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Anatomical sciences > Kidney Physiopathology > Flashcards

Kidney Physiopathology Flashcards

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1
Q

medulla of the kidney

A

inner part of the kidney, consists of the medullary collecting ducts, loops of Henle, vasa recta and the interstitium.

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2
Q

cortex of the kidney

A

The renal cortex is the outer part of the kidney. It contains the glomerulus and convoluted tubules

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3
Q

renal pelvis

A

The area at the center of the kidney. Urine collects here and is funneled into the ureter, the tube that connects the kidney to the bladder.

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4
Q

nephron

A

The functional unit of the kidney is the nephron. Each kidney consists of millions of nephron which plays a significant role in the filtration and purification of blood.
1.5 million

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5
Q

how much sodium is filtered, excreted and reabsorbed per day

A

filtered = 25000 mEq
excreted = 150 mEq
reabsorbed = 99%

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6
Q

how much water is filtered, excreted and reabsorbed per day

A

filtered = 180 lt
excreted = 1.5 lts
reabsorbed = 99%

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7
Q

podocytes

A

cells in Bowman’s capsule in the kidneys that wrap around capillaries of the glomerulus.
adapted to kidney function

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8
Q

what is in the glomerular filtrate

A

water
glucose
amino acids
urea

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9
Q

components of the filtration membrane

A
  • capillary endothelial fenestrations
  • gel like basement membrane
  • slit diaphragms within filtration slits between the pedicels of podocytes
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10
Q

Why is ultrafiltration important

A

Maintaining homeostasis

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11
Q

where does ultrafiltration of blood occur

A

Across the glomerulus filtration barrier

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12
Q

what are 2 types of glomerulopathies

A

nephrotic syndrome
nephritic syndrome

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13
Q

Nephrotic syndrome symptoms

A
  • high levels of protein in urine
  • low albumin in blood.
    -edema
    -hyperlipidemia (increase triglycerides and cholesterol)
  • lipiduria
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14
Q

Nephritic syndrome symptoms

A
  • mild levels of protein in urine
  • hematuria - brown urine
  • hypertension
  • blurred vision
  • azotemia
  • oliguric
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15
Q

what is post streptococcal glomerulonephritis

A
  • 10-14 days after skin or throat infection
  • not caused by bacteria
  • autoimmune reaction
  • immune complexes deposit at the glomerular membrane
  • damage filtration barrier = loss of protein/ albumin in urine
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16
Q

post streptococcal glomerulonephritis symptoms

A
  • hematuria
  • loss of protein = proteinuria
  • decrease of albumin in blood
  • edema (puffy face, pitting edema)
  • oliguria
  • hypertension
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17
Q

post streptococcal glomerulonephritis diagnosis

A
  • kidney biopsy
  • stain glomerulus
  • immuno deposits
  • flourescence
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18
Q

post streptococcal glomerulonephritis treatment

A
  • no specific treatment
  • relive symptoms
  • antibiotics = destroy streptococcal bacteria
  • blood pressure medicine and diuretic drugs = control swelling and high blood pressure
  • corticosteroids
  • anti inflammatory medicine - not effective
  • limit salt in the diet = control swelling and high blood pressure
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19
Q

role of diuretics

A

drugs that increase urine output

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20
Q

Glomerular capillaries

A

have high permeability to water and electrolytes
20% of plasma = filtered into Bowmans space and PCT

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21
Q

exampled of diuretics

A

Mannitol, Acetazolamide, Furosemide, spironolactone, triamterene, amiloride

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22
Q

function of mannitol

A

*inert
*increases plasma osmolarity
*filtered at glomerulus and poorly reabsorbed
*increases osmotic pressure in glomerular filtrate
*decreases H2O reabsorption
*doesnt enter brain or eye - draws fluid from tissues

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23
Q

uses of mannitol

A
  • forced diuresis (poisonings)
  • actor glaucoma
  • cerebral oedema
  • slow IV infusion
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24
Q

what happens to mannitol when it gets to the tubule

A

eliminates and drugs all the water with it
glucose and sodium will be reabsorbed whereas mannitol is not - so drags out all the water

