body.
ADH: increases water absorption in the collecting ducts of the kidney nephron.
hypotonic/ hyponatremic: caused by loss electrolytes esp sodium. causes intravascular water to shift to extracellular space
Hypertonic/ hypernaturemic: from water loss
isotonic/ isonaturemic: loss of both water and electrolytes - most common in people
sx: headache, low BP, dizziness (orthostatic hypotension)
Any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes.
hydrostatic pressure generated by the heart pushes water out of the capillaries. The water passes from a high concentration outside of the vessels to a low concentration inside of the vessels, but equilibrium is never reached because the constant blood flow. removed through the surrounding lymph vessels, and eventually ends up rejoining the blood.
defines the forces across a semipermeable membrane and allows calculation of the net flux. The solution to the equation is known as the net filtration or net fluid movement.
increased blood/ tissue acidity (arterial pH below 7.35 is dxable). it's the process that leads to acidemia. can be due to increased production of metabolic acids or decreased renal excretion.
lungs compensate for metabolic by increasing exhalation of CO2.
Respiratory acidosis is due to increased CO2 in blood usually from hypoventillation, bicarbonate may be normal or increased.
increased alkalinity of blood/ tissues (pH above 7.45). can be respiratory (from hyperventilation and resultant loss of CO2) or metabolic (often due to prolonged vomiting reducing hcl in st). could also be diuretics, dehydration, endocrine disorders or alkali consumption.
retained by rennin-angiotensin-aldosterone system (atrial peptide causes sodium loss)
release renin, which turns angiotensinogen into angiotensin which is converted to angiotensin II.
Angiotensin II causes constriction of blood vessels and inc sodium retention by effect proximal renal tubule and through causing synth/ release of aldosterone (acts on the sweat ducts and colonic epithelium to conserve sodium)
loss of sodium by the kidneys: it is secreted from the heart in high sodium states due either to excess intake or cardiac disease. Elevated blood pressure will also tend to cause Na+ loss and a low blood pressure usually leads to sodium retention.
most of body potassium is in cells, next largest is bones.
ca absorption controlled by vit D, excretion controlled by parsthyroid hormones.
3 forms: ionized, nonionized, protein bound
kidneys maintain pH homeostasis through excretion of waste products.
Acidosis causes more bicarbonate to be reabsorbed from tubular fluid while collecting ducts secrete more hydrogen to generate more bicarbonate; and more NH3 buffer is formed.
Alkalosis causes the kidney to excrete more bicarbonate as there is reduced secretion of hydrogen ions and more ammonium is excreted.
Place the following blood vessels that carry blood to and within the kidney in the order in which blood passes through them.
1. afferent arteriole
2. efferent arteriole
4. peritubular capillary
- a series of straight capillaries in the medulla. They lie parallel to the loop of Henle. branch off the efferent arterioles of juxtamedullary nephrons (closest to the medulla), enter medulla, & surround the loop of Henle.
- very slow rate, help countercurrent exchange that prevent washout of the concentration gradients established in the renal medulla.
- descending portion NaCl & urea reabsorbed into blood, water secreted. Ascending portion NaCl & urea are secreted into interstitium, water is reabsorbed.
- afferent arteriole feeds into
- portal system: first capillary bed is glomerulus, goes to
- efferent arteriole,
- second capillary bed is peritubular capillaries
- then venules
ADH: increases renal water absorption
Aldosterone: increases NA reabsorption and K secretion
Angiotensin II: increases ADH and Aldosterone secretion, increases BP via cardiovascular effects, increase thirst
natriuretic peptides: increases GFR, decrease Na reabsorption & decrease vasopressin & angiotensin II
Main Action: collecting duct permeability to Na (steroid from adrenal cortex - made on demand)
low BP, activate RAS pathway to cause release aldosterone to act on P cells
@ P-Cell: Aldosterone combo w/ int cell receptor, travel to nucleus & influence transcritpt/ tnslt of protein channel & pumps inc na/k atpase & other for increase Na reabsorb and increase secretion of K
high extracellular potassium: refelx adrenals to produce b/c aldosterone is potassium wasting
RAS: renin from kd (smooth muscle around afferent arteriole - control gfr - renin in proportion to amt of constriction) - renin turins ATG( made by liver) -> ATI (ACE tns to) -> ATII Stim production and release of aldosterone
act on brain to cardio response,
act on hypothalamus to thirst and ADH,
act on prox tubules to help aldosterone absorb sodium to increase bp/bv
(posterior pituitary) act on collecting duct to control amt aquaporins (no aquaporins - osmolarity max dilute).
