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What are some causes of metabolic acidosis?

1) Increased acid production

a) Lactic acidosis
-poort tissue perfusion
-CO or cynaide poisoning

b) Diabetic ketoacidosis (DKA)
-beta-hydroxybutyric and acetoacetic acids 
-failure of oxygen delivery to the tissues

2) Decreased acid excretion

a) Renal failure

b) Renal tubular acidosis
-Failure of tubular acid secretion

3) Bicarbonate loss
a) Severe biarrhoea, ileostommy


What would you see in 

Acute respiratory alkalosis?

Acute metabolic alkalosis

Acute respiratory acidosis

Acute metabolic acidosis

1) pH
2) bicarbonate
3) pCO2



Normal pH of the body is...



Describe the detailed 4-step approach to interpreting acid-base data

  • 1) What is the primary diagnosis?
  • -Acidaemia/alkalaemia first, then is it primary or acidosis or primary alkalosis? (look at pH)
  • -Is the primary disturbance respiratory or metabolic? (look at the pCo2, bicarbonate and Base excess)


  • 2) Is the compensation appropriate?
  • -Use an acid-base map or use a 'rule of thumb' (inappropriate compensation implies a mixed disorder)


  • 3) Calculate the anion gap
  • -A high anion gap implies metabolic acidosis is present and can determine the diagnosis (+ urine serum anion gap if serum anion gap is normal)
  • AG = cations - anions
  • AG = (Na+K) - (Cl+ bicarbonate)
  • (Normal AG reflects mainly protein anions)
  • Increased AG indicates the presence of unmeasured anions 


  • 4) Calculate the delta anion gap/delta HCO3 ratio
  • This helps to identify the presence of a co-existing metabolic acidosis or alkalosis
  • Delta ratio = increased anion gap / decrease [HCO3-]
    • Meausred AG - Normal AG
    • Normal [HCO3] - measured [HCO3]
  • If the delta ratio is lesser than 1 = concurrent with normal AG acidosis
  • (e.g. DKA and diarrhoea) (two conditions which result in acidosis)
  • If the delta ratio is between 1-2 = pure AG acidosis
  • If the delta ratio is greater than 2, it indicates concurrent metabolic alkalosis (e.g. lactic acidosis and vomitting). (one condition which result in acidosis and the other resulting in alkalosis)


Case report:

-42 year old man who is semi-comatosed with seizures

-pH is low
-PO2 is normal
-pCo2 is low
-Bicarbonate is very very low
-Base Excess = -19

Na, K and Cl are normal.

What can we determine from this?

Metabolic acidosis

AG = (140+4) - (102+8)
AG = 34 (high)


Ethylene glycol poisoning (dry-freeze) is suspected. Treatment was commenced with an ethanol infusion


What are some causes of normal Anion Gap acidoses  (Metabolic acidosis)

Non-renal causes (most common) 
-Normal renal acidification by the kidneys but loss of bicarbonate from non-renal causes
1) Diarrhoea
2) GI ureteral connections, ileostomy
3) External loss of pancreatic or biliary secretions

Renal causes 
-failure of renal acidification
1) Proximal renal tubular acidosis (type 2 RTA) 
2) Hypokalaemic distal renal tubular acidosis (type 1 RTA)
3) Hyperkalaemic distal renal tubular acidosis (type 4 RTA)
4) RTA of chronic kidney disease (failing kidney, but not quite failed)


What is Renal Tubular acidosis (RTA)?

-Defects in acid excretion: urine pH > 5.5 and urine ammonium not increased (inappropriate for metabolic acidosis)

-Proximal (Type 2) or distal (Type 1) types
-Usually hypokalaemia


Why does chronic vomitting cause muscle weakness?

1) Loss of HCl due to vomitting causes alkalosis

2) Hypokalemia is due to 
a) alkalosis
b) K+ loss to due to excessive laxative use (in chronic diarrhoea, K+ loss predominates due to the NaK exchange in the colon. In acute diarrhoea, Na+ loss predominates)

3) Hypokalemia causes muscle weakness (hyperpolarises exciatble cells)


What are the boarders of the Inguinal Canal?

Anterior Wall = 
1) Aponeurosis of External Oblique 
2) Internal Oblique (in Lateral 1/3) 

Floor = 
1) Inferior rolled edge of External Oblique aponeurosis (Inguinal Lig.) 
2) Lacunar Lig. (Medial)

Roof = 
1) Fibres of Internal Oblique 
2) Transversus Abdominis

Posterior Wall = 
1) Transversalis Fascia 
2) Conjoint Tendon (Medial 1/3)


What is the Hesselbach's (Inguinal) Triangle?

