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Semester 2 (1st year) > Wk 28 > Flashcards

Wk 28 Flashcards

1
Q

What forms the inorganic component of bones?

What forms the organic part?

A

Calcium phosphate

Collagen

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2
Q

How does a muscle cell work? (The steps)

AP arrives, triggering what?

What destroys left over Ach?

What channels are opened and what happens?

Ca binds to what? (exposing what?)

What heads bind to what?

What is pumped out of the what with ATP?

What complex slides back and what heads are blocked again?

A

Action potential arrives –> releases Ach, which triggers a muscle action potential

(Acetylcholinesterase destroys left over Ach so no more muscle APs occur)

Muscle AP opens Ca channels in the sarcoplasmic reticulum, so Ca flows into the sarcoplasm

Ca binds to troponin (exposing the binding site for myosin)

Myosin heads bind to actin and muscle contracts

Ca is pumped out of sarcoplasm with ATP

Troponin-tropomyosin complex slides back where myosin heads are blocked again= muscle relaxes

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3
Q

Plasma calcium is tightly maintained between what values?

A

2.1-2.6 mmol/L

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4
Q

__% of calcium is circulating ‘ionised’ = free and physically available

__% is bound to what plasma protein?

Which out of those 2 is maintained and which is more changeable?

A

44%

46% (mostly albumin)

(other 10% bound to other molecules like HCO3)

Free fraction is maintained while bound fraction more changeable

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5
Q

What is the main role of phosphate?

What other 5 roles is it involved in?

A

Bone mineralisation

pH buffering 
Nucleic acids 
Attached to proteins and lipids 
Energy production 
Intracellular signalling (phosphorylation)
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6
Q

What are osteoprogenitor cells?

What are osteoblasts?

What are osteocytes?

What are osteoclasts?

What are bone lining cells?

A

Stem cells

Blasts= secrete bone matrix

Cytes = mature bone cells

Clasts= breakdown bone matrix

Bone lining cells= contribute to matrix maintenance

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7
Q

What is Wolff’s Law?

A

Bone grows or remodels in response to demands placed on it

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8
Q

Where are osteocytes located?

How do osteoclasts detect stresses?

A

Lacunae

They monitor bone matrix and communicate with osteoblasts and osteoclasts to regulate remodelling

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9
Q

What do osteoblasts secrete new bone as and what does it contain?

A

Osteoid

It contains collagen and Ca binding proteins (which attract ECF Ca)

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10
Q

What 2 things do osteoblasts secrete and how do they affect bone resorption?

(The balance of these secretions regulates osteoclast activity)

A

RANK Ligand (RANKL)= stimulates bone resorption

Osteoprotegerin (OPG)= reduces bone resorption

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11
Q

What 2 things do osteoclasts secrete?

What substance does this resorb?

A

Acid and collagenases

Calcium (to increase plasma calcium)

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12
Q

What 3 main hormones promote osteoblast differentiation? (And therefore bone growth/ mineralisation)

Which hormone increases bone resorption by promoting osteoclast activity?

A

Growth Hormone
IGF-1
Sex hormones (estrogen)

Thyroid hormone

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13
Q

What cells secrete Calcitonin?

What does it do?

A

Thyroid parafollicular cells

Decreases blood calcium and phosphate and puts it into bone (inhibits osteoclast activity)

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14
Q

Parathyroid hormone secretion…

Low Ca _______ PTH secretion

High Ca _______ PTH secretion

A

Stimulates

Inhibits

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15
Q

What cells secrete parathyroid hormone?

What are the effects of PTH?

A

Chief cells of parathyroid glands

Increase plasma Ca and Mg

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16
Q

What are the 4 main effects of PTH?

A

Increases activity of osteoclasts

Increases Ca reabsorption in kidneys

Increases phosphate excretion in kidneys

Increases conversion of calcitriol (active Vit D) which also increases plasma Ca

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17
Q

What is the Vit D called what you get in your diet?

What is the Vit D you get from UVB exposure?

And what is it called when the kidneys activate it?

A

Ergocalciferol (D2)

Cholecalciferol (D3)

Calcitriol

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18
Q

What are the effects of calcitriol in the gut, kidney and bone?

What effect does it have on PTH secretion?

What effect does it have on further calcitriol production?

