Physiology Exam 3

anskorczewski12's version from 2016-04-14 15:20

Section 1

Question Answer
Renal Processes: 1.glomerular filtration (20% nondiscriminant of protein-free plasma) 2.Tubular reabsorption (selective) 3.Tubular secretion (selective)
renal corpusglomerular capillaries and bowman's space
kidney layers1.renal cortex (has renal corpuscle & convoluted tubules) 2.renal medulla (has renal pyramids, juxtamedullary nephrons, collecting ducts)
types of nephrons1.juxtamedullary (20%, long loops, generate gradient in medulla for diluting urine, has vasa recta) 2.cortical (short/no loops, do not contribute to hypertonic medullary interstitium)
vasa rectaperitubular capillaries branch into this around juxtamedullary loops of Henle
three layers for glomerular filtration1.capillary endothelium/glomerular cap. wall (single layer, many large pores) 2.basement membrane (neg. charge so repels proteins) 3. Bowman's epithelium (has podocytes that can contract)
podocytespart of Bowman's Epithelium that wrap around glomerular blood vessel and create pathway for fluid leaving glomerular capilarry into capsule (can open/close pores)
regular GFR125 mL/min
Starling fores in filtration1. glomerular capillary bp (favors filtration, exerted from blood force&resistance to flow) 2.plasma-colloid osmotic pressure (opposes filtration, unequal plasma protein across membrane-H20 wants in) 3.Bowman's capsule hydrostatic pressure (opposes, fluid pressure from Bowman's space fluid
justaglomerular apparatuscomposed of 1.granular cells (on affarent arteriole, sense bp by stretch&constrict) 2. Macula densa (on distal convoluted tubules, detect salt level and release ATP to constrict afferent arteriole)
sympathetic input on filtration: contract mesangial cells (on glomerular membrane) to decrease surface area of afferent arteriole/GFR), causes renin secretion from granular cells

tubular reabsorption

Question Answer
possible routes for reabsorption (99% is reabsorbed)1. luminal membrane to basolateral membrane to renal interstitial fluid to peritubular capillaries 2.tight junctions(vary by region) to renal interstitial fluid to peritubular capilalries
reabsorption modes: 1.diffusion (if lipid soluble, doesn't need carriers, small, nonpolar) 2.mediated transport (large/charged, glucose)
Na+ reabsorption65% in proximal tubules (not regulated, symport transport with other nutrients from lumen into the cell, pump in basolateral mem. makes gradient so Na comes in), 25% in ascending limb (nonregulated), 10% distal and collecting duct (regulated, channels from aldosterone in luminal mem. allow Na in, and is NOT directly coupled to water reabsorption-that depends on vasopressin)
aldosterone rolebuilds Na channels and Na/K pumps in distal/collecting tubes (when Na load in body is low)
routes for water reabsorption1.paracellular (between cells in leaky tight junctions, main water route in proximal tubules, non-regulated) 2. transcellular (through aquaporins, main water route in distal/collecting duct, requires aquaporins regulated by vasopressin)
renin-angiotensin-aldosterone systemregulates Na amount (granular cells secrete renin in blood, renin activates angiotensinogen (from liver), becomes angiotensin I which becomes angiotensin II by ACE in lungs, which stimulates secretion of aldosterone/constricts arterioles to increase BP, stimulates thirst, and stimulates vasopressin)
ways to trigger reningranular cells sense stretch in afferent arteriole, macula densa sense low Na, sympathetic input sense low BP)
to produce more excretion of NaAtrial natriuretic peptide (ANP-made in atrial cells) or brain nutriuretic peptide (BNP-made in ventricles) both released when heart stretched to inhibit Na reabsorption (inhibit renin secretion and aldosterone and vasopressin and increase GFR with dilation of arterioles and constrict efferent arterioles)
glucose and amino acid reabsorptionin prox. tubules by secondary active transport, symport carriers with Na across luminal membrane then passively diffuse into plasma (limited because need transport carriers)
renal thresholdplasma concentration where max. reabsorption is reached and substance begins to get excreted
countercurrent multiplicationestablishes required gradient (fluid becomes progressively more concentrated down descending limb and more diluted up ascending limb); used to concentrate fluid so urine is more concentrated than body fluids (and more dilute)
vasopressin mechanism(when low BP from low stretching) binds with receptor on basolateral membrane (g-protein coupled) activates cAMP pathway, increases permeability of luminal membrane by inserting aquaporins (only in distal and collecting ducts)

tubular secretion

Question Answer
tubular secretionforeign chemicals and toxins (H+ in all tubules and K+ in distal tubule), usually involves active transport coupled with Na reabsorption,
increased K levels(in distal tubules, K leaky channels in luminal membrane make K secretion; in prox. tubules, K leak channels on basolateral mem to put back in ECF) increases aldosterone(increase Na)
renal plasma clearancevolume of plasma completely cleared of that substance by kidneys per minute (urine conc. X urine flow rate / plasma conc. of the substance) -shows how efficient kidneys are
H+filtered and secreted (GFR is smaller than RPC)
glucose and ureafiltered and reabsorbed (RPC is smaller than GFR)
inulin and creatinefiltered ONLY (GFR = RPC)


Question Answer
to increase bpsecrete renin (angiotensin II reabsorbs more Na, triggers thirst, constricts arterioles,stimulates vasopressin),
diabetes insipidusfailure to release vasopressin or failure of kidney to respond to vasopressin (more water loss)
diabetes mellitusfailure to reabsorb glucose (glucose in urine causes water to be not reabsorb)
Conn's syndrometumor on adrenal cortex secretes unregulated aldosterone (high BP from more water retention), lower renin (from high BP and high stretch), slightly higher urine output (vasopressin still triggered by osmolarity of blood, but lower than normal), lower K levels (increased secretion)
dehydration(hypertonicity of ECF) from low water intake 2.excessive water loss 3.diabetes insipidus (deficiency in vasopressin) [lowers bp]
overhydration(hypotonicity of ECF) from renal failure (can't excrete dilute urine), rapid water ingestion, inappropriate vasopressin secretion
Carbonic Acid Buffering SystemCO2 + H20 = H2CO3 = H+ + HCO3- (bicarbonate)
respiratory acidosislungs fail to eliminate CO2 (hyperventilation-shallow fast breaths) happens in respiratory diseases (renal response is increase H secretion and excretion, increase bicarbonate reabsorption, no bicarbonate excretion, acidic urine)
metabolic acidosis(causes are severe exercise, hypoxia, fasting, diabetes)
respiratory alkalosishyperventilation (too much CO2 out) fast/deep breaths (from fever, anxiety, high altitude) (renal response is to decrease H secretion, excretion, bicarbonate reabsorption, and increase bicarbonate excretion, alkaline urine)
metabolic alkalosis(persistance vomiting/ loss of H+)

respiratory system

Question Answer
collapsed lungatelectasis
air in the chestpneumothorax
how much air is left after quiet exhalefunctional residual capacity
flow of airP(alv.)-P(atm) / resistance
compliancehow much effort required to stretch (change of lung volume based on change in transmural pressure gradient), which high, stretches more; fibrous tissue decreases this/emphysema increases)