Site of Direct Heria- pushes through weakened abdominal wall

Corresponds to weak anterior wall (superficial inguinal ring)

Lateral Boarder: Rectus abdominis

Inferior Epigastric artery

Inguinal Ligament


Name the arteries found in the spermatic cord

3 Arteries - 

1) Testicular a. (from L2 level Abdominal Aorta)
2) Artery of Vas Deferens (Deferential a.)
3) Cremasteric a.


Name the nerves found in the spermatic cord

1) Genital branch of Genitofemoral n. - (L1-2)
2) Sympathetic nerves (from Testicular plexus)
3) (Ilioinguinal n. - L1) - (DOESN'T actually travel in cord)


A 16 year old NZ European boy presents with severe pain in his left testis associated with some swelling. It started an hour ago and is excruciating. He has otherwise been well in the past.

What is wrong with this patient?

testicular torsion

Spermatic cord twists round, cutting of blood supply (causing Ischaemia)


Describe the cremasteric reflex

Reflex that indicates whether torsion has occured in the testis

Normal Reflex
-Stroke superior medial thigh
-Stimulates sensory fibres of Femoral branch of Genitofemoral n. & Ilioinguinal n. (L1-2 origins)
-This in turn stimulates motor fibres of Genital Branch of Genitofemoral n. 
-Cremaster muscle contracts on Ipsilateral side, raising the testis

If Torsion has occured:
-Reflex not present 
-NB: Method is not infallible!
-Ultrasound confirmation = very reliable (Distinguishes torsion from epididymitis by showing lack of blood flow to testis)
-6 hour window of opportunity - chance of saving testis drops significantly after this time


What are Inguinal Hernias?

Inguinal hernias = protrusion of abdominal contents through inguinal canal

2 types: Indirect & Direct


DIRECT: Abdominal contents herniate through weak spot in fascia of posterior wall of Inguinal canal - Hesselbach's Triangle (don't travel into the groin)


Direct: **MEDIAL to Inf. Epigastric a.

More older in elderly patients


INDIRECT: Herniation goes through D.I.R. and through ENTIRETY (this is the difference between direct and indirect) of inguinal canal into scrotum Within Spermatic Cord

Indirect: LATERAL to Inf. Epigastric a.

More common in younger patients



How do you differentiate between inguinal or femoral hernia? 

1) Inguinal Ligament
-Inguinal: Superior to the inguinal lig (also more common in males)

-Femoral: Inferior to the inguinal lig (more common in females)

2) Pubic tubercle **
-Inguinal: Above and medial
-Femoral: Below and Lateral


How do you differentiate between the 3 hernias?

Q: Is there a Hernia?
Test: Cough impulse & reducibility
A: Positive cough impulse / lump is reducible = Hernia

Q: Is it Femoral or Inguinal?
Test: Find Pubic Tubercle and reference hernia to this point
A: Above & Medial = Inguinal, Below & Lateral = Femoral

Q: If Inguinal, is it direct or indirect? (Without Imaging)
Test: Using your knowledge of the surface anatomy place fingers over D.I.R and have patient cough
A: No Bulge = Indirect


What is Nephrotic Syndrome?

Nephrotic syndrome is often caused by damage to small blood vessels in the kidneys that filter waste and excess water from the blood. 

1) >3.5g/day urinary protein
2) Low serum albumin
3) Oedema (due to the loss of albumin which reduces oncotic pressure and results in aggregation of fluid in the interstitial space)

4) Frothy urine
5) Hypercholesterolaemia
6) Blood clots

7) Renal function may be normal or impaired (GFR)


What is the difference between Nephritic and Nephrotic syndrome?

Nephrotic ( o = odemia)

Nephritic = acute kidney injury


What are the root values of Sciatic Nerve?



What causes the rectum to be bent?


What is the significance of this?

