Urinary 3 Flashcards

(23 cards)

1
Q

ECF osmolarity

A

isotonic = same concentration of solute and solvent
hypertonic = ECF has higher salt concentration than cell, resulting in water to leave the cell causing shrinkage in the cell
hypotonic = ECF has lower salt concentration than cell, water enters into cell from surrounding causing cell to swell and rupture

increase ECF osmolarity = hypertonic
decrease ECF osmolarity = hypotonic

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2
Q

disturbance to plasma/serum osmolality + compensatory mechanism

A

occurs due to 2 reasons
1) dehydration, lost of water resulting in increase plasma osmolarity and volume decrease

2) presence of osmotically active substances eg: glucose, can result in increase in plasma osmolarity but volume remains constant

compensatory mechanism- increase body fluid water

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2
Q

disturbance to volume + compensatory mechanism

A

occurs as a result of vomiting, diarrhea, or lost of blood
loosing both electrolytes and water

decrease in volume but osmolality remains constant

compensatory mechanism- increase fluid and electrolytes in body

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3
Q

what are the 2 key reasons that lead to increase ECF osmolality

A

1) dehydration/lost of water > increase plasma osmolarity, increase thirst mechanism allowing for reduction in ECF osmolality

2) the increase in ECF osmolality results in increase ADH secretion > water retention > decreasing ECF osmolality

increase in ECF osmolality is the main driving force that stimulate ADH secretion

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4
Q

what is the other reason that leads to ADH levels increasing?

A

1st reason: increase in ECF osmolality is the main driving force that stimulate ADH secretion

2nd reason: decrease in ECF volume and decrease in blood pressure and volume

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5
Q

explain the mechanism of how ADH (vasopressin) is secreted

A

ADH is synthesized in the hypothalamus and stored in the posterior pituitary

1st reason: increase in ECF osmolality is the main driving force that stimulate ADH secretion
detected by osmoreceptors in the anterior hypothalamus that leads to increase secretion and release of ADH

2nd reason: decrease in ECF volume and decrease in blood pressure and volume
detected by baroreceptors leading to increase secretion and release of ADH

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6
Q

stimuli affecting vasopressin secretion (ADH)

A

ADH secretion increase
- ECF osmolality increase
- blood pressure decrease
- ECF volume decrease

ADH secretion decrease
- ECF osmolality decrease
- blood pressure increase
- ECF volume increase
- alcohol intake > inhibits ADH activity

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7
Q

what increases/decreases thirst mechanism

A

increase thirst mechanism
- plasma osmolarity increase
- blood volume decrease
- blood pressure decrease
- angiotensin II increase

decrease thirst mechanism
- plasma osmolality decrease
- blood volume increase
- blood pressure increase
- angiotensin II decrease

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7
Q

ADH helps to increase water reabsorption at the late distal tubules and at the collecting duct but it also ____

A

helps to increase the reabsorption of urea. Tho urea is a toxic substance but it also helps with regulating the concentration gradient and maintenance of the countercurrent mechanism.

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8
Q

describe the MOA of ADH

A

increase plasma osmolality > ADH secretion binding to V2 receptors at the late distal tubules and at the collecting duct > allows for incorporation of more aquaporin 2 water channel in this region > increase efficiency of water reabsorption by making this region more permeable to water > urine osmolality increase as lesser water is excreted out of the body

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9
Q

clinical implications of ADH

A

too much ADH secretion - increase water retention leading to swelling and oedema

failure to produce ADH - diabetes insipidus
1) central diabetes insipidus
hypothalamus fails to secrete ADH hence ADH levels is decreased/absent
due to tumor or pituitary disease

2) nephrogenic diabetes insipidus
ADH levels are normal but distal tubules and collecting duct unresponsive to ADH (receptor issue)

When there is deficient ADH/failure to produce ADH > there is a inability to produce concentrated urine which means that the urine is very diluted > triggers thirst mechanism

by giving synthetic vasopressin (desmopressin) this can help to identify which diabetes insipidus isit

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10
Q

What are the 5 mechanism that occurs when there is a decrease in ECF volume and a decrease in blood volume, pressure and reduce in kidney perfusion?
to restore the ECF volume

A

1) RAAS (renin angiotensin aldosterone system) main mechanism
2) increase ADH secretion
3) thirst mechanism
4) increase sympathetic activity
5) reduce ANP (arterial naturietic peptide)

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11
Q

describe RAAS

A

when there is a decrease in ECF volume

1) juxtaglomerular cells lining the afferent and efferent arterioles release renin

2) renin is involved in conversion of angiotensinogen to angiotensin I

3) angiotensin I is converted to angiotensin II by ACE (angiotensin converting enzyme)

angiotensin II is a potent vasoconstrictor so it results in vascular constriction leading to increase in vascular resistance > increase blood pressure (heart)
this is important for people with low blood pressure, since the constriction of the blood vessels would allow for increase in systolic and diastolic pressure to ensure that blood is constantly supplied to vital organs

in kidney, the angiotensin II would stimulate the increase in aldosterone levels as it stimulates the zona glomerulosa of the adrenal cortex.
Aldosterone would result in the increase in sodium reabsorption at the principal cells, since sodium increase in reabsorption, water follows as well.
