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Flashcards in Physiology Deck (55):

What is acidosis?

Decrease in pH <7.4


What is alkalosis?

Increase in pH > 7.4


What is normal blood pH?

pH 7.4


What is pH?

Power of hydrogenium (as H are very reactive so can act on proteins, too much= change function)
Only free H ions involved in pH balance


What is normal quantity of carbonic acid in the blood?

Depends on amount of C02 dissolved in the plasma


What is normal PC02 levels?



What is normal HC03 levels?



What is a normal GFR?



What does the proximal convoluted tubule reabsorb?

NaCl, water AAs, glucose, anions, low molecular weight proteins


What does the distal tubule secrete and reabsorb?

Secretes- K, H
Reabsorb- NaCl, Water


What does the descending loop of henele cause reabsorption of ? How does this happen?

Water via aquaporins
Water follows higher conc. of Na and Cl (excreted from ascending loop) out into efferent arteriole (higher tonicity causes osmotic flow)


What does the ascending loop of henle cause reabsorption/ secretion of\?

Na, Cl


What is the simple function of the glomerulus?

Filtration- Reabsorption- Secretion


What is the blood flow to the kidneys?

1200mls/min (20-25% of cardiac output- therefore takes 5mins for who cardiac outflow to run through)


What is the function and purpose of hydrostatic and oncotic forces?

Colloid osmotic (oncotic) pressure- exerted by proteins (albumin) in a blood vessel's plasma, pulls water into the circulatory system (favour reabsorption)
Hydrostatic Pressure- due to gravity, increases filtration by pushing fluid out of capillaries
=Starlings Forces


Describe the pressures acting on a glomerulus that result in filtration/ reabsorption . What is the net filtration?

Hydrostatic (BP)- 55mmHg
Fluid Pressure (created by Bowmans capsule)= 15mmHg
Colloid Osmotic (oncotic)- 30mmHg
55- (30+15)=10mmHg filtration pressure


How do you increase pressure in glomerulus?

Short and wide afferent arterioles= little resistance to flow
long and narrow efferent arterioles= inc friction + resistance= Inc pressure + High resistance in efferent arterioles causes and increase in hydrostatic (filterative forces) up stream (afferent) so more will be taken out NOTE: causes a decrease in pressure down stream


What extrinsic control is there over GFR?

1. Sympathetic- afferent + efferent vasoconstriction
2. Circulating catecholamines (adrenaline + noradrenaline from adrenal medulla)- Inc blood flow to other organs so decreases GFR by decreasing hydrostatic pressure
3. Ang 2- High Conc (afferent + efferent= normal), Low (Act of efferent to inc GFR)


What are the intrinsic controls over GFR?

Autoregulation- within 60-130mmHg
-Inc MAP= Afferent arteriolar constriction (prevents rise in glomerular pressure)
-Dec MAP= Afferent arteriolar dilation(try and inc pressure to keep filtration going)


How/ Why would autoregulation be overridden?

In seriously compromised BV/BP (eg./ haemorrhage) where autoregulation is over-ridden by sympathetic output (vasoconstriction) to liberate blood to immediately important organs- prolonged reduction can disrupt the kidneys role in homeostasis=death


What substances does the kidney reabsorb? How does it do this?

Glucose, Water, Na, Cl, urea via high TTp>Ppc (high osmolarity and low hydrostatic)


Explain the anatomy of the basement membrane

Epithelial Podrocytes- wrap around capillaries leaving filtration slits, podrocytes attach to BM via pedicles (foot process)
Basement Membrane- 3 layers, prevent plasma proteins from being filtered out of blood
Endothelium- large pores with solutes (plasma proteins and fluid can pass through but blood cells cannot)


What mechanisms are used to absorb nutrient back into the efferent arteriole after they can been filtrated by the glomerulus?