Puborectalis from the Pubococcygeus part of the Levator Ani


Levator Ani is innervated by:

-pundendal nerve (S2-4)
-nerve to levator ani (S3-4)


If this is damaged, you lose the ability to control your bowel movements


What is Guevedoces? (DHT syndrome)

Condition characterised by lack of Androgen DHT (5α-Dihydrogen Testosterone) during development 
- 5α-Reductase deficiency (5a-reductase converts testosterone to DHT)
- DHT = 2-3x more potent androgen than testosterone

Males born with female primary sexual characteristics (i.e. no/underdeveloped penis - genitally ambiguous)

Sex = Male but Gender = Female due to lack of conspicuous male genitalia

Puberty: Raised androgen sex hormones may result in radical virilisation and development of Male genitalia

- Choice about whether they want to adopt the male gender identity or remain female



If the right renal artery becomes abnormally constricted, what will happen to renin secretion by the right kidney and the left kidney?


Also state what would happen to the BP

Right: Decrease flow, so Renin secretion will increase (constrict)

Left: May see increased flow because BP goes up (because of the increase in renin secretion by the right side). Renin secretion will decrease

Overall: Acute increase in renin. Will hit the rest of the body. BP will go up.


What stimulates release of aldosterone?

Angiotensin II (High NaCl)

High Potassium


What is the consequence of aldosterone activity?

1) Increase sodium and water re-uptake

  • Due to aldosterone binding onto the minteralocorticoid receptor,  and therefore the insertion of the ENac channel. This allows sodium to pass through the channel from the tubular lumen back into the body.


2) Lose more K+


What is Hyperaldosteronism treated by?

Treated by antagonists to the minerocorticoid receptors. (Spironolactone)


If you lose the function of your adrenal glands. What would you observe in the tubular secretion patterns?

Increased sodium excretion (due to loss of aldosterone-dependent sodium reabsorbtion)


What are the mediators of
1) osmolality

2) extracellular fluid volume


1) Osmolality: Antidiuretic Hormone (ADH)

2) ECF volume: Renin-angiotension system and Sympathetic Nervous system


How is decreased ECF volume compensated for?

Decreased ECF volume is compensated by increased renal reaborption of Na+

When ECF volume increases, there is less reabsorption of Na+

Increased Na+ reabsorption

  • -RAA (renin, angiotensin, aldosterone) system
  • -Sympathetic nervous system
  • -ADH

Decrease Na+ reabsorption

  • -ANP
  • -Decrease RAA and SNS activity
  • -Domapine
  • -Prostaglandins


Name 3 things that increases sodium reabsorption

-RAA (renin, angiotensin, aldosterone) system
-Sympathetic nervous system


What does ANP do?

What does it result in?

Atrial natriuretic peptide (inhibit Na+ reabsorption)

-Released from the atria in response to increased filling pressure and increased atrial stretch


This decreases Na+ reabsorption in DT and outer medullary CT by blocking ENac and by inhibiting Na, K-ATPase

1) Inhibits release of aldosterone
2) Inhibit renin release
3) Vasodilates afferent arteriole to increase GFR


What happens during dehydration?

1) (if change is 1-2%)

  • -Increased osmolarity
  • -Sensed by osmoreceptors in the hypothalamus
  • -Release ADH
  • -ADH binds to the V2 receptor.
  • -This leads to aquaporin 2 insertion into the tubular-lumen membrane.

2) (if the dehydration is enough to change the volume ~10%)

  • -Decreased atrial stretch
  • -Atrial stretch receptors feedback to the hypothalamus
  • -Increase in ADH


If someone has Syndrome of inappropriate antidiuretic hormone secretion (SIADH)...

1) What would you expect ADH levels to be in this patient (provided normal ADH levels can range from 1-5 picograms per milimeter)

Greater than 5

(faint = low BP)


If someone has Syndrome of inappropriate antidiuretic hormone secretion (SIADH)...

What would expect the osmolality levels in this patient to be? (provided normal range between 275-295 mm/kg)


Lower than 275 (reabsorb lots of water)


What is kidney failure?

Renal failure = decrease in GFR (glomerular filtration rate)

Normal = ~100ml/min

(A condition in which the kidneys lose the ability to remove waste and balance fluids.)

Two main forms:
1) Acute Kidney Injury
2) Chronic Kidney Disease


What is the normal glomerula filtration rate?

Normal = ~100ml/min


Plasma creatinine ______ as GFR _____


plasma creatinine rises as GFR falls


What is eGFR?

Estimate Glomerular filtration rat using plasma creatinine 

1) Weight (muscle mass)
2) Age (again, muscle mass and probably reduction in nephron)
3) Gender (women tend to have less muscle than men)

eGFR is inaccurate if muscle mass is unusally high or low (e.g. amputees, body bulders)


What are the 2 types of renal failure?


