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Renal Flashcards

1
Q

Where does most reabsorption occur in the kidneys?

A

Proximal convoluted tubule

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2
Q

What are the two synthetic functions of the kidney?

A

Make EPO

Make vitamin D

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3
Q

Renal blood flow is approximately what percentage of cardiac output?

A

20%

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4
Q

What charge do the channels through the podocytes covering the glomerulus have?

A

Negative charge

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5
Q

What is the formula for net filtration pressure in the glomerulus? What is the approximate value for normal net filtration pressure?

A

NFP = hydrostatic pressure – oncotic pressure

Approximately 14 mmHg

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6
Q

What are the two mechanisms of myogenic autoregulation in the kidney? What does each mechanism do to renal blood flow and GFR?

A

Autoregulation 1: Dilates afferent arteriole, increases RBF but does nothing to GFR
Autoregulation 2: Constricts efferent arteriole, does nothing to RBF but increases GFR

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7
Q

When is adenosine released and what does it do to the kidneys with regard to renal blood flow and GFR? How does it do this?

A

Adenosine is released when the body is in its hydrated state. It constricts the afferent arteriole to decrease renal blood flow and GFR. It inhibits renin release and it is switched off with decreased filtrate flow to ensure filtrate flow doesn’t get too low.

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8
Q

Angiotensin II is a vasoconstrictor in itself. When is Angiotensin II released and what does it do to the kidneys with regard to renal blood flow and GFR? How does it do this?

A

Angiotensin is produced from the renin cascade
Angiotensin II is released when blood pressure is lower/hypovolaemia.
It constricts the efferent arteriole to maintain GFR. It is produced from the renin angiotensin system to increase water retention and blood pressure. It promotes the release of vasopressin.

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9
Q

When is PGE2 released and what does it do to the kidneys with regard to renal blood flow and GFR? How does it do this?

A

PGE2 is produced in the DCT
PGE2 is released in response to hypovolaemia due to decreased filtrate flow. It maintains renal blood flow by dilating the afferent arteriole. It suppresses vasopressin (ADH). Its action can be inhibited by NSAIDs, so NSAIDs can be dangerous in hypovolaemia.

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10
Q

What are the two main ways that sodium is resorbed in the PCT?

A

Na+/H+ antiporter

Na+/glucose symporter

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11
Q

How do loop diuretics work?

A

Blocking the NKCC cotransporter in the loop of Henle to prevent the reabsorption of Na+, K+, and 2Cl-so more water remains in the tubule instead of being reabsorbed so more water is passed out in urine.

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12
Q

Aldosterone is a steroid hormone, so how exactly does it work on principle cells in the DCT to increase Na+ resorption?

A

Aldosterone works intracellularly and regulates gene expression. It increases the production of Na+/K+ channels in principal cells to increase the reabsorption of Na+ in exchange for the secretion of K+.

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13
Q

What type of aquaporins are inserted into the collecting duct?

A

Aquaporin 2

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14
Q

What do the juxtaglomerular cells mainly release? If the JGA is stimulated, what does this cause?

A

JGA cells mainly release renin. If the JGA is stimulated this causes dilation of the afferent arteriole.

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15
Q

Triggering of what sort of receptors is responsible for JGA releasing renin?

A

Triggering of Beta-1 adrenergic receptors can cause the JGA to release renin.

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16
Q

What is the main muscle of the bladder?

A

Detrusor muscle

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17
Q

What is the smooth triangular region of muscle in the bladder called?

A

Trigone

It is the internal surface of the the bladder base.

The ureters open at the superior end obliquely with valve-like effect to prevent reverse flow to the kidneys.

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18
Q

How do the sympathetic and parasympathetic nervous systems control micturition? From what spinal levels do these nerves arise and what are the nerves called?

A

Sympathetic NS encourages storage of urine by causing relaxation of the detrusor muscle. This occurs via the hypogastric nerve which arises from levels T12-L2.
Parasympathetic NS encourages peeing by causing contraction of the detrusor muscle. This occurs via the pelvic nerve, from S2-S4.

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19
Q

What nerve provides voluntary/somatic control of micturition and from what spinal levels does it arise?

A

The pudendal nerve allows voluntary control of micturition by permitting the contraction of the external urinary sphincter. The pudendal nerve is from S2-S4.

