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1. HUMAN & ANIMAL PHYSIOLOGY > leanne (L1-2) > Flashcards

leanne (L1-2) Flashcards

1
Q

Renal function and contribution to homeostasis

A 
Blood ionic composition
Blood pH
Blood Volume 
Blood Pressure
Blood osmolarity (concentration of solutes)
Excretion of waste 
Hormone production
Glucose levels
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2
Q

diseases from extreme body fluid volume

A

HYPOVOLAEMIA
too little body fluid vol
dehydrated

HYPERVOLAEMIA
too much body fluid vol
fluid overload

SYMPTOMS AND SIGNS L1 S6

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3
Q

define JVP and oedema

A

JVP - jugular venous pulse / pressure

Oedema - tissue swelling (peripheral, pulmonary, ankles etc)

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4
Q

Regulation of fluid balance

A

Kidneys play major role in regulating body fluid homeostasis

Regulate both volume and composition

Kidneys do this by altering volume and composition of plasma, which in turn influences the other fluid compartments

Maintenance of volume linked to regulation of extracellular sodium and water – this in turn controls blood pressure.

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5
Q

define

  • osmolarity
  • osmotic pressure
  • oncotic pressure
  • hydrostatic pressure
A

OSMOLARITY - the measurement of solute concentration or osmotically active solutes = osmoles (osmol/L) or (Osm/L) or (mOsm/L)

OSMOTIC PRESSURE - The pressure which needs to be applied to the solution to prevent an inward movement of fluid across a semipermeable membrane.
High osmolarity = high osmotic pressure (strong inward pull on water).

ONCOTIC PRESSURE / COLLOID ONCOTIC PRESSURE - The osmotic pressure exerted by the proteins in the blood plasma or exudate/filtrate which attracts/pulls water into that compartment.

HYDROSTATIC PRESSURE - The force exerted by a fluid against a capillary wall.

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6
Q

Tonicity and osmolarity

A

cell in hypo-osmotic solution
water will move into the cell
low osmotic pressure outside the cell (high in cell)

cell in iso-osmotic solution
water will be balanced, no net movement
high osmotic pressure in and out of cell

cell in hyper-osmotic solution
water will move out of the cell
very very high osmotic pressure out of the cell (high in the cell)

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7
Q

if Pc > osmotic pressure

A

so fluid will leave the capillary promoting filtration of the plasma.

bottleneck effect in capillary –> wide afferent / narrow efferent
HIGH HYDROSTATIC PRESSURE IN CAPILLARY
LOW OSMOTIC PRESSURE IN TISSUE

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8
Q

if Pc < osmotic pressure

A

so fluid will leave the capillary still

bottleneck effect is lower but still pushes water through
LOW HYDROSTATIC PRESSURE IN CAPILLARY
HIGH OSMOTIC PRESSURE IN TISSUE

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9
Q

STRUCTURE OF KIDNEY

A

DIAGRAM IN L1 S12

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10
Q

NEPHRON - FUNCTIONAL UNIT

A

DIAGRAM IN L1 S13

- renal corpuscle
bowman's capsule
glomerulus
- renal tubule
proximal convoluted tubule (PCT)
loop of henle
distal convoluted tubule (DCT)

several nephrons empty into the collecting duct
several collecting ducts converge into the papillary duct - minor calyces

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11
Q

JUXTAMEDULLARY NEPHRON

A

DIAGRAM L1 S14

Cortical nephrons are much shorter than the juxtamedullary nephrons
So C nephrons don;t play a role as important in altering the outputs

Loop of henle helps to conc the urine composition output
THIN descending limb and THICK ascending limb

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12
Q

FUNCTIONAL OVERVIEW - STEPS THROUGH THE NEPHRON

A

FILTRATION
Filtration under pressure – water & blood plasma solutes = Glomerular Filtrate. (GFR =180 L/day 125 mL/min)

TUBULAR REABSORPTION
99% of water and many solutes – reabsorbed back into the blood via passive and active processes (Glucose, Amino acids, Urea; Ions - Na+, K+, Ca2+ , Cl-, HCO3- and HPO42-

TUBULAR SECRETION
Renal tubule and duct cells secrete wastes, drugs, excess ions etc. out of the blood into the filtrate

URINE EXCRETION
Renal tubule and duct cells secrete wastes, drugs, excess ions etc. out of the blood into the filtrate