1) Acute
-acute kidney injury

2) Chronic
-chronic kidney disease

Both have increased creatinine and decreased GFR


What are the aetiologies of Acute Kidney Injury?

1) Pre-renal (before kidneys e.g. renal artery)

  • -Low BP
  • -Not enough blood to kidneys (dehydration, septic shock, haemorrhage, cardiogenic shock, severe renal artery stenosis)

2) Renal (kidney)

3) Post-renal (after kidney e.g. ureter)


What is the word for "very low urine output"



What sort of things would you see in a blood test of someone with Acute Kidney Injury (Pre-renal aetiology)

1) High creatinine

2) Potassium: hyperkalaemia
3) Phosphate: high
4) Calcium: may be low


How would you treat someone with Pre-renal Acute Kidney Injury?

Fix the underlying problem (usually increase BP)

1) Rehydrate
2) Treat bleeding
3) Fix heart
4) Antibiotics for sepsis
5) ICU treatment for persistent low BP (with inotropes)


What is Acute Tubular Necrosis?

Acute tubular necrosis (ATN) is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys. 

  • ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI. 
  • This makes up the "renal" part of the Acute Kidney Injury

-Mainly develops from Pre-renal causes.
-Persistant Oliguria and renal failure after correction of underlying pre-renal condition
-May take 4-6 weeks to recover.

-High creatinine
-Low urine output
-High potassium


How would you treat Acute Tubular Necrosis? (ATN)


-Maintain normal BP
-Treat the underlying problem

-If kidneys keep getting worse, put them on dialysis (usually when GFR <10ml/min)


What is Glomerulonephritis?

Inflammation of glomerulus can cause both acute kidney injury as well as chronic kidney disease


What are some Post-renal causes of Acute Kidney Disease?

Plumbing issues, tips are blocked or squashed

1) Kidney stones
2) Tumour
3) Prostate hypertrophy
4) Urinary retention

(cause Hydronephorsis and hydroureter)


What is the best way of Diagnosing post-renal failure?



What is Chronic Kidney Disease?

Gradual decline in renal function


Once your kidney is scarred, it will never go away. We just try and stop it from getting worse

1) elevated creatinine
2) elevated urea
3) Usually normal urine output


What is observed in tests of chronic kidney disease?

1) elevated creatinine
2) elevated urea
3) Usually normal urine output


What happens (in terms of hormones) in dehydration?

1) Water deficit
2) Increase in extracellular osmolality (sensed by osmoreceptors in the hypothalamus)
3) Increase in ADH secretion (posterior pituitary)
4) Increase in plasma ADH
5) Increase in H2O permeability in distal tubules, collecting ducts
6) Increase H2O reabsorbtion
7) Decrease H2O excretion


If we need to correct osmolarity what would you use?



If we need to correct ECF volume/blood volume what would you use?

angiotensin II


ADH is released in response to....

  1. increased osmolality- less than 1% change
  2. decreased volume- greater than 10% change of the ECF.


Describe the action of ADH

ADH (released from posterior pituitary) binds to the V2 receptors (intersititial side)

Causes insertion of Aquaporin-2 receptors on the tubular side

Causes water comes through the aquaporin-2 and the body reabsorbs water.


How can you differentiate between Central and nephrogenic diabetes insipidus

Central and nephrogenic diabetes insipidus (tasteless urine)

1) Central origin (can't produce ADH, due to brain injury or tumour)
2) Nephrogenic (enough ADH but receptor problems- problem to V2 receptor).

-Can be diagnosed by measuring levels of ADH in blood. If high, they're nephrogenic, if low, central

-Can also be diagnosed by giving them ADH and seeing if symptoms improve.
(Water deprivation test)


What is SIADH?

Syndrome of inapporpiate ADH secretion

-Plasma ADH levels higher than normal for the person's plasma osmolality and volume
-Patient retains water inappropriately (has negative free water clearance)

-Plasma osmolarity is significantly lower than normal

-If patient's water intake is not controlled a hypoosmolal
state results with possible dire consequences

-SIADH may be caused by brain injury or tumor, by certain anti-cancer drugs, and by lung cancer and certain other cancers.

-Patients "restricted" from drinking water


What is renin?

Secreted from Granula (JG) cells from the afferent vessels.