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20
Q

In what part of the brain is the micturition centre?

A

The micturition centre is in the pons.

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21
Q

Largely, what type of MACh receptors are present in the bladder?

A

M2

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22
Q

What is acute kidney injury? What are some of the symptoms of acute kidney injury?

A

An abrupt loss of kidney function, usually in <7 days, shown by a sharp drop in GFR. Symptoms include a metabolic acidosis, hyperkalaemia, flank pain, decrease in urine output.

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23
Q

How is GFR normally calculated?

A

GFR 1/plasma creatinine concentration

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24
Q

Name 3 examples of antibiotics that interfere with bacterial cell walls.

A

Penicillins, vancomycin, cephalosporins

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25
Q

Name 5 examples of antibiotics that interfere with bacterial protein synthesis.

A

Macrolides, Chloramphenicol, Fusidic Acid, Aminoglycosides, Tetracyclines

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26
Q

Name some examples of antibiotics that interfere with bacterial nucleic acid synthesis.

A

Antifolates – sulphonamides, Quinolones – fluoroquinolone, Metronidazole, Rifampicin (RNA synthesis inhibitors)

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27
Q

What is the first line of antibiotic treatment for a UTI?

A

Trimethoprim

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28
Q

What is the difference between uric acid and urea?

A

Uric acid is a biproduct from nucleic acid breakdown, urea is a biproduct from protein breakdown.

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29
Q

What effects does aging have on the function of the human kidney and how?

A

Aging decreases GFR, kidneys less functional, as no. of nephrons you have over time decreases, less surface for filtration, increased BP with age too.

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30
Q

Over time, what happens to the sensitivity of the body’s blood vessels to NO?

A

Overtime, the blood vessel’s sensitivity to NO decreases. So as you get older, NO is not a very potent vasodilator any more, so you get a higher risk of stenosis, blood vessels’ diameters cannot be as easily changed.

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31
Q

What are the effects of aging on the immune system?

A 
Less CD4 cells, Less CD8 cells
B cell Ig class switching is reduced – antibody classes cannot be easily switched in response to an infection
Low complement
Low serum immunoglobulins
Low levels of naïve T cells.
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32
Q

How do NSAIDs affect the renal arteries?

A

NSAIDs block the action of prostaglandins at the renal arteries. PGE2 dilates the afferent arteriole to increase renal blood flow in response to hypovolaemia. NSAIDs can block the action of PGE2 so the renal afferent arteriole cannot dilate as easily.

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33
Q

What is the blood supply to the ureter?

A

Branches of the renal, gonadal and vesicular arteries.

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34
Q

An aneurysm in what branch of the aorta can cause compression on the left renal vein?

A

An aneurysm in the superior mesenteric artery can compress the left renal vein as the SMA passes over it.

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35
Q

What is the lymphatic drainage of the kidneys?

A

Left and right lumbar (caval or aortic) lymph nodes

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36
Q

At what spinal level do the renal arteries arise?

A

Renal arteries arise between L1 and L2

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37
Q

At what spinal level is the transpyloric plane?

A

Transpyloric plane is at L1

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38
Q

What sort of glands are the suprarenal glands?

A

Endocrine glands

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39
Q

The suprarenal glands are highly vascularised and they receive blood from two sources, what are these two sources?

A

Superior and inferior suprarenal arteries from the phrenic arteries
Middle suprarenal artery from the abdominal aorta

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40
Q

The venous drainage of the right and left suprarenal glands is different, what is the venous drainage pattern of each?

A

Right suprarenal gland drains directly into the IVC, left suprarenal gland drains into the inferior phrenic vein and then into the left renal vein.

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41
Q

There are no ganglion/synapses in the nerve supply to the suprarenal gland, why is this?

A

The chromaffin cells which are in the adrenal medulla itself act like the post ganglionic neurons anyway and the medulla itself is like a synapse as it originated from nervous tissue embryologically.

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42
Q

What are the two types of suprarenal medullary tumour called and what sort of symptoms would both present with and why?

A

Phaeochromocytoma – affects the chromaffin cells, symptoms are due to an excess in catecholamine secretion.
Neuroblastoma – derived from sympathetic nerve cells or ganglia outside the medulla, symptoms are due to an excess in catecholamine secretion.

