anatomy 2 Flashcards
kidneys
Wilms’ tumor
kidney tumor assoc. with aniridia
kidney functions
acid base balance, controling Na (&H20) excretion and thereby also controling BP, eliminate waste like urea, uric acid and creatinine, PRODUCE erythropoietin and vitamin D3, degrade insuline and PTH
what % of body weight is water?
60%
what % of body weight is INTRA-cellular
40%
what is in EXTRA-cellular body fluid?
20% and has interstitial fluid, plasma, transcellular, NaCl and NaHCO3
what is macula densa and where is it?
MD monitors fluid composition @ tubular lumen at the JG apparatus (in front of Lacis cells)
what are lacis/ extraglomerular mesanglial cells?
they lie behind macula densa layer at the entrance near Bowman’s capsule–transmit info from macula densa to the granular cells
what are granular cells? aka JG cells?
smooth muscles with epi appears @ AFFERENT arteriole near glomerulus–synthesize renin (vasoconstrictor when low BP)
when do JG cells produce renin?
beta-1 adrenergic stimulation, JG detected low renal perfusion P-meaning when there’s low fluid P at JG, and low NaCl re-absorption by the macula densa due to a low GFR
what is the equation for urine formation?
excreted: filtered - reabsorbed + secreted
what is the quation for renal clearance in word form?
clearance= (urine concentration * flow rate) / plasma concentration—measured in RATIO to clearance of INULIN (same as GFR)
what does it mean to have a LOW clearance? less than 1
low Clearance ratio= need MORE of it in the body= increase reabsorption of product
why do we use inulin for GFR clearance? what’ a normal value?
inuline= fructose polymer that just stays in the tubule and goes to pee, nontoxic and normal= 110-125mL/min
what is GFR?
rate at which plasma is filtered (out into bowman’s and into Prox. tubule) by the glomeruli
what is creatinine? how’s it related to GFR?
from creatine phosphate and is always stable in blood unless there’s disease. has INVERSE relationship w/ GFR
what does high creatinine clearance in pee mean?
good, efficient kidneys! they are working well to maintain stable plasma creatinine levels. low PLASMA creatinine= good filtration= high GFR!
name something that should NOT be in urine?
glucose, protein, AA, RMC, WBC, bilirubin, ketones (acidosis)
what is glucose TH for diabetics?
over 200+mg in pee= diabetic
what type of diabetes is likely in someone with ketones in their urine?
type 1
what is bilirubin?
yellowing in brusing, from break down of blood. Usually means liver problem, but can be in newborns who are making too much RBC and liver is killing off the excess so there’s increase in bilirubin–that’s normal
what % of cardiac output goes to renal blood flow? what is that in L/min?
20% – 1.2L/min
assuming HIGH BP, what is the myogenic mechanism?
Ca channels open and contract smooth vessel walls which decrease the diameter= vaso-CONSTRICTION= increases resistance to “brace” for the high BP
assuming HIGH BP, what is the tubuloglomerular feedback?
highBP= higher GFR to help get rid of some fluid to decrease the P. This happens with ATP released @ macula densa via adenosine release—a vasoconstrictor at the local level (also stops reninproduction which is for low BP)
what are some vasoconstrictors?
renin during low BP, adenosine during high BP, angio2 @ lungs, thromboxane for hemostatis, vasopressin
what are some vaso-dilators?
dopamine when happy/relaxed, histamine, prostaglandins, kinins
what do the JG cells have that allow it to control what goes in/out? how?
has podocytes w/ food processes on the VISCERAL layer that work with endo. fenestrations/pores (RBC’s can’t leave cuz of this). slit membranes on the apical side facing Bowman’s Space prevent mid-size proteins leaving, Basal lamina (middle layer, BM) prevents large proteins from leaving
what is the net filtration P? and what are the average values in and out?
net= 10mmHg, with 55= capillary P pushing OUT, and P of bowman’s + colloid osmotic P pressing ON capillaries= 45—55-45=10
what is filtration fraction?
% of plasma flowing through the kidney’s that’s filtered–20%
what is going OUT of prox tubule and into the prox. cells to be reabsorbed to blood?