  • In the blood, renin acts on a protein known as angiotensinogen, resulting in the release of angiotensin I. 
  • Angiotensin I is cleaved to form Angiotensin II by ACE enzymes


Angiotensin II functions

1) Increase in aldosterone
2) vasoconstriction of efferent arteriole
3) Increase in proximal Na+ reabsorption
4) Increase in thirst
5) Increase in ADH release
6) Decrease in RBF, but maintains GFR
7) Decrease in Na+ and H2O excretion

8) (Can cause vasodilation if they bind to AT2 receptors but we have more AT1 receptors than AT2)


Factors that promote renin secretion:

1) decrease in afferent arteriolar pressure

2) Increase in sympathetic activity

3) Decrease in macula densa NaCl delivery



What are the consequences of Angiotensin II release?

Angiotensin II functions

​1) Increase in aldosterone
2) vasoconstriction of efferent arteriole
3) Increase in proximal Na+ reabsorption
4) Increase in thirst
5) Increase in ADH release
6) Decrease in RBF, but maintains GFR
7) Decrease in Na+ and H2O excretion

8) (Can cause vasodilation if they bind to AT2 receptors but we have more AT1 receptors than AT2)


What are ACE inhibitors?

Block ACE enzyme function

Cause decrease in angiotensin II (decrease in vasoconstriction)


Contrast ADH and Angiotensin II

ADH mainly reabsorbs water

Angiotensin II drags salt and water follows.

Way to correct osmolarity = use ADH

Way to correct volume = use angiotensin II


If you have a high salt diet, what happens? (not in terms of hormones)

-new balance is achieved.
-weight gain due to water retention (in order to maintain constant ECF osmolality).

1) Transient increase in plasma osmolality
2) Increase renal salt excretion (but with a few days lag)
3) Increased thirst (water retained to maintain ECF osmolality proportional to extra salt loaded).
4) Plasma osmolality returns to normal but at the expense of larger ECF volume.
5) Larger ECF volume continues while the high Na+ diet continues.
6) ECF volume returns to normal if less Na+ is ingested or renal Na+ excretion increases (e.g. diuretic).
7) As ECF volume increases, BP increases and renal Na+ loss increases ('pressure natriuresis').


What is the most important factor in determining the volume of the ECF?

Because the osmolality of the ECF is kept ~constant, the amount of Na+ in the body determines the volume of the ECF.

To maintain a constant ECF volume, the amount of Na+ excreted needs to match Na+ input by the diet.


What are the functions of the urinary system?

1) Filter out blood and remove waste 
2) Blood pressure/volume regulation
3) pH balance
4) Electrolyte balance


Describe the surface anatomy of kidneys

RK sits behind and below rib 12

LK sits behind and below rib 11/12 (higher because no liver)

Located posteriorly in abdomen (retroperitoneally)

Sitting on top of Psoas and quadratus lumborum in the abdominal cavity.


Describe the surface anatomy of ureters

Ureters exit kidney at L1 (Transpyloric plane)


What vessel is found in the midline of the body?

Abdominal aorta


Describe the arterial supply to the kidneys

Renal Arteries (lateral @L1/2)
- anterior & posterior branches
- (into segmental branches)

Right Renal artery is longer than Left (pass IVC)

Runs posterior to IVC


How does the L.renal vein run?


What is the significance of this?

L. renal runs under the SMA at the L1 plane

(note compression of left renal with aneurism of either SMA or Aorta)

Runs Anterior to Aorta, Under SMA & Posterior to Splenic v./Body of Pancreas


How does the ureter travel?

Leave the kidneys at @L1

Extend vertically down from hilum on surface of Psoas muscle

Crosses Bifurcation of Common Iliac Artery

Passes on lateral wall of Pelvis (Ilium) towards the Ischial Spine

Enters Bladder on inferior surface at the Trigone


Where are the 3 possible constrictions of the ureter?

1) Junction of the ureters and the renal pelvis (Pelvic-ureteric junction PUJ). *

  • *Most common sites of renal calculus obstruction

2) Where ureters cross the pelvic brim

3) As they enter the wall of the bladder (UVJ/VUJ). *



Name the regions in the male urethra

4 Distinct regions:

1) Pre-Prostatic

2) Prostatic
Widest part - many ducts emptying in

3) Membranous
Thinnest part - Through deep perineal pouch

4) Spongy
Through Corpus Spongiosum


What is the clinical significance of the Lateral Femoral Cutaneous nerve?