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43
Q

What are the effects of cortisol?

A

Increases blood glucose by encouraging gluconeogenesis, decreases bone formation, suppresses the immune system, aids in the metabolism of fats, proteins, carbohydrates.

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44
Q

What are the symptoms of Cushing’s syndrome? What can it be caused by?

A

Can be caused by excess in ACTH production, adrenal cortical neoplasms or iatrogenic. Its symptoms are caused by an excess in glucocorticoid (cortisol) secretion, symptoms include: HTN, diabetes, hirsutism, osteoporosis.

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45
Q

What hormone is there an excess of with Conn’s syndrome? What can it be caused by?

A

Excess in aldosterone.

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46
Q

Concentration of what substance holds fluid inside blood vessels?

A

Albumin

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47
Q

What substances can stimulate and inhibit ADH release?

A

Stimulate ADH release: angiotensin II, nicotine

Inhibit ADH release: Alcohol, caffeine, ANP

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48
Q

What hormone is the main controller of Na concentration in the body and what sort of hormone is it? Where does it act in the body?

A

Aldosterone, steroid hormone, acts at principal cells in DCT of kidneys.

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49
Q

Why can high levels of aldosterone cause hypokalaemia?

A

Aldosterone works to increase the number of Na+/K+ channels in principal cells in the DCT in the kidneys, which reabsorb Na+ into the blood in exchange for K+ which is secreted into renal tubules. High levels of aldosterone therefore lead to lots of Na+ reabsorption at a consequence of lost K+.

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50
Q

Why is ANP released? What does it do?

A

ANP is released from the atria in response to atrial stretch due to high blood pressure. It antagonises the effects of aldosterone. It causes more sodium, and therefore more water, to be passed out in urine to lower blood volume and therefore pressure.

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51
Q

Name some things that can cause hyponatraemia and why is hyponatraemia dangerous?

A

Diarrhoea, loop diuretics, adrenal failure

It can cause cerebral oedema as water enters brain cells via osmosis.

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52
Q

What is the difference between osmolarity and osmolality?

A 
Osmolarity = number of osmoles per LITRE of solution
Osmolality = number of osmoles per KILO OF SOLVENT
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53
Q

What is tonicity?

A

Tonicity is the remaining osmotic pressure of a solution after the loss of any particles from the administered solution e.g. glucose taken up by cells.

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54
Q

What is the main intracellular cation?

A

K+ is the main intracellular cation

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55
Q

What two types of cell in the DCT and collecting duct control K+ secretion? What happens in each of these cells?

A

Principal cells: Na+ reabsorbed, K+ secreted

Intercalated cells: K+ reabsorbed, H+ secreted

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56
Q

What can cause hypokalaemia?

A

Diuretics (loop diuretics), Diarrhoea and vomiting

57
Q

Where do loop diuretics principally act and how can they be the cause of hypokalaemia?

A

Principally act on NKCC cotransporter in the loop of Henle, they can cause hypokalaemia as less sodium is reabsorbed in the loop of henle, there is a compensatory release of aldosterone in an attempt to reabsorb more sodium at the distal convoluted tubule. As a result, more sodium is reabsorbed in principle cells but more potassium is secreted into renal tubules and passed out in urine, hence causing hypokalaemia.

58
Q

What can cause hyperkalaemia? What is the treatment of hyperkalaemia?

A

Renal failure, acidosis, aldosterone impairment

Treatment with Insulin and glucose to draw K+ back into cells. Insulin is called ‘actrapid’ in IV preparation.

59
Q

What hormone increases plasma Ca2+ and what hormone decreases it? How do each of these hormones work to control processes in the bones, gut and kidneys?

A

Parathyroid hormone increases plasma Ca2+ by increasing osteoclast activity, freeing up minerals from bone, increasing Ca2+absorption in the small intestine and increasing Ca2+ reabsorption in the kidneys.
Calcitonin decreases plasma Ca2+ by decreasing osteoclast activity and increasing osteoblast activity it also increases renal Ca2+ activity.

60
Q

What are the causes and effects of hypocalcaemia and hypercalcaemia?