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13
Q

bowman’s capsule structure

FUNCTIONS OF : mesangial cells / parietal layer / visceral layer

A

DIAGRAM IN L1 S16

Mesangial cells are smooth muscle cells (around vasculature and around afferent arteriole)
They contract and impact the diameter and SA available for filtration
They contract vasculature and change hydrostatic pressure

Parietal layer - outer squamous epithelial cell of the bowman’s capsule

Visceral layer - made out of podocyte cells which have digits that can lock in and create another filter … BEAUTIFUL

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14
Q

describe the feedbakc mechanisms of the bowman’s capsule

A

Cells from the afferent arteriole, called juxtaglomerular cells, are touching the macula densa cells of ascending limb - very important because they create juxtaglomerular apparatus (she says juxtamedullary though)

This is a feedback mechanism

  • macula densa cells act as chemoreceptors, they detect the amount of sodium chloride in the filtrate
  • juxtaglomerular cells act as mechanoreceptors, they detect stretch in capillary wall

We now have mechanisms to detect conc of the filtrate and blood volume
Both mechanisms manage glomerular filtration rate (GLR)

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15
Q

glomerular filtration - what 3 characteristics allow the filtration?

A

1 – FENESTRATIONS
they are pores in the glomerular endothelial cells that prevent filtration of blood cells but allows all components of blood plasma to pass through.
Fenestrations 0.07 – 0.1µm diameter , everything but RBC and platelets.

2 – BASAL LAMINA
prevents filtration of larger proteins
BL negatively charged prevents large negatively charged molecules.

3 – SLIT MEMBRANE BETWEEN PEDICELS
this prevents filtration of medium-sized proteins
Spaces between pedicels = Filtration slits covered by membrane allow molecules less than 0.006 – 0.007µm in diameter e.g. water, glucose, vitamins, ammonia, urea, ions small plasma proteins and some albumin.

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16
Q

define filtration and which membranes/pressures allow it to happen

A

The use of pressure to force fluid through a membrane.
The difference between the forces that promote filtration and the pressures that oppose filtration.

This happens to a greater extent in the renal corpuscle than any other capillary bed of the body. – Why?

  • Large surface area of glomerular capillaries – regulated by mesangial cells.
  • Endothelial membrane is thin and fenestrated ~50X leakier than other capillaries.
  • Blood pressure is much higher owing to the differences in diameter of afferent and efferent arterioles.
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17
Q

NFP definition and equation

A

NFP = GBHP - CHP - BCOP

nfp - net filtration pressure (the totla pressure that promotes filtration
gbhp - glomerular blood hydrostatic pressure Pgc
chp - capsular hydrostatic pressure Pbc
bcop - blood colloid osmotic pressure πgc

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18
Q

Three mechanisms control GFR:

A
  1. Renal Autoregulation a) Myogenic and b) Tubuloglomerular feedback
  2. Neuronal regulation
  3. Hormonal regulation

These work in two different ways:

  1. Adjustment of blood flow into and out of the glomerulus
  2. Alteration of glomerular capillary surface area
19
Q

Renal autoregulation - MYOGENIC MECHANISM

A

Maintenance, by the kidneys themselves, of a constant renal blood flow and GFR in response to everyday alterations in blood pressure.

Myogenic Mechanism - in response to ↑BP and ↑GFR
Myogenic autoregulation - rapid, musculature, increase in blood pressure

↑ BP stretches the walls of the afferent arterioles
JG Smooth muscle fibres contract
Narrowing the lumen of afferent arteriole
↓renal blood flow and GFR

In response to ↓BP and GFR the opposite happens

20
Q

Renal autoregulation - TUBULOGLOMERULAR FEEDBACK

A

Negative feedback regulation via Macula densa cells. Slower mechanism.

↑flow of filtrate into renal tubules (fast).
↓reabsorption of ions and water
Sensed by JGA - ↓NO release
Afferent arterioles constrict
 ↓in blood flow and GFR
21
Q

role of juxtaglomerular apparatus

A

JUXTAGLOMERULAR APPARATUS DOES 2 THINGS

  • Secretes ?, this is the long distance hormonal effect
  • Decreases its secretion of nitric oxide (vasodilator), this is the local effect

Local effect of it in the kidney will allow the efferent arteriole to constrict - will remove the vasodilatory impact and allow the decrease in blood flow through glomerulus and decrease in GFR

22
Q

Substances filtered/reabsorbed and excreted

A

TABLE IN L1 S26

23
Q

water reabsorption

A

Most water reabsorbed in proximal (convoluted) tubule and Loop of Henle

Fine tuning and hormonal regulation of water reabsorption occurs mainly in (medullary) collecting ducts

