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Anatomical sciences > Kidney Physiopathology > Flashcards

Kidney Physiopathology Flashcards

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
Q

what happens in the proximal convoluted tubule

A

reabsorption of sodium water and bicarbonate
655 of sodium is reabsorbed in PCT

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26
Q

tubular transport of glucose

A

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.
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27
Q

how much glucose is reabsorbed normally in PCT

A

100% reabsorption
SGLUT2 transporter

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28
Q

glucose reabsorption in diabetes

A

hyperglycemias
high filtered load of glucose
filtered loas exceeds reabsorption capacity
glucose in urine

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29
Q

what can be used as a diabetes treatment in PCT

A

GLUT2 inhibitors = prevent glucose reuptaek = treatment

30
Q

function of carbonic anhydrase

A

catalyses the reversible reaction of bicarbonate to water and CO2
circulating H+

31
Q

role of sodium potassium ATPase

A

pumps NA+ out of the cell and K+ into the cell; the ratio is 2:3

32
Q

what type of diuretic is axetazolamide

A

carbonic anhydrase inhibitor

33
Q

what happens when we inhibit carbonic anhydrase

A

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
Q

what dies acetazolamide do

A
  • 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
Q

when is acetazolamide used

A

acute mountain sickness
restores acid base balance in heart failure or those who hyperventilate - get metabolic alkalosis

36
Q

which side of the loop of Henley is impermeable to water

A

thick ascending limb

37
Q

what does the thick ascending limb reabsorb

A

sodium potassium and chloride (co transport)
25% os sodium from original filtrate reabsorbed in TAL

38
Q

what does interstitial hyper osmotic mean

A

Loop of Henley
very permeable to water
water is reabsorbed

39
Q

why is the countercurrent multiplication in loop of henle used

A

The loop of Henle utilizes the countercurrent multiplier system to increase the concentration of solute and ions within the interstitium of the medulla

40
Q

mechanism of counter current system

A

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
Q

how do loop diuretics work

A

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
Q

mechanism of Furosemide

A

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
Q

what happens in the distal convoluting tubule

A

also impermeable to water
5% of sodium reabsorbed
co transport with chloride

44
Q

What type of diuretic is hydrochlorothiazide?

A

thiazide

45
Q

how do thiazides diuretics work

A
  • 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
Q

limitations of thiazides

A

lower blood volume
renine secretion
angiotensin formation and aldosterone secretion
slower

47
Q

what happens in the collecting duct

A

1-2% of sodium reabsorbed
exchange with potassium and hydrogen

48
Q

what is collecting duct activity regulated by

A

activity - dependent on tubule conc of sodium
activity is regulated by aldosterone (adrenal cortex) and ADH

49
Q

how is water excretion controlled by ADH

A

rate of water excretion set by ADH - vasopressin
ADH = increases water permeability of the cortical and medullary collecting ducts and DCT(sometimes)

50
Q

what happens when there is no ADH

A

walls of distal nephron are impermeable to water

51
Q

where does ADH come from

A

posterior pituitary gland

52
Q

how is the release of ADH regulated

A
  • 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
Q

volume of urine with no and max ADH release

A

no ADH = 23L urine
max ADH = 400 ml urine
normal = 1.4 L urine

54
Q

site of ADH synthesis

A

supraoptic and paraventricular nuclei

55
Q

what does ADH do

A

*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
Q

disease as a result of reduced output of ADH

A

diabetes insipidus

57
Q

symptoms of diabetes insidious

A

excretion of large volumes of dilute urine
thirst

58
Q

pituitary (central) diabetes insipidus

A

head
no or reduced release of ADH from pituitary gland
treated = nasal spray = ADH replacement

59
Q

nephrogenic (peripheral) diabetes indipidus

A

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
Q

3 types of potassium sparing fiuretics

A

ENaC blocker
- triamterene
- amiloride

Aldosterone antagonist
- spironolactone

61
Q

how doe ENaC blocked work ( triamterene, amiloride )

A
  • 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
Q

how do Aldosterone antagonist work (spironolactone)

A

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
Q

what is the site of synthesis storage and release of resins

A

Juxtaglomerular cells

64
Q

where are juxtaglomerular cells

A

in afferent/efferent arterioles of the glomerulus

65
Q

RAAS

A

angiotensinogen + renin -> angiotensin I + ACE -> angiotensin II _> aldosterone

66
Q

what does vitamin D deficiency result in

A

deformed bones
cardiovascular disease

67
Q

how is the active form of vitamin D formed

A

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
Q

what does EPO release lead to

A

EPO binds to receptors in bon emarroe
red blood cell production
increases bloods oxygen carrying capacity

69
Q

synthesis of erythropoietin (EPO)

A

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
Q

what can recombinant EPO be used for

A

renal failure
cancer (as a side effect of chemotherapy is destruction of RBC)

71
Q

what is EPO

A

both endogenous and recombinant EPO = GLYCOPROTEINS
can be distinguished in urine sample

Anatomical sciences (12 decks)

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