A

Increased absorption in the gut, kidney and bone

Inhibits PTH secretion

Inhibits further calcitriol production

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19
Q

Fibroblast Growth Factor 23 (FGF23) is secreted from bone in response to what?

What does it do and how does it do it?

A

Increased plasma phosphate

Reduces blood phosphate levels by reducing gut absorption (decreases calcitriol production) and stimulating kidney excretion of phosphate

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20
Q

What are the 3 mechanisms of controling pH in the body?

A

Buffer systems (1st response)

Respiratory regulation (2nd to respond)

Renal mechanisms (3rd to respond)

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21
Q

Lungs can only eliminate _____ acid (volatile acid) as ____

Only the kidneys can excrete fixed (_____) acids

A

Carbonic acid as CO2

Metabolic acids

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22
Q

Major key renal activities that maintain acid/ base balance:

1) Reabsorption of filtered _________ associated with H+ secretion
2) Production of new _______ via glutamine metabolism and ammonia secretion
3) Excretion of _____ ______ accociated with production of new bicarbonate

A

Bicarbonate

Bicarbonate

Fixed acid

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23
Q

__% of the filtered bicarbonate is reabsorbed by the ______ _______

(This process is dependent on ___ secretion in the tubular fluid by renal cells)

A

80% by the proximal tubule

Dependent on H+ secretion into urine (so bicarb wants to leave because too concentrated in tubules)

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24
Q

What is the acid base buffer formula?

A

CO2 + H2O H2CO3 HCO3- + H+

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25
Q

For each H+ secreted by _____ cells into the tubule lumen (urine), there is ___ bicarb ion reabsorbed into blood

A

Renal cells

One bicarb (1 for 1)

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26
Q

Most of the buffering of excess H+ in tubule fluid is carried out by what buffering system?

A

Ammonium buffering system

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27
Q

Glutamine comes into the kidney and makes __________ and _______ (____)

Which of these goes into the blood and which is excreted into urine?

A

Bicarb and ammonium (NH4)

Ammonium into urine and bicarb into blood

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28
Q

Which cells of the renal collecting ducts can generate new bicarb ions while excreting H+ ?

Which buffer system does this involve?

A

Type A intercalated cells

Phosphate buffer system

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29
Q

The net effect of excretion of one H+ into urine is the reabsorption of _______ and ______ into the blood

A

1 Bicarb and 1 Na

30
Q

Resp acidosis= hyper or hypoventilation

Resp alkalosis= hyper or hypoventilation

What is the blood pH for resp acidosis vs resp alkalosis

A

Resp acidosis is a build up of CO2 so not breathing it off enough= hypoventilation

Resp alkalosis is not enough acid/ CO2 so breathing too much= hyperventilation

Resp acidosis pH= below 7.35
Resp alkalosis pH= above 7.45

31
Q

Metabolic acidosis can be due to what? (Why?)
(2 causes)

Metabolic alkalosis can be due to what? (Why?)
(1 cause)

A

Acidosis can be due to renal disease (inadequate bicarb absorption or acid secretion) or severe diarrhoea (because no time for absorption of bicarb from GI lumen back into blood, all lost in stool)

Alkalosis can be due to severe vomiting (causes H+ to be drawn from the blood to replace stomach acid so less acid in blood now)

32
Q

What is the 1st line of defence against pH shift? (Give the 3 types)

What is the 2nd line of defence against pH shift? (2 types)

A

1st line= chemical buffer systems (bicarb buffer system, phosphate buffer system and protein/ ammonium buffer system)

2nd line= physiological buffers (resp mechanism= CO2 excretion, renal mechanism= H+ excretion and bicarb retention and production)

33
Q

How do the proximal convoluted tubules deal with metabolic acidosis?
(3 things)

A

More H+ secreted in urine

Ammonium secreted in urine

More bicarb produced and reabsorbed

34
Q

How do Type A intercalated cells deal with metabolic acidosis?
(2 things)

A

More H+ secreted into urine by phosphate buffer system

More bicarb and K reabsorbed into blood

35
Q

What is the body’s response to metabolic alkalosis?

3 things

A

Chemical buffer systems release H+

Respiratory compensation (breathing slower and shallower allows CO2 to accumulate in blood)

Kidneys retain H+ and excrete bicarb

36
Q

How do Type B intercalated cells of the collecting ducts react to metabolic alkalosis?