ADH present in blood, flow through esp vasa recta capillaries, diffuse into intersitial fluid and work on ADH receptors on surface of collecting duct cells, activate second messenger act throu cAMP, translocate storage vesicles to transfer aquaporins into membrane
Stim for synth/ release ADH
decrease BP: baroreceptors arteries - sensory neuron to hypothalamus
decreased artial stretch: sensory neurons to hypothalamus
increased osmolarity: hypothalamic osmoreceptors, interneuron to appropriate
- Other factors: surface area of glomerulus (#capillaries) and premeability between capillary and bowmans (both should be unchanging normally) - kd problems can effect these
organic anion transported: tertiary indirect active tnspt (powered by Na concentration low in cell, sodium dicarboxylate pump, dicarboxylate passive tnspt coupled to active inport of organic anions into cell. from there can passive diffuse into tubule lumen (penicillin cleared by OAT, used to collect urine and reextract penicillin, but found another chemical that competes for binding with OAT )
Describe the tubular elements of the nephron
glomerulus (capillary bed) seeps into in bowman’s capsule (first part of tubules), filtrate pass through proximal tubule, descending and ascending loop of henle, to distal tubule and collecting duct. ongoing exchange with blood specifically the peritubular capillaries.
Suggest two possible mechanisms to explain why the kidney would excrete excess glucose, and what abnormality may underlie those conditions.
- in the case of diabetes, the amount of glucose in the blood exceeds the tubular maximum for glucose.amt in glomerular filtrate is more than can be absorbed as the filtrate passes through the proximal tubule where glucose reabsorption takes place.
- impairment in the body's ability to reabsorb glucose. as in renal glycosuria - tubules are unable to properly reabsorb glucose from the filtrate despite otherwise normal blood glucose and kidney function.
- glucose is unable to get into the cells so lots in blood.
- if the level of glucose in the blood climbs above the renal threshold for glucose some will be excreted in the urine. (inititally in filtrate but if healthy all will be absorbed in proximal tubule)
- This causes osmotic diuresis, (concentration of glucose leeches water out of the blood into urine). This causes more water to be excreted than should have been, leading to polyuria and dehydration.
Diabetes mellitus produces ketoacidosis, which results from excessive accumulation of by-products of fat metabolism, as the body cannot meet energy needs from carbohydrate metabolism. Sally is a teenaged diabetic not taking her insulin. Her mother takes her to the hospital because her breathing has become deep and gasping. Explain. What other compensatory responses may occur, and would they occur earlier or later than the respiratory response?
Her breath is deep and gasping because the primary way that we regulate pH is through respiratory regulation of CO2 concent in blood. She is breathing that way because her body is attempting to exhale maximum CO2. She may also be using the secondary renal compensatory mechanisms like tubular cells reabsorbing more bicarbonate, collecting duct cells secreting more hydrogen and generating more bicarbonate.
Calculate the body mass index of a woman who is 5'5" tall and weighs 180 lbs. Now calculate the BMI of a man with those dimensions. 1 kg = 2.2 lbs, 1 m = 39.24 in. Is either individual considered obese? Explain. Could BMI be misleading as a means of indicating obesity? Explain.
BMI is lb/(height in inches squared)
BMI calculations do not consider age, gender, frame size, muscle mass, or fat distribution (visceral vs distributed).
- mostly borken down into aminos which can be take up into lumen cells by cotransported with sodium for both steps.