A

Hypocalcaemia is caused by hypoparathyroidism, kidney failure and hyperventilation. It can cause muscle spasms and paraesthesia.
Hypercalcaemia is caused by hyperparathyroidism and malignancy – especially bone cancers that increase osteoclast activity. It can cause “bones, moans, stones and groans” – confusion, abdominal pain, ureteric stones and bone pain.

61
Q

What is meant by the term base excess?

A

The measure of how much base there is in the blood, with the primary basic component being HCO3-. It can tell you whether an acid-base disturbance is metabolic/respiratory as HCO3 is primarily a metabolic base. A negative number for base excess means there is an excess of HCO3 whereas a positive indicates a deficit.

62
Q

What would be causing an acidosis with a high anion gap?

A

Organic acid disturbance.

63
Q

What are the normal values for blood pH, pCO2, pO2, HCO3- and BE?

A 
pH = 7.35-7.45
pCO2 = 5.1-5.5 kPa
pO2 = 11.5-14.5 kPa
HCO3- = 24-28 mmol
BE = 0 mmol
64
Q

What happens to the cell cycle when a cell ages?

A

Permanent cell cycle arrest

65
Q

What sort of cells contain telomerase?

A

Germ cells contain telomerase

66
Q

What happens to the telomeres within cells over time?

A

They get shorter over time

67
Q

What are the three stages of oliguria?

A

Pre-renal, renal and post-renal.

68
Q

Why might extension of the hip joint increase pain from the paranephric region?

A

The close relationship of the kidneys to the psoas major muscle explains this.

69
Q

What are the 4 renal capsules? From inside out

A

Proper capsule
Perinephric fatty capsule
Renal fascial capsule
Paranephric capsule

70
Q

What structure lies posterior to the kidney?

A

Costodiaphragmatic recess of pleura

71
Q

Where are the 3 main areas of ureter constriction?

Why are these clinically important areas?

A

Where the renal pelves meet the ureter
Where the ureter crosses the brim of the pelvic inlet
During the passage through the wall of the urinary bladder

72
Q

What is the blood supply to the kidneys?

A

Branches from:

Renal artery
Abdominal artery
Common iliac artery
Internal iliac artery
Testicular/Ovarian artery
73
Q

What is the order of structures within the renal hilum? Anterior to posterior

A

Vein
Artery
Ureter

74
Q

Name the sphincter at the bottom of the urinary bladder.

A

Sphincter vesicae

75
Q

What is the average volume that the bladder can hold?

A

300-500ml

76
Q

What is the arterial supply to the urinary bladder?

A

Superior and inferior vesicle arteries

- branches of the internal iliac artery

77
Q

What is the venous drainage of the urinary bladder?

A

Vesical venous plexus

- communicates with the prostatic plexus which then drains into the internal iliac vein

78
Q

What is the lymphatic drainage of the urinary bladder?

A

Internal and external iliac nodes

79
Q

What is the nerve supply to the urinary bladder?

A

Pelvic plexus AKA inferior hypogastric

80
Q

Which muscle contracts to cause emptying of the bladder?

A

Detrusor muscle

81
Q

What structure relaxes to allow micturition?

A

Internal urethral sphincter

82
Q

Where does the autonomic innervation to the pelvis originate?

A

Sympathetic T11-L2

Parasympathetic S2-S4

83
Q

What is the process of micturition?

A

Reflex action which is voluntarily controlled after 2-3 years.

Initiated by stretch of the bladder muscle

Nerve impulses cause contraction of detrusor muscle and relaxation of the internal sphincter

Once urine enters the urethra, additional affronts fire impulses to the spinal cord and reinforce the reflex action

In adults, the process is inhibited by the cerebral cortex

84
Q

What is a coincident suprarenalectomy?

A

The suprarenal glands are enclosed by the renal fascia, and are only separated from the kidneys by a thin fascial septum. As a result, the suprarenal gland may be removed accidentally during removal of the kidney.

85
Q

What is the embryological origin of the cortex of the adrenal gland?

A

Mesoderm

86
Q

What is the embryological origin of the medulla of the adrenal gland?

A

Neural crest cells

- associated with sympathetic nervous system

87
Q

What is produced in the zona reticularis of the adrenal cortex?

A

Androgens

- dehydroepiandrosterone

88
Q

What is produced in the adrenal medulla?

A

Catecholamines

  • adrenaline
  • noradrenaline
89
Q

What is produced in the zona glomerulosa of the adrenal cortex?