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25
what happens in the proximal convoluted tubule
reabsorption of sodium water and bicarbonate 655 of sodium is reabsorbed in PCT
26
tubular transport of glucose
glucose nephron tubular lumen -> Proximal tubules epithelial cell -> blood capillary via facilitated diffusion SGLT2 1. Na+/K+ ATPase on the basal membrane creates a gradient for Na+ 2. Na+/glucose symporter (SGLT-2) on the luminal membrane->GLUT2 transporter on the basal membrane.
27
how much glucose is reabsorbed normally in PCT
100% reabsorption SGLUT2 transporter
28
glucose reabsorption in diabetes
hyperglycemias high filtered load of glucose filtered loas exceeds reabsorption capacity glucose in urine
29
what can be used as a diabetes treatment in PCT
GLUT2 inhibitors = prevent glucose reuptaek = treatment
30
function of carbonic anhydrase
catalyses the reversible reaction of bicarbonate to water and CO2 circulating H+
31
role of sodium potassium ATPase
pumps NA+ out of the cell and K+ into the cell; the ratio is 2:3
32
what type of diuretic is axetazolamide
carbonic anhydrase inhibitor
33
what happens when we inhibit carbonic anhydrase
The H+ is not generated if dont exchange the H+ out of the cell cannot reabsorb Na+ inside the cell in the blood. get a build up of carbonic acid drag the water out
34
what dies acetazolamide do
- suppresses H+ production, thus reduces Na+-H+ exchange = less Na+ reabsorption - increases excretion of HCO3- = causes mildly alkaline urine and metabolic acidosis - effect is self-limiting
35
when is acetazolamide used
acute mountain sickness restores acid base balance in heart failure or those who hyperventilate - get metabolic alkalosis
36
which side of the loop of Henley is impermeable to water
thick ascending limb
37
what does the thick ascending limb reabsorb
sodium potassium and chloride (co transport) 25% os sodium from original filtrate reabsorbed in TAL
38
what does interstitial hyper osmotic mean
Loop of Henley very permeable to water water is reabsorbed
39
why is the countercurrent multiplication in loop of henle used
The loop of Henle utilizes the countercurrent multiplier system to increase the concentration of solute and ions within the interstitium of the medulla
40
mechanism of counter current system
solutions in the two tubes flow in opposite directions. In one tube 0% concentration of the solution starts to flow from one end, and in the other tube, 100% concentration of the solution starts to flow from the opposite end. constant gradient so constant movement of ions
41
how do loop diuretics work
nhibits the cl- pump, so K+ and Na+ are no longer reabsorbed, so no gradient - means all the ions stay in the (lumen) urine and drag the water with them.
42
mechanism of Furosemide
loop direction inhibits Na+ /K+/2Cl- co transporter cause 15-25 of filtered sodium to be excreted = torrential urine production result in increased osmotic pressure in filtrate delivered to distal tubule - decreases water reabsorption very fast - emergencies
43
what happens in the distal convoluting tubule
also impermeable to water 5% of sodium reabsorbed co transport with chloride
44
What type of diuretic is hydrochlorothiazide?
thiazide
45
how do thiazides diuretics work
- block Na+/Cl- co-transporter -results in higher osmolarity of urine and decreased water reabsorption - effect is self-limiting - effect doesnt act as fast as furosemide.
46
limitations of thiazides
lower blood volume renine secretion angiotensin formation and aldosterone secretion slower
47
what happens in the collecting duct
1-2% of sodium reabsorbed exchange with potassium and hydrogen
48
what is collecting duct activity regulated by
activity - dependent on tubule conc of sodium activity is regulated by aldosterone (adrenal cortex) and ADH
49
how is water excretion controlled by ADH
rate of water excretion set by ADH - vasopressin ADH = increases water permeability of the cortical and medullary collecting ducts and DCT(sometimes)
50
what happens when there is no ADH
walls of distal nephron are impermeable to water
51
where does ADH come from
posterior pituitary gland
52
how is the release of ADH regulated
* increase ECF osmolarity is detected by osmoreceptors * shrink leading to increased frequency of nerve impulses to posterior pituitary gland * increase frequency of nerve impulses causes secretion of ADH from nerve terminals
53
volume of urine with no and max ADH release
no ADH = 23L urine max ADH = 400 ml urine normal = 1.4 L urine
54
site of ADH synthesis
supraoptic and paraventricular nuclei
55
what does ADH do
*ADH binds to V2 receptors in basolateral cell membranes of principal cells in the collecting ducts *This up regulates the expression of aquaporins (water channels) = inserted into the apical cell membranes of principal cells *water moves osmotically from tubular fluid in distal nephron into surrounding interstitial fluid -> blood
56
disease as a result of reduced output of ADH
diabetes insipidus
57
symptoms of diabetes insidious
excretion of large volumes of dilute urine thirst
58
pituitary (central) diabetes insipidus
head no or reduced release of ADH from pituitary gland treated = nasal spray = ADH replacement
59
nephrogenic (peripheral) diabetes indipidus
kidney unresponsive to circulating ADH lack of V2 receptors in CD genetic disease = disrupts ability to synthesise aquaporins water balance only be maintained by increase water intake to compensate for increase water excretion
60
3 types of potassium sparing fiuretics
ENaC blocker - triamterene - amiloride Aldosterone antagonist - spironolactone
61
how doe ENaC blocked work ( triamterene, amiloride )
- directly block epithelial sodium channel In distal tubule, collecting tubules and collecting ducts (limited diuretic efficacy) - used in conjunction with loop and thiazide diuretics to miantain K+ balance
62
how do Aldosterone antagonist work (spironolactone)
aldosterone on sodium reabsorption - early phase = increases opening of ENaC -later phase = probes DNA transcription - increases synthesis of ENaC - increases synthesis of Na+, K+ ATPase
63
what is the site of synthesis storage and release of resins
Juxtaglomerular cells
64
where are juxtaglomerular cells
in afferent/efferent arterioles of the glomerulus
65
RAAS
angiotensinogen + renin -> angiotensin I + ACE -> angiotensin II _> aldosterone
66
what does vitamin D deficiency result in
deformed bones cardiovascular disease
67
how is the active form of vitamin D formed
cholesterol derivative in food (sunlight on skin) cholecalciferol (liver) 25 hydrocycholecalciferol (kidney) 125 dihydroxycholecalciferol = increase absorption of calcium and phosphate from gut and kidney
68
what does EPO release lead to
EPO binds to receptors in bon emarroe red blood cell production increases bloods oxygen carrying capacity
69
synthesis of erythropoietin (EPO)
reduced oxygen delivery to renal cortex (CO poising, anaemia, haemorrhage, altitude, respiratory disease) - O2 sensory in interstitial cells in renal cortex HIF - increase rate of transcription of EPO genes by interstitial cells EPO stimulates bone marrow cells and erythrocytes
70
what can recombinant EPO be used for
renal failure cancer (as a side effect of chemotherapy is destruction of RBC)
71
what is EPO
both endogenous and recombinant EPO = GLYCOPROTEINS can be distinguished in urine sample

Anatomical sciences (12 decks)

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