NaCl w/ water passively following, bicarbonate, glucose, AA, proteins, phosphate, Cl (exchanging base)
@ prox. tubule, what’s going out of cell and INTO BLOOD ultimately?
Na (via Na/K ATPase pump), K& water passively, glucose, AA, P, Cotransport: Cl&K, Na & HCO3
what’s going OUT from blood into urine @ prox. tubule?
H+ and base
what’s an INHIBITOR @ prox. tubule? what will decrease reabsorption?
carbonic anhydrase= acetazolamide (diuretic)—decrease HCO3 resorp.= decrease Na resorp= water goes to pee!
what happens at DESCENENDING loop of henle?
only water leaves tubule to go towards blood (impermeable to NaCl)
what happens at ASCENDING loop of henle?
water cannot do anything here. NaCl &K all cotransport out to blood via Na/K ATPase
what is a INHIBITOR @ascending limb that blocks the NaCl&K cotransport? what disease can happen from this?
diuretic furosemide= increase EXCRETION= more pee with less resorption—can lead to hypokalemia= low K
what happens at distal tubule?
unless there’s Aldosterone from adrenal glands or ADH water will not do anything here. mostly just Na, Ca (passive into cell, active to blood) and Cl cotransport to blood
what hormone enhances the Ca channel to increase Ca absorption?
PTH parathyroid
what INHIBITS @ the distal tuble…stopping NaCl cotransport to blood?
diuretic (thiazide)= more pee!
what happens at he collecting duct?
Primary: K regulation via Na/K ATPase out of blood & passive to the tubule
what is the 2ndary action at the collecting duct during acidosis? via ____ cell?
intercalated cells that adjust during ketoacidosis (too much acid in blood)–H/K ATPase @ lumenal membrane—excrete H+ and keep HCO3 and K in blood
what is the mechanism for urinary concentration?
counter-current @ medulla: opposite fluid flow in adjacent structures.
what type of counter-current is the loop? what about the vesa recta?
loop= CC multipliers
vasa recta= CC exchangers (reduce dissipation of solute gradient)
which part of the tubule re-absorbs most of urea?
prox. conv. tubule
as water is reabsorbed, urea is ___? resulting in ___ urea @ inner medulla?
more water in body= more urea in pee
where does the ADH act on? what does it do?
ADH= vasopressin and acts on cortical collecting to make them water permable= increase water retention
where is urea IMPERMEABLE?
- ascending limb of loop
- DCT
- outer collecting tubule
what is diabetes insipidus?
even tho you drink less water, you still excrete highly diluted urine= polyuria
what is cranial Diab. Insipidus?
low ADH release from post. potuitary
what is nephrogenic diab. insipidus?
ADH insensitivity by collecting ducts= water still impermeable
what is dipsogenic diab. insipidus?
excessive thirst from hypothalamus issue
how does atrial natriuretic factor affect urine formation?
atrial cells that regulate Na sense volume expansion on atrial wall causing 1. vasodilation 2. decrease aldosterone=decrease angio2= vasodilate 3. decrease renin—all leads to more Na excreted=more water excreted!
increasing K levels will ___ aldosterone levels?
increase K = increase Aldosterone= decrease BP by increasing plasma K
if a pt has diabetc acidosis, why do they have to watch K levels when using insulin treatment?
insulin promotes decrease of K levels in blood by moving them INTO cells, but you could move too MUCH out of the cell causing “hypokalemia” if they originally had too low of K levels
is it harder for body to deal with alkalosis or acidosis? why?
harder to deal with alkalosis because there is a loss of H+ which causes an increase in bicarbonate (since you can’t turn it into h2o and CO2)= body then decreases respiration to preserve HCO3 which just makes things MORE basic
does the parasymp. or the symp. system regulate micturition (urination?)
PARASYMP!! mediates internal spincter contraction and relaxation
what is the effect of atrial natriuretic factor? what type of patients are these?
bed ridden pts. heart cells sense “stretching” and more Na is excreted= more water in pee too! (leads to DIURESIS= bad)