A

Mineralocorticoids

- aldosterone

90
Q

What is produced in the zona fasciculata of the adrenal cortex?

A

Glucocorticoids

  • cortisol
  • cortisone
  • corticosterone
91
Q

What is the arterial supply to the adrenal glands?

A

Superior and inferior suprarenal arteries
- from the phrenic arteries

Middle suprarenal arteries
- from the abdominal aorta

92
Q

What is the venous drainage of the adrenal glands?

A

Right suprarenal vein
- drains into inferior vena cava

Left suprarenal vein

  • joined by the inferior phrenic vein to drain the left suprarenal gland
  • drains into the left renal vein
93
Q

What is the nerve supply to the adrenal glands?

A

From the coeliac plexus and the abdominopelvic splanchnic nerves

Presynaptic sympathetic fibres synapse with the chromatin cells within the medulla

T10 - L1

94
Q

What is the most likely clinical diagnosis?

Hypertension
Sweating
Headaches
Nervousness

A

Phaeochromocytoma

  • adrenal medulla tumour
  • derived from chromatin cells
  • symptoms are due to excess catecholamine secretion
  • may be malignant

OR

Neuroblastoma

  • rare but highly malignant adrenal medulla tumour
  • derived from sympathetic nerve cells outside the medulla
  • symptoms are due to excess catecholamine secretion
95
Q

What is the most likely clinical diagnosis? What is the pathophysiology of this condition?

Hypertension
Diabetes
Hirtuism
Osteoporosis

A

Cushing’s syndrome

Due to excess ACTH (adrenocorticotropin hormone) secretion from the pituitary, adrenal cortical neoplasms or iatrogenic.

ACTH causes increased production and release of cortisol

Symptoms are due to excess glucocorticoid secretion

Increase in cortisol inhibits sodium loss through small intestine, leading to sodium retention and hypertension

Sodium load augments K+ excretion by cortisol; in order for K+ to move out of cell, cortisol moves an equal amount of Na+ ions into the cell, leading to hypokalaemia

Hypernatraemia
Hypokalaemia

96
Q

What is the most likely clinical diagnosis?

Weight loss
Hypotension
Pigmentation

A

Suprarenal cortical insufficiency

Due to autoimmune adrenalitis
- lack of mineralocorticoids and glucocorticoids and androgens

97
Q

What tumour causes Conn’s syndrome?

A

Adenoma of zona glomerulosa

Resulting in hyperaldosteronism

  • hypertension
  • headaches
  • poor vision

Not very many symptoms

98
Q

What are the functions of the kidneys?

A
  • Remove waste products and excess fluid from the body (as urine)
  • Regulation of body salts, potassium and acid content
  • Remove drugs
  • Production of hormones that regulate blood pressure
  • Production of hormones that produce red blood cells (EPO)
  • Produce active form of Vitamin D
99
Q

What are the divisions of the blood supply to the kidneys?

A 
Aorta
Renal artery
Segmental artery
Interlobar artery
Arcuate artery 
Cortical radiate artery 
Afferent arteriole
Glomerulus
Efferent arteriole 
Peritubular capillaries (vasa recta)
Cortical radiate veins
Arcuate veins 
Interlobar veins 
Renal vein 
Inferior vena cava
100
Q

What are the normal values for:

pH
PCO2
PO2
HCO3-
Base Excess
A 
pH = 7.35-7.45
pCO2 = 5.1-5.5
pO2 = 11.5-14.5
HCO3- = 24-28 
BE = 0
101
Q

Is aspirin an acidic or basic drug?

A

Aspirin is salicylic acid therefore is an acidic drug

102
Q

How is most of the acid produced in the body?

A

Through respiration
- Carbonic acid from CO2 and H2O

Metabolic production of lactic acid, sulphuric acid etc. accounts for less than 1% of total acid produced in 1 day

103
Q

Are pancreatic secretions and gastric secretions acidic or alkaline?

A

Pancreatic

  • alkaline
  • contains high amounts of bicarbonate

Gastric

  • acidic
  • contains high amounts of H+

If either is lost in substantial quantities, acid/ base disturbance can result

104
Q

How are inorganic and organic acids metabolised?