Bernhardt-Roth Syndrome 
(Meralgia parasthetica)

- numbness of outer thigh due to compression of the nerve as it passes under the Inguinal lig.

- Many causes (e.g. seat belts, exercise, tight clothing)


What is hyponatremia?

Hyponatremia is a condition that occurs when the level of sodium in your blood is abnormally low.


When this happens, your body's water levels rise, and your cells begin to swell.


What is absorbed at different parts of the nephron?

1) Proximal tubule reabsorbs 2/3 of filtered water, Na+ and Cl-,
and 90% of HCO3-. and 100% of glucose. Na+ coupled transport dominates. Filtrate remains at 300 mOsm (as water follows the Na+). pH drops only slightly as most H+'s are used to reabsorb HCO3-. Some new HCO3-made from glutamine.

2) Loop of Henle. Thick ascending limb pumps out NaCl but water cannot follow.
Countercurrent multiplier established by short loops in outer medulla (300-600
mOsm gradient). In long loops, when ADH is high: NaCl moves from tip and ascending
thin limb into inner medulla by osmosis, urea is deposited in inner medulla by collecting duct. Inner medulla gradient established (600-1200 mOsm) and draws water from descending thin limb and collecting duct to concentrate the urine.

3) Early distal convoluted tubule: impermeable to water. More NaCl absorbed (blocked by thiazide diuretics eg Furosemide). Urea
becomes concentrated.

4) Late distal convoluted tubule, connecting tubule and cortical collecting duct, what happens depends on ADH. 

Absence of ADH: No
aquaporins inserted, tubule is impermeable to water. NaCl continues to be reabsorbed by ENaC (target of K+ sparing diuretics). Urine stays dilute. 

Presence of ADH: tubule becomes water permeable. Urine concentrated (300 mOsm). Intercalated cells secrete H+ (some used to
reabsorb HCO3 - some freely excreted (pH balance).

5) Medullary collecting duct: what happens depends on ADH.

Absence of ADH: No aquaporins inserted, tubule is impermeable to water. NaCl continues to be reabsorbed. Urine stays dilute.

Presence of ADH: tubule becomes water permeable and more urea permeable. Urea
deposited into medullary interstitium. NaCl moves osmotically from long thin loops to interstitium. Urine becomes concentrated (max 1200 mOsm).

Intercalated cells secrete H+
(some used to reabsorb HCO3
- some freely excreted (pH balance). pH can drop to 4.5.
Additional H+ excreted by NH4
+ 'diffusion trapping'.


What happens if you vasoconstrict the afferent arteriole

Decrease blood flow

Decreased glomerular hydrostatic pressure

Decreased GFR


What happens if you vasodilate the afferent arteriole

Increases blood flow

Increase glomerular hydrostatic pressure

Increase GFR


What happens if you constrict the efferent arteriole

Moderate vasoconstriction

Increase glomerular hydrostatic pressure

Increased GFR


What are the mechanisms of renal autoregulation?


(Extrinsic and Intrinsic)

Extrinsic mechanisms

1) Renin-angiotensin II: constriction of the efferent arteriole - increase GFR)
2) Arterial natriuretic peptide ANP and BNP: dilation of the afferent arteriole- increase GFR)
3) Sympathetic nervous system: constriction of the afferent arteriole - decrease GFR - important in shock

Intrinsic mechanisms

1) Myogenic: increased arterial pressure stretches the afferent arteriole inducing it to constrict: offsets pressure increase and keeps GFR stable

2) Tubuloglomerular feedback: macula densa cells monitor NaCl levels in in distal tubule, if high they signal to the afferent arteriole to constrict (decrease GFR to return it to the stable setpoint).


Describe when the Renin-angiotension mechanism is activated and desribe how it works

One of the extrinsic mechanisms

1) Low GFR
2) Less NaCl passes the macular densa cells in the JGA
3) Paracrin signals released
4) JG cells release Renin
5) angiotensin II produced

6a) constriction of efferent arteriole
7a) Increase GFR

6b) Aldosterone released
7b) Increase Na+ uptake from distal nephron
8b) Increase blood volume


What % of things are reabsorbed in the proximal tubule?

~66% water and inorganic ions (Na+, Cl-, K+ etc.)

~100% glucose and amino acids

~90% of bicarbonate (filtrate becomes acidified)


What is the Fanconi syndrome?