Water reabsorption from collecting ducts is passive & if we want to concentrate urine requires :

  1. Insertion of water channels (aquaporins) - regulated by antidiuretic hormone (ADH)
  2. An osmotic gradient - generated by the countercurrent system in loop of Henle
24
Q
  1. Glucose reabsorption in the PCT
A

Reabsorption of glucose through sodium glucose transporters (SGLTs)

At normal levels of plasma glucose, all glucose in the filtrate is reabsorbed via the PCT

It is co-transported with Na+ at the luminal membrane by a Na+/glucose cotransporter

It then diffuses from the cell into the interstitial fluid then into the peritubular capillaries

25
Q
  1. Reabsorption of sodium ions and secretion of hydrogen ions in PCT
A

In the PCT, we can reabsorb Na ions back into the blood and get rid of H+ ions
So we can secrete it into the filtrate - which helps us with buffering

CO2 in H2O in association with carbonic anhydrase = carbonic acid H2CO3
Broken down into a H ion which will will be pushed into the Na/H antiporter

Na+ comes in to give us gradients for other mechanisms
We can get rid of our bicarbonate which can then get reabsorbed (and we can pump out Na)
Na reabsorbed from surrounding tissues back into the blood
Get rid og H ions by secreting it back into the filtrate

26
Q
  1. The distal part of the PCT is involved in passive reabsorption of certain ions and urea
A

A lot of passive diffusion down conc gradient

Cells are leaky - pericellular movement (between cells) and transcellular movement (through linked channels)

27
Q
  1. Reabsorption in the Loop of Henle
A

The descending limb is permeable to water (15%)

The ascending limb is impermeable to water but cells have Na+ - K+ - 2Cl- symporters in the apical membrane

28
Q
  1. Reabsorption and secretion in the DCT and CD
A

The amount of water and solute reabsorption in the late DCT and CD varies depending on the body’s needs.

Water - heavily influenced by the action of Anti Diuretic Hormone (Arginine vaspressin)

29
Q

Control of ADH release

A

Low pressure sensors in atria, pulmonary vasculature
High pressure sensors in carotid sinuses & aortic arch
Stretch receptors in afferent arterioles (indirect via release of angiotensin II)

↓ pressure/stretch → ↑ADH

IN HYPOTHALAMUS - we have detectors as osmoreceptors and the thirst center (which has msgs coming into it as a result of cellular dehydration)

ON PERIPHERY - extracellular dehydration (plasma and interstitial fluid)
Low plasma volume - can be detected by pressure sensors (can detect high/low pressures and can send signals to the hypothalamus)

30
Q

ADH

where is it made? how is it transported? its 2 functions?

A

Produced in supraoptic & paraventricular nuclei of hypothalamus
Transported to the posterior pituitary
Short plasma half life.

TWO main functions:-

  • Reduce water excretion (antidiuretic)
  • Stimulate vasoconstriction

We get messages from osmoreceptors/thirst centers etc
It talks via the paraventricular neuron and supraoptic neuron
Will secrete the ADH from the posterior lobe of the pituitary
This will travel via the circulatory system and will bind to receptors and the principal cells of the collection duct

31
Q

ADH mediated AQP2 export to the apical membrane

A

We have our vasopressin 2 receptor and our vasopressin adh (also called arginine vasopressin)
It binds and we have a CAP dependent system where it leads to the activation of PKA
Leads to the phosphorylation of our proteins within a vesicle
Leads them to be shuttled to the apical membrane of the cell
Which inserts the aquaporins

We also have aquaporin 3 expressed on the basal lateral
Which means we now have a transcellular pathway (from tubule fluid, through the cell, into the interstitial fluid, and into the vasculature)

32
Q

urine production

A

Minimum urine production ~500 mL /day (20-30 ml/h)

Obligatory urine volume needed to excrete waste solutes – typically ~600 mOsm / day.

Owing to the limited ability of the kidney to concentrate urine to 1200mOsm/L.

Maximum urine production ~ 20 000 mL /day (20 litres /day)

Normal urine production ~1500ml /day = 1 mL /min

Diurnal variation.

Mechanisms of urine production allow rapid responses to changes in water intake / loss

33
Q

DIAGRAM OF ALL THE NEPHRON

A

DIAGRAM AND LECTURE CAPTURE

L1 S37

34
Q

countercurrent multiplier LoH

A

defined as - the formation of increasing osmotic gradient in the medullary interstitial fluid.

Na+ and Cl- are concentrated in the medulla interstitial fluid as they are transported by symporters in the thick ascending limb of LoH and urea recycling.