A

Inorganic
- excreted by kidneys unchanged

Organic
- undergo liver metabolism

105
Q

Name 3 mechanisms of acid-base homeostasis

A

Buffers

  • immediate
  • seconds- minutes

Respiratory

  • rapid
  • minutes - hours

Metabolic (renal)

  • slow
  • hours - days
106
Q

Name some buffers

A 
Proteins
- albumin
- haemoglobin 
Phosphate 
- HPO4 2- + H+ = H2PO4-
Carbonic acid
H2O+CO2 = H2CO3 = H+ + HCO3-

Carbonic acid is the main extracellular buffer

107
Q

Where is the final urine acidity determined?

A

In the distal convoluted tubule by intercalated discs

Urine pH can vary from 4.5-8

108
Q

Where does most of the H+ secretion and HCO3- reabsorption take place?

A

In the proximal convoluted tubule

109
Q

What acid/base disturbance can result from impaired renal function?

A

Acidosis

- acid is constantly being produced through respiration and so impaired renal elimination leads to acidosis

110
Q

How does erythropoietin affect RBC count?

A

Fall in O2 levels in renal tissues
- pO2 low

EPO secretion by peritubular cells in kidney

Stimulated RBC precursors in bone marrow and their differentiation to RBC

NOTE: anaemia is likely with untreated chronic kidney disease

111
Q

How does vitamin D affect bone density?

A

Cholecalciferol (vitamin D3) is produced from dietary precursors and from the reaction between skin and vitamin D.

D3 is then converted to 25-hydroxycholecalciferol in the liver

25-OH D3 is the converted to 1,25-dihydroxycalciferol (1,25- (OH)2 D3

1,25- (OH)2 D3 raises serum Ca2+ by

  • promoting GI absorption
  • decreasing renal excretion (increase tubular reabsorption)
  • stimulating bone reabsorption

Rickets or osteomalacia can result from hypocalcaemia secondary to renal disease

112
Q

What is oncotic pressure?

A

A form of osmotic pressure exerted by proteins, namely albumin

113
Q

What are the boundaries for the stages of CKD?

A 
Greater than 90 = normal 
60-90 = mild 
30-59 = moderate
15-29 = severe 
Less than 15 = failure
114
Q

What are the processes of autoregulation?

A

When the arterial pressure drops this leads to

  • fall in renal blood flow
  • fall in glomerular filtration rate

Afferent arteriole dilates

  • improves renal blood flow despite a lower afferent arteriole pressure
  • causes decrease in filtration fraction

Efferent arteriole constricts

  • improving glomerular filtration rate
  • despite lower renal blood flow
  • this increases the filtration fraction

In reality, both of these processes occur simultaneously and so filtration fraction will be maintained

115
Q

What is the filtration fraction?

A

The filtration fraction represents the proportion of fluid reaching the kidneys which passes into the renal tubules

116
Q

What is the equation for the filtration fraction?

A

Filtration fraction = glomerular filtration rate/ renal plasma flow

117
Q

What GFR marker can be used in clinical practice?

A

Creatinine

  • main marker
  • there is minor tubular secretion and so a slight overestimation

Cystatin C

  • no tubular secretion
  • small protein produced by most cells

Inulin
- has to be infused at a steady state

118
Q

Give a brief overview of the main roles of each part of the nephron

A

Glomerulus
- produce filtrate through high pressure filtration of blood

Proximal convoluted tubule
- conservation of majority of useful filtration components (Na+, HCO3-, glucose)

Descending loop of Henle

  • permeable to H20 but not ions
  • creates a hypertonic filtrate

Ascending loop of Henle

  • permeable to ions, but not to H20
  • pumps ions into the interstitial fluid
  • creates a hypertonic interstitial fluid

Distal convoluted tubule
- final regulation of the amount of Na+, K+ and H+ excreted in urine

Collecting duct

  • final regulation of H2O excretion and thereby urine concentration
  • normally impermeable to all but can have aquaporins inserted to make urine more concentrated
119
Q

What can cause an osmotic diuresis?

A

Osmotic diureses is the increase in urination rate caused by the increased presence of certain substances in the tubules.

It can occur the a patient has hyperglycaemia; as the concentration of glucose in the filtrate is higher, the transport maximum is reached before all of the glucose can be reabsorbed.