Either hereditary or acquired results from an impaired ability of the proximal tubule to reabsorb HCO3-, Pi, amino acids, glucose and low-MW proteins resulting in increased urinary excretion of these solutes.


What sets up the Na+ gradient in the medulla in the short loop of nephrons? (describe the channels involved)

  • NKCC2 and Na/K ATPase mediates Na+ transfer to ECF
  • (Pumps Na+ and 2xCl- and K+ into the cell.)
  • ROMK channel recycles some fo the K+
  • Tight junctions are water-tight
  • ECF becomes hypertonic ('single effect').
  • NKCC2 is the target of the diuretic Furosemide


NKCC2 is the target of the _______ diuretic

NKCC2 is the target of the diuretic Furosemide


The Na/Cl transporter is blocked by _______________

The Na/Cl transporter is blocked by thiazide diuretics


What does the thiazide diuretic block?

Na/Cl transporter (in the arly distal convoluted tuubule)


What is Gittleman syndrome?

Mutation in the Na/Cl transporter (in the early distal convoluted tubule)

This results in Na+ and Cl- wasting, hyperaldosteronism and resultant hypokalemic metabolic alkalosis.

Patients are hypo-calciuric and hypomagnesemic.


What are the 2 cells found in the distal convoluted tubule, connecting tubule and collecting duct?

1) Principal cells (red)
2) Intercalated cells (green)


Describe Principal cells

Found in the distal convoluted tubule, connecting tubule and collecting duct.

Principal cells reabsorb Na+ and secrete K+ (K+ increases in the urine)

Absorbed via the Electrogenic Sodium Channel (ENaC)
-Reabsorption of Na+ makes lumen electronengative, which drives the K+ secretion.
-More lumenal Na+ present, the more K+ secreted

-This is important because if the Na/Cl is blocked in the early distal convoluted tubule using thiazide, there's going to be more Na+ uptake by the principal cells, and more K+ will be secreted
-This can cause hypokalemia, which can cause ventricular arrhthmias

-This channel is the target of Potassium-sparing diuretics e.g. amiloride


What do the Potassium-sparing diuretics e.g. amiloride target?


ENaC channels

Electrogenic sodium channel (in collecting duct/principal cell)


Describe the Electrogenic Sodium Channel (ENaC)

Found in the prinicpal cells

-Reabsorption of Na+ makes lumen electronengative, which drives the K+ secretion.
-More lumenal Na+ present, the more K+ secreted

-This is important because if the Na/Cl is blocked in the early distal convoluted tubule using thiazide, there's going to be more Na+ uptake by the principal cells, and more K+ will be secreted

-This can cause hypokalemia, which can cause ventricular arrhthmias

-This channel is the target of Potassium-sparing diuretics e.g. amiloride


What is the Liddle's Syndrome?

Mutation that causes increase in number of ENaC.

Too much NaCl is reabsorbed, leading to increased ECF volume and hypertension.


Describe the effects of Aldosterone on the principal cells

Aldosterone stimulates Na+ reabsorption and K+ secretion by gene expression changes:

Up-regulates activators that open ENaC channels AND induces more ENaC and Na/K ATPase

(more K+ is secreted)

Spirolactone (weak K+ sparing diuretic) blocks aldosterone


What does the Spirolactone diuretic block?



Describe Intercalated cells

Found in the distal convoluted tubule, connecting tubule and collecting duct

1) Important for acid-base balance and K+ absorption
2) Usually secrete H+ (H+ ATPase and H+/K+ ATPase)
3) Some H+ aer used to reabsorb HCO3-
4) Some H+ can be freely secreted (generates NEW HCO3-)
5) Some are just lost (way of losing acidity)


How does ADH work? (late distal convoluted tubule, connecting duct, CORTICAL collecting duct)

This depends on the level of anti-diuretic hormone (ADH) aka Arginine Vasopressin (AVP)

Binds to V2 receptor which activates cAMP

ADH causes aquaporin water channels to be inserted into the apical membrane

Now water gets reabsorbed rather than excreted into the urine (tube fluid can be 300mOsm)

In the absence of ADH, water remains in the tubule lumen

Response to ADH is rapid (vesicles rapidly inserted or re-internalised)


High ADH-> _____water reabsorption -> ______urine

Low ADH -> _____water reabssorption -> ____urine

High ADH-> high water reabsorption -> concentration urine

Low ADH -> low water reabssorption -> dilute urine