Osmosis is inhibited due the reduced permeability of the cells to water.

The continued movement of fluid through the tubules means there is a constant build-up of ions = the formation of an osmotic gradient from 300 mOsml/L to 1200 mOsml/L

35
Q

loop of henle structure

A

Thin descending limb – permeable to water - no active reabsorption or secretion of solutes

Thin ascending limb – impermeable to water - essentially no active reabsorption or secretion of solutes

Thick ascending limb – impermeable to water
- active reabsorption of sodium & other solutes

36
Q

Formation of dilute urine

A

Osmolarity of tubular fluid INCREASES as it flows down the descending limb LoH.
Owing to increase in osmolarity of the surrounding interstitial tissue of renal medulla so fluid moves out of the tubule.

Osmolarity of tubular fluid DECREASES as it flows up the ascending limb LoH.
Owing to the removal of ions by Na+, K+ and Cl- symporters : and retention of water because the cells of the thick limb are impermeable to water. So solutes are leaving but water can not follow.

Osmolarity of tubular fluid further DECREASES as it flows through DCT and CD.
Some solutes are further removed and reabsorbed, in the absence of ADH the DCT and CD are impermeable to water so the tubular fluid is very dilute at this point = 65-70 mOsml/L.

37
Q

steps of formation of dilute urine

A

From ascending limb of loop of Henle the tubule is relatively impermeable to water.

∴ as pumps move solutes out of tubule lumen they leave behind a dilute tubular fluid when compared to plasma

This leads to a dilute urine being excreted

38
Q

steps of formation of concentrated urine

A

The distal & collecting tubules / ducts are permeable to water in the presence of antidiuretic hormone (ADH)

Water will move so that there is osmotic equilibrium with surrounding interstitium

Note osmolarity of medullary interstitum ~1200mOsm/L/H2O

This leads to a concentrated urine being excreted

39
Q

Counter-current exchange

A

Hairpin arrangement allows the nutrients to be delivered & water removed whilst minimising disruption to the medullary concentration gradient – counter current exchange

Constant flow of urea and NaCl (lumen to interstitium and via vasa recta) - stops them precipitating in medulla

MORE INFO IN L1 S44

40
Q

Renal regulation

A

Renal function is regulated by neural and hormonal influences.

Renal sympathetic nerves
Renin-angiotensin-aldosterone system
Antidiuretic Hormone (ADH) or Arginine vasopressin
Atrial natriuretic peptide (ANP)
Parathyroid hormone (PH)
41
Q

Renin- Angiotensin-Aldosterone system

A

When blood volume and BP is low walls of the afferent arteriole are less stretched and the juxtaglomerular cells secret RENIN (enzyme).

Ultimately leads to Angiotensin II (potent vasoconstrictor)

  • Vasoconstriction of afferent and efferent arterioles – lower GFR
  • Increases reabsorption of Na+, Cl- and water by activating Na+/H+ antiporters.
  • Stimulate the adrenal cortex to release aldosterone – reabsorption of water increasing blood volume and BP.
42
Q

Renin –Angiotensin – Aldosterone - System

A

DIAGRAM AND LECTURE CAPTURE IN L1 S47

43
Q

Angiotensin Converting Enzyme

A

ACE – produced from both renal and lung epithelia

ACE Inhibitors clinically very important.
They are used as hypertension drugs, will stop systemic vasoconstriction
They are commonly prescribed to stop impact of high BP

MAJOR TARGET FOR HYPERTENSION DRUGS
benazepril (Lotensin)
captopril (Capoten) 
enalapril (Vasotec), 
fosinopril (Monopril), 
lisinopril (Prinivil, Zestril) 
moexipril (Univasc), and 
perindopril(Aceon), 
quinapril (Accupril), 
ramipril (Altace),
trandolapril (Mavik)
44
Q

Diuretics and the control of Blood pressure

A

Diuretics are substances that promote the loss of Na+ and water.

  • Natural diuretics.
  • Osmotic diuretics.
  • Loop diuretics (Lasix, Frusemide) are the most powerful diuretics because they inhibit the formation of the medullar gradient.
  • Thiazide diuretics (Chlorithiazide, Diuril) acts on the DCT - reduces Na+ reabp.
  • Spironolactone is an aldosterone receptor antagonist. This is known as a K+ sparing diuretic. It acts because the K+ in the urine is from aldosterone-driven active tubular secretion into the late DCT and collecting ducts.

1. HUMAN & ANIMAL PHYSIOLOGY (8 decks)

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