A

They increase the excretion of bicarb and K into urine and retain H+ in blood

37
Q

What happens to potassium balance in the blood in acidosis and alkalosis?

A

K follows bicarb so in acidosis, kidneys retain bicarb and K in blood so can get hyperkalaemia

In alkalosis, bicarb and K are excreted in urine so can get hypokalaemia

38
Q

In chronic heart failure, patients get oedema in lungs because back up of blood (pump failing) and low cardiac output causes sympathetic NS to go crazy and constrict peripheral arteries (increases afterload- making it harder for heart) and also Renin Angiotensin System is turned on to retain water and further vasoconstrict (making afterload even larger so harder for heart)

Which drugs are used to improve oxygenation by getting rid of oedema in the lungs?

Which drugs reduce intense sympathetic NS drive on heart?

How would you reduce afterload (due to SNS and RAS activation)?

A

Diuretics

B Blockers

Block RAS

39
Q

What is a natriuretic?

A

Something that promotes Na excretion into the urine (most diuretics are natriuretics)

40
Q

Where do loop diuretics, thiazides, amiloride and spironolactone stop the reabsorption of Na and Cl in the nephron?

A

Loop diuretics= Thick ascending limb of loop of Henle

Thiazides= distal convoluted tubule

Amiloride and Spironolactone= Collecting Tubule

41
Q

What do osmotic diuretics do?

What is an example of one?

A

The drug gets filtered and not reabsorbed so increases water excretion because osmotic effect drags water into lumen

E.g. Mannitol

42
Q

What is the main loop diuretic drug?

A

Furosamide (Lasix)

43
Q

__-__% of filtered sodium is reabsorbed in loop of Henle so Furosemide is very potent because it blocks this much reabsorption

What is a potential problem with Furosemide?

A

15-20%

Furosemide stops the absorption of Na into the blood so there is a lot of Na left in the urine tubule so in the collecting duct, there is more Na to exchange with K (a bit of Na is reabsorbed here and lots of K is excreted)
= hypokalaemia

44
Q

What is Spironolactone (acts on collecting duct) antagonising?

How is this potassium sparing?

A

Aldosterone

Blocking the action of aldosterone increases sodium excretion without potassium loss

45
Q

Why can’t you use cortical collecting duct diuretics on patients with chronic renal failure?

A

Because in Chronic Renal Failure, patients already have trouble excreting K so they need to excrete as much as possible in the CCD and if you use K sparing diuretics, it will block the excretion of K and patients will get hyperkalaemia (risk of cardiac arrest)

46
Q

What 3 things stimulate renin release?

A
  • SNS activation
  • Low Renal perfusion/ Low BP
  • Increase in Na+ in urine/tubule (after diuretic use) to try and increase BP
47
Q

What does renin form angiotensin 1 from?

What converts angiotensin 1 to angiotensin 2?

A

Angiotensinogen

ACE (angiotensin converting enzyme)

48
Q

What 2 receptors does Angiotensin 2 act on and what do they do?

A

AT-1 receptor (vascular)
- Vasoconstriction (to increase BP)

AT-2 receptor (adrenal)
- Aldosterone secretion (increases Na and H2O reabsorption to increase cardiac output)

49
Q

What do ACE inhibitors reduce the formation of?

How do they reduce blood volume (antihypertensive effect)?

When _____ are used, ACE inhibitors should also be used- why is this?

A

Angiotensin 2

By reducing sodium reabsorption

Diuretics
- Because when diuretics are used, renin is released and symp drive is increased so ACE inhibitors block these effects so diuretics can do their thang

50
Q

ACE is also important in the inactivation of _______

When on ACE inhibitors, patients don’t get this inactivation so they have the effects of ______ which are ______ and __________

A

Bradykinin

Bradykinin

  • Vasodilation
  • Bronchoconstriction
51
Q

How do ACE inhibitors lower BP? (2 mechanisms)

A
  • Block Angiotensin 2 formation so reduced vasoconstriction

- Production of aldosterone reduced so less Na retention (so water excretion and less blood vol)

52
Q

What do ACE inhibitor drugs all end with?

A

Pril

53
Q

What are ARBs?

What effects do they have to lower BP?