- some proteins into di and tri peptides - co transported with hydrogen ions (then cotransported with NA),
- peptides may stay of get further broken down in epithelial/ lining cell.
- More rare - proteins into large peptide (7-9 aminos) too big for tnspt so cross cell in trans cytosis
animal - heme taken through facilitated diffusion, broken into porforin ring and iron ions,
plant source: active tnspt iron - hydrogen cotransport then either type exported into extracellular fluid by ferroportins - regulate how many ferroportins present controls absorption of iron depending on needs
paracellular pathway between enterocytes and go directly into interstitial. most taken up by enterocytes - low concnetration inside like all so tnspt is passive. export on basolateral side ca regulated via a vitamin d regulated pathway
through si and li. sodium and chloride - lots of tnspts throughout (cl passive out of cell, sodium active tnspt out of cell), presence of ions attract water and potassium through paracellular pathway (between enterocytes) potassum going down concentration gradient, water attracted by sodium and chloride concnetration
process of homeostasis over caloric intake and output through work and heat production. change expenditure and appetite depending.
regulation of feeding/ energy balance theories
glucostatic theory: most important stim is blood sugar - glucose sensing neurons in hypothalamus
lipostatic theory: fat stores regulate eating - adiposcytokines produce hormones
Leptin: member of cytokine. more fat tissue -> more leptin. 1st adipocytokine discovered
BOTH are true and other stuff too
heat input: internal (metabolism, skeletal muscle contraction) and external heat production (sun etc)
heat output: evaporative heat loss, other heat loss
unregulated: heat is byproduct - muscle contraction (voluntary) normal metabolism
reg heat production: shivering and maybe non-shivering thermogenesis (brown fat) -
fed: insulin rise, glucagon goes down. insulin increases uptake nutrients by cells. use glucose, make glycogen for storage, store triglycerides, increase protein synthesis
plasma glucose levels - more means more insulin (pancreas and hypothalamus sense glucose levels)
plasma amino acids (like glucose)
feed forward of gut hormones inc GLP 1 - make insulin go up in response to stomach stress before nutrients get into blood
parasympathetic activate insulin secretion
sympathetic activity suppress insulin sensitivity
Esophagus: the fibromuscular tube through which food passes, aided by peristaltic contractions, from the pharynx to the stomach.
Stomach: secretes protein-digesting enzymes called proteases and strong acids to aid in food digestion, before sending partially digested food to the small intestines.
Duodenum: the first section of the small intestine and may be the principal site for iron absorption.
most of the small intestine and all of the large intestine . According to some sources, it also includes the anus.
Duodenum: juices from pancreas (enzymes) and GB (bile) mix together. enzymes break down proteins and bile emulsify fats into micelles. bicarbonate from Brunner's glands and pancreatic juice neutralize hydrochloric acid CHEMICAL DIGESTION
Jejunum:ABSORPTION. contains plicae circulares & villi to increase surface area
Ileum: Has villi, where all soluble molecules are APSORBED into the blood (capillaries and lacteals).
Cecum: appendix is attached to the cecum.
Colon: Includes the ascending colon, transverse colon, descending colon, and sigmoid flexure. The main function of the colon is to absorb water, but it also contains bacteria that produce beneficial vitamins like vitamin K.
supports abdominal organs and conducts blood, lymph vessels and nerves.
2 layers: outer (parietal) attached to abdominal wall and inner (visceral) wrapped around internal organs
space between filled with serous fluid so cal slide freely
exocrine cells, ducts arranged in clusters (acini). filled w/ secretory granules of inactivated enzymes, mainly trypsinogen, chymotrypsinogen, pancreatic lipase, & amylase, secreted acini lumen
also bicarbonate ions from the ductal cells to neutralize the acidic chyme
exocrine function of the pancreas is controlled by the hormones gastrin, cholecystokinin, and secretin
bile can directly SI via CBD or be stored in GB.
major role in metabolism: glycogen storage, plasma protein synthesis, and drug detoxification.