This results in glycosuria and diuresis as the increased glucose causes an increased osmotic pressure within the tubules, causing retention of water within the lumen, increasing urine output.

120
Q

What are the 2 mechanisms of Na+ reabsorption in the PCT?

A

Na+/H+ antiporter

  • Na+ moves into tubular cell
  • H+ moves into tubule lumen
  • Na+ then moves into interstitial fluid in co-transport with HCO3-

Na+/glucose symporter

  • Na+ and glucose move from tubule into tubular cell
  • Na then moves into interstitial cell through the Na+/K+ ATPase active pump
121
Q

Explain the counter current system

A

The vasa recta vessels run in the opposite direction to the Loop of Henle.

Electrolytes leaving the ascending limb of the loop move into the descending limb of the vasa recta vessel. This increases the osmotic pressure in the vasa recta.

As the osmotic pressure in the vasa recta has risen, the water leaving the descending limb of the loop moves into the vasa recta.

The osmolarity of the blood within the vasa recta on the venous return is almost the same as the osmolarity within the vasa recta before reaching the loop of Henle.

122
Q

Explain the mechanism of action of the NKCC in the ascending loop of henle

A

NKCC channel is a K+, Na+, Cl- co-transporter. it transports 1Na+, 1K+ and 2 Cl- ions into the tubular cell. The Na+ and K+ then move into the interstitial fluid via the Na/K+ ATPase active pump

123
Q

What channel does the drug furosemide - loop diuretic - work on?

A

NKCC

Furosemide inhibits the action of the NKCC channel to decrease reabsorption of Na+ and thus decrease reabsorption of H20

124
Q

Through which channels does H2O leave the descending loop of Henle?

A

Aquaporin 1

By (passive) diffusion

125
Q

Where are principle cells found, what do they control and what channel do they use to control this?

A

Found in the distal convoluted tubule, they control final Na+ excretion through ENaC

Aldosterone stimulates increased ENaC synthesis and ENaC pump activity

  • Increased ENaC synthesis increases Na+ reabsorption and K+ excretion
  • Increased pump activity keeps intracellular Na+ down by pumping the Na+ out of the principal cell into the interstitial cell
  • Aldosterone therefore increases blood pressure

ENaC is stimulated by

  • aldosterone
  • increased K+
  • Alkalosis
  • Increased tubular flow
126
Q

Where are intercalated cells found, what do they control and what channel do they use to control this?

A

Found in the distal convoluted tubule, control acid-base balance through H+/K+ ATPase pump.

The H+/K+ ATPase pump excretes H+ and reabsorbs K+ depending on the acid base balance

If there is a lot of H+ in the blood, the H+/K+ pump will excrete H+ into the tubule. In response to this, the pump will force K+ out of the tubule and into the intercalated cell.

The H+/K+ pump is stimulated by

  • acidosis
  • hyperkalaemia
127
Q

What hormone causes insertion of aquaporins into the collecting duct? What aquaporins does it cause insertion of?

A

ADH (vasopressin) - released from posterior pituitary under control of osmoreceptors in th hypothalamus.

Aquaporin 2

ADH binds to the ADH V2 receptor on the interstitial side of the tubular cell. This G coupled protein receptor causes increased cAMP, which causes insertion of aquaporin 2 on the luminal surface of the tubular cell.

Due to the high osmotic pressure within the tubular cell (remember that the interstitial fluid is extremely concentrated), water rushes into the tubular cell through the aquaporin. Water then moves across the cell and moves into the interstitial fluid through other constant aquaporins.

This causes more water to moves into the vasa recta and thus BP to increase.

128
Q

What are the types of ADH receptors?

A 
V1a
- peripheral circulation 
- vasoconstriction 
 V2 
- renal collecting duct 
- aquaporin 2 insertion 
V2 
- endothelium 
- clotting factor release
V3 
- CNS
- ACTH released
129
Q

Explain the process of bicarbonate buffering

A

HCO3- carried in the tubule reacts with H+ excreted by the tubular cell through the Na+/H+ ATPase pump.

This forms H2CO3 which then breaks down into H20 and CO2 - catalysed by carbonic anhydrase.

CO2 diffuses into the tubular cell where it binds with H20 to form H2CO3, which then dissociates into H+ and HCO3-.