A

Angiotensin 2 receptor blockers or Angiotensin 2 receptor antagonists

They are basically ACE inhibitors without inhibiting the breakdown of bradykinin

They still stop vasoconstriction and production of aldosterone (and hence Na retention) so patients on ARBs have vasodilation and lower blood vol

54
Q

What is an example of an ARB?

A

Sartans

55
Q

In chronic kidney disease…

Does GFR go up or down?

Does Permeability of arterioles and glomerulus go up or down?

Does clearance of drugs (dependent on filtration and/or renal transporters for elimination) increase or decrease?

A

GFR reduces

Permeability of arterioles and glomerulus increases

There is reduced clearance of those drugs

56
Q

What are some markers of CKD?

5

A

Oedema

Anaemia

Metabolic acidosis

Bone problems (hyperkalaemia, osteodystrophy)

Hypertension

57
Q

What are the 3 causes of anaemia?

A

Drop in haemoglobin

Drop in erythrocyte count

Drop in blood oxygen

58
Q

In CKD, drop in kidney function leads to a drop in the production of what? (needed for RBC synthesis)

A

Erythropoetin (EPO)

59
Q

The kidney reabsorbs bicarb and excretes H ions through buffering by _____ (produced by kidney) and filtered _______

A

ammonia

phosphates

60
Q

How do you treat metabolic acidosis in patients with CKD?

A

Give them sodium bicarbonate

61
Q

What is the cause if the anion gap is high?

What is the cause if the anion gap is normal?

A

Increase in organic acids (not in equation so makes the gap bigger)

Loss of Bicarb (Cl- reabsorption increases to keep equation same)

62
Q

The treatments for hyperkalaemia in CKD…

What does IV glucose with insulin do?

What does IV sodium bicarb do?

Polystyrene sulfonate resins?

(There is also dialysis and diet)

A

Insulin stimulates glucose uptake (to glycogen) and K+ uptake into cell

Sodium bicarb corrects acidosis and this allows K+ to go from blood to cells in exchange for H+

It draws out K+ into faeces

63
Q

What is the term for reduced bone mineralisation

A

Osteomalacia

64
Q

Do CKD patients get hyper or hypo for the following things…

___ phosphataemia

___calcaemia

____prathyroidism

A

hyperphosphatemia (because less phosphate excreted by damaged kidney)

Hypocalcaemia (because kidneys wrongly excreting all calcium)

Hyperparathyroidism (because trying to get more calcium in blood)

65
Q

What are the 2 treatments for osteodystrophy in CKD?

A

Dietary restriction of phosphorus

Phosphate binding agents (limit absorption of dietary phosphates, promoting the excretion in stools)

66
Q

What is the treatment for Vit D deficiency in CKD?

A

More in diet and more sun

Give calcitriol (active form of vit D)

67
Q

Why would you use a calcium supplement such as Cinacalcet in patients with CKD?

A

It reduces the excessive PTH secretions so bones can keep their calcium and the blood can use the calcium from the supplement

68
Q

Describe the vicious circle of hypertension and CKD?

A

Hypertension damages kidneys so promotes CKD and CKD means there is a lot more retention of Na and water into blood which increases BP even more and this damages kidneys even more :(

69
Q

What are the 2 main anti-hypertensive agents for CKD?

A

ACE inhibitors (pril)

ARBs (sartans)

(they both promote fluid loss and vasodilation= reduce BP)

70
Q

How do calcium channel blockers reduce BP?

Example of one:

A

Reducing the entry of calcium into cells decreases artery contraction, causing dilation and reducing BP
(Verapamil)

71
Q

How do NSAIDs contribute to renal failure?

A

They block prostaglandins (which normally promote block antidiuretic hormone and hence promote excretion of Na and water) so without prostaglandins, excessive Na and water is retained and this slowly promotes renal failure over time

72
Q

Summary…

What treatment do you give for CKD patients with:

Anaemia= 1
Metabolic acidosis= 1
Hyperkalaemia= 3
Osteodystrophy= 3
Fluid overload/ HTN= 2
A

Anaemia= EPO

Metabolic acidosis= sodium bicarbonate

Hyperkalaemia= glucose/ insulin, sodium bicarb, resins

Osteodystrophy= phosphate binders, Ca and Vit D

Fluid overload/ HTN= diuretics and antihypertensives

Semester 2 (1st year) (13 decks)

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