portal system connect digestive system capillaries to lv capillaries - nutrients go ht for distribution).
lv is 70-80% hepatocyte (rough ER & ribosomes- so can protein synth, store, carb tns, cholesterol synth, bile salt synth & phospholipid synth)
stores bile - muscle wall contracts to release bile in response to cholecystokinin (peptide hormone from SI)- emulsifies fat and neutralized acid. connected to the liver and the duodenum by biliary tree.
gallbladder is connected to main bile duct through the cystic duct, which connects to duodenum. The cystic duct serves as an entrance and exit to the gallbladder. divided into fundus, body and neck
lined w/ mucus membrane & juice secreting cells
2 smooth muscle sphincters (cardiac and pyloric)
cardiac region: esophagus enpty into the stomach
fundus: upper curve
body: main/ central region
pylorus/ atrium: lower part, empties into SI
kills most of the bacteria in food, stimulates hunger, and activates pepsinogen into pepsin; and denatures the complex protein molecule as a precursor to protein digestion.
secretin diminishes stomach acid secretion
inhibited by somatostatin
is in the duodenum and signals the secretion of sodium bicarbonate in the pancreas and it stimulates the bile secretion in the liver.
is in the duodenum and stimulates the release of digestive enzymes in the pancreas and the emptying of bile in the gall bladder.
(or duodenal glands) are compound tubular submucosal glands found in that portion of the duodenum which is above the hepatopancreatic sphincter (Sphincter of Oddi). produce a mucus-rich alkaline secretion (containing bicarbonate) in order to neutralize the acidic content of chyme. alkaline condition for optimal intestinal enzyme activity, thus enabling absorption to take place, and lubricate the intestinal walls
Patches of lymphoid tissue or lymphoid nodules on the walls of the ileal-small intestine. immune surveillance system of the intestinal lumen and facilitating the generation of the immune response within the mucosa.
li absorb products like short fatty acids, vits & fiber.
vitamin K, biotin, b12, thiamine, riboflavin
train immune system
prevent bad bacteria growth
regulate gut development
produce some fat storage hormones
cephalic phase: gastric secretion begin think food
Gastric phase: swollowed food, stretch stomach & raise pH-> release hcl. and other stuff
intestinal: response arrival of chyme (moderates gastric activity via nervous and hormone)
acid trigger inhibitory signals to the stomach
Gastric inhibitory peptide (GIP) -
connections of carb, protein and lipid energy pathways:
cholesterol and tryglycerides are the fats that can enter pathways of glucose catabolism
synthesis of cholesterol starts with actyl groups from actyl CoA and goes only one way so must have glucose metabolism to make cholseterol
triglycerides can be made or broken down in glocose catabolism pathways
There is only one way to lose weight without actually removing a body part: consume fewer calories than you expend. Is this statement true or false? Explain, citing a fundamental law of physics. Why is it difficult for many people to lose weight? Many weight-loss gimmicks work. Explain why they work, and why they may not work forever.
The law of conservation of energy -energy can neither be created nor destroyed. So the only way to lose weight is to take in less energy than you expend and use some of the stored energy. It would be more difficult to lose weight if you have a low metabolic resting rate, that is if your basic body functions expend less energy than average. Similarly, someone with an efficient metabolism would burn fewer calories to do the same work so exercise would be less effective at leading to weight loss.
high-density lipoproteins (HDLs).
Which of the following is the sequence of layers from the lumen to the outer wall of digestive tract?
A) mucosa, submucosa, serosa, muscularis externa
B) serosa, submucosa, mucosa, muscularis externa
C) submucosa, muscularis externa, serosa, mucosa
D) submucosa, mucosa, serosa, muscularis externa
E) mucosa, submucosa, muscularis externa, serosa
E) mucosa, submucosa, muscularis externa, serosa
creating glucose from glycerol, amino acids, or lactate
sweating and dilation of cutaneous blood vessels.
spontaneous cycles of depolarization and repolarization.
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