HCO3- is then co-transported with Na+ into the interstitial fluid from where it moves into the blood.

This whole process of bicarbonate buffering is essentially the process of bicarbonate reabsorption into the blood from the tubule.

This process occurs in the PCT

130
Q

Explain the process of buffering by phosphate

A

HPO42- in the tubule binds to H+ which is excreted into the tubule by the Na+/H+ pump, forming H2PO4 which is then excreted in the urine.

As the H+ has been excreted from the cell, HCO3- is added to the blood.

This process occurs in the DCT

131
Q

Explain the process of buffering by ammonia

A

Ammonia is formed from amino acid breakdown, particularly glutamine.

Ammonia leaves the tubular cell and enters the lumen where it reacts with H+ released from the H+/K+ ATPase pump to form NH4+ which is then excreted in the urine.

This process occurs in the DCT.

It is through this mechanism that we can get rid of most of the H+ in the tubule when the blood is too acidic.

132
Q

Describe the location and role of the juxtaglomerular apparatus.

A

Located between the afferent arteriole and the DCT. It therefore receives inputs from both areas.

The juxtaglomerular apparatus has 2 main cell types

Granular cells
- sense decrease in pressure

Macula dense cells
- sense decrease in tubular Na+ flow

133
Q

A patient is involved in a serious road traffic accident and has suffered from a ruptured spleen. Explain the physiological changes that take place with regards to blood pressure.

A

As patient has lost blood, they will become hypovolaemic.

Hypovolaemia leads to decreased renal blood flow. This is sensed by the granular cells of the juxtaglomerular apparatus. The macula densa cells of the JGA then release renin into the blood.

Renin converts angiotensinogen in the blood into Angiotensin I. Angiotensin I is then converted to Angiotensin 2 by ACE in the lungs.

Angiotensin II causes vasoconstriction of arterioles; including the efferent arteriole of the nephron to maintain GFR. The constriction of other arterioles throughout the body helps to increase BP.

Angiotensin II also acts on the zona glomerulosa of the adrenal gland to cause it to release aldosterone.

Aldosterone acts on the cells of the DCT, causing them to increase Na+ reabsorption and thus increase BP.

Aldosterone also stimulates ADH release from the posterior pituitary gland. ADH acts on the cells of the collecting duct, causing insertion of aquaporin 2 on the luminal side of the tubular cell. This causes increased reabsorption of water and thus an increase in BP.

ADH also causes vasoconstriction

Additionally, the low BP is sensed by peripheral baroreceptors. This signal is sent to the medulla oblongata which causes increased HR, vasoconstriction and neural stimulation of JGA cells to release renin.

134
Q

What condition would cause a +ve base excess?

A

Base excess if the extent to which HCO3- exceeds the expected value.

+ve BE = metabolic alkalosis
-ve BE = metabolic acidosis

135
Q

What acid disturbance would cause a raised anion gap?

A

Anion gap is a a measure to help identify the cause of a metabolic acidosis as being a disturbance of either

  • organic acid
  • inorganic acid

raised anion gap = organic
normal anion gap = inorganic

Normal range is between 8-16mmol/L

The normal anion gap is mostly caused by albumin

136
Q

Name 4 factors that can affect ADH release

A 
Stimulated by
- Angiotensin II (as part of shock response)
- Nicotine 
Inhibited by 
- Alcohol 
- ANP
137
Q

What are the effects of Atrial Natriuretic Peptide?

A

ANP is released when the atria is stretched due to increase blood volume

It causes

  • increased GFR
  • decreased aldosterone secretion
  • decreased renin release
  • decreased ADH release

Overall increasing Na+ excretion

138
Q

What are the clinical implications of hyponatraemia? What may cause hyponatraemia?

A

In hyponatraemia, water moves in the brain cells by osmosis causing ‘cerebral oedema’

Cerebral oedoma causes drowsiness –> convulsions –> coma –> death

There is a greater risk in children

Hyponatraemia is caused by

  • diuretics
  • vomitting/ diarrhoea
  • adrenal failure (Addison’s)

Hypernatraemia is caused by

  • heart failure
  • inappropriate ADH secretion
  • SIADH may be caused by tumours, infections, SSRIs and hypothyroidism
  • intake excess through oral or IV

GI (3 decks)

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