1. Carrier Mediated Transport- open 1 side at a time (not freely passing), have a Tmax when all sites saturated (limiting- rest will enter the urine) eg./ Glucose
2. Active Transport eg./ Na passive enters and leaves via NaKATPase (keeps gradient going) creates an electrochemical gradient driving anion eg./ Cl absorption + water movement
3. Diffusion- permeable solutes eg./ K, Ca, urea
4. Sodium- Dependent Glucose Transporter- SGLT1 moves Na + glucose, GLUT2 takes it out (linked to ATP hydrolysis-releases energy)


What is renal threshold?

Plasma concentration at which saturation occurs
Tm- Transport rate at saturation


How are substances transported from peritubular capillaries into tubular lumen?

Protein bound substances (secretion at glomerulus is limited) + harmful substances via carrier mechanisms eg./ for drug excretion


What levels demarcate hyper + hypo kalemia? What is the clinical consequence?

1. Hyperkalemia >5.5mmol/L= dec in RMP of cells- VF-death
2. Hypokalemia <3.5mmol/L= Inc RMP so hyper polarises cells= arrhythmia- death


How is potassium secreted and reabsorbed in the kidney tubularies? What can regulate its levels?

Filtered out at glomerulus and reabsorbed at proximal tubule
Aldosterone regulates K
Inc K(extra)- Inc Aldosterone- secretes K and keeps Na (water follows) useful in hypovolemia


What is the osmolarity of isosmotic fluid in the proximal tubularly?



How is the renal gradient set up?

The renal tubules have a 300mosmole/L isotonic gradient. Active reabsorption of Na + Cl (ascending limb) decreases osmolarity in the tubule and increases it in the interstitum. Water moves out via the vasa recta (due to inc in colloid osmotic pressure (oncotic).
With every turn tubularly gets more concentrated due to active NaCl and osmotic shift of water.


What is the difference between osmolarity in the ascending vs descending loop at any given time?



How do proteins, non-polar drugs and pollutants leave the renal system?

Albumin and some non-polar drugs and pollutants are highly lipid soluble to when water moves (descending loop) they move too


What is the vasa recta? What is its function?

Pertitubular capillaries of the juxtmedullary nephrons
Freely permeable to H20 and solutes- equilibrate with medullary interstitial gradient
Delivers 02 to medulla and removes volume (H20) from interstitum)


What is the job of the collecting duct? What hormone controls here?

Site of water regulation
ADH (vasopressin acts here)
-osmoreceptors- detect inc BP
-Baroreceptors (aortic arch, carotid sinus) detect decreased BP)
PP releases ADH= vasoconstriction


What kind of molecules cannot cross the GBM?

Blood Cells- RBC, WBC, high molecular weight proteins eg./ albumin, globulin


Explain the process of osmolarity and how this acts on ion movement out and into cells

Inc Osmolarity (low water conc.)= water flows out of cell- cell shrinks- stretch sensitised ion channel opens- change membrane potential- Inc neural discharge- ADH inc (stops water being secreted)
Dec Osmolarity (high water conc.)= water flows into cell- cell swells- decrease in stretch discharge- ADH dec (water secreted from collecting duct)


What do stretch receptors in cells sense?

OSMOLARITY not tonicity (non- penetrating solutes) BUT particles that move across the membrane freely (no tonicity) result in no osmotic drag so stretch receptors not stimulated
eg./ ureic syndrome (inc in urea) has no affect on osmoreceptors as is a penetrating particle aka it has no affect on tonicity


What is the action of ADH in collecting ducts?

ADH (vasopressin)-binds to membrane receptor- receptor activates cAMP- cell inserts AQUAPORIN into apical membrane- water absorbed by osmosis into blood (medullary gradient)
1. ADH present- water able to leave collecting ducts
2. ADHmax- contents equilibrate with medullary interstitum- water uptake by vasa recta + high conc urine


What happens to urine production if there's a secondary disorder of ADH secretion at the posterior pituitary?

No ADH secreted- medullary gradient not established/ not enough to bring water in so stays in collecting tubule= large volumes of dilated urine produced (diabetes insipidus)


What role does urea have in concentrating urine?

An increase in urea concentration in collecting ducts (due to water moving out via ADH) then moves out with water (reinforces medullary gradient, otherwise water would stay due to increased tonicity in collecting ducts) can result in uraemia (high levels of plasma urea) coupled with rehydration


What would happen to excretion if an individual drank sea water?

Sea Water- salty- Hypertonic (low water conc)
Therefore a higher solute load to be excreted so more water + urea has to be lost with it= dehyration (as more water required to excrete solute load than what was with it)


What toxic substance decreases ADH(vasopressin) secretion from the hypothalamus?

Alcohol= pee more as less ADH to bring water out


How do you treat central vs peripheral Diabetes Insipidus?

ADH insuffiency via
1. Central- Hypothalamic insufficency- give ADH
2. Peripheral- collecting ducts irresponsive to ADH- DON'T give ADH (as loose thirst mechanism)
=polydipsia + polyuria


What is respiratory acidosis? What does this produce? What can cause it?

Reduced ventillation= Inc in CO2 in blood (retension) which is exchanged for H+ (equation moved to right). This drops the pH in the body and HCO3 stays normal unless chronic, in which case levels will eventually increase
= Inc PCO2, Inc H+= Inc pH, Inc HCO3 (chronic)
Acute- Drugs eg./ barbiturates, opiates, airway obstruction
Chronic- Lung Disease eg./ bronchitis, asthma, emphysema (here HCO3 Inc- problem if renal function also off)


What is respiratory alkalosis?

Inc ventilation= CO2 blown off. Reduced CO2- shifts equation to left so less H+ produced= Inc in pH.
HCO3 normal unless chronic, in which case levels will eventually decrease.
= Dec CO2, Dec H+= Inc pH, Dec HCO3 (eventually)
Acute- voluntary hyperventilation, aspirin, first ascent to altitude
Chronic- long term residence at altitude, dec P02 (peripheral chemoreceptors kick in)


What is metabolic acidosis?

Decreased HCO3 due to inc buffering of H or loss of HCO3. To protect pH drop PCO2 via ventilation
Cause- Inc acid production due to ketoacidosis/ lactic acidosis; renal failure means can't excrete normal H (diet); loss HCO3 (eg./ diarrhoea)


Why does a metabolic correction response take longer than the immediate respiratory response?

Respiratory response is immediate correction (eg./ hypo/hyperventilation)- protects pH
Renal response (metabolic) takes longer due to glutamate takes 4-5 days to reach max


What happens to pH during vomiting?

Lose NaCl + Water= hypovolemic- catecholamines- tubule- direct BF to other organs (away from kidney) so less filtration + aldosterone reabsorbs Na in favour of K out.
Lose HCl- metabolic alkalosis- respiratory compensation (inc PCO2)- inc H- adds HCO3 to plasma (exacerbates)
Restoration of volume takes presedence- give NaCl- restores volume- alkalosis corrected


When is aldosterone released? What can you ingest that can have the same affect?

Aldosterone is secreted when ECF is decreased
Ingesting large quantities of liquorice can also cause metabolic alkalosis


What is the anion gap? What is an increase of it indicative of?

Difference between the sum of principle cations (Na, K) and principle anions (Cl, HCO3)
Measure in metabolic acidosis
No change- When acidosis is due to loss of bicarbonate (compensated by an increase in chloride)
Increase- when reduction in bicarbonate is replaced by other anions eg./ lactate, acetylate in lactic or diabetic acidosis


How is fluid split in the body?

2/3 (28L) in ICF
1/3 in ECF- 3L plasma, 11L interstitial fluid


What are the major ECF osmoses?

Na and Cl


What are the major ICF osmoles

K salts


Change in what concentration of ion dictates total body water concentration?



What detects change is ECF/ circulating volume?

High + Low pressure baroreceptors


How does the body compensate for hypovolemia?

Vomiting, Diarrhoea = excessive sweating cause NaCl and water loss.
Dec plasma volume= Dec venous pressure- Dec venous return- Dec atrial pressure- Dec End systolic pressure- Dec stroke volume- dec cardiac output= Dec BP
Baroreceptors detect drop in atrial pressure- Inc sympathetic discharge- Inc Vasoconstriction- Inc TPR- Inc BP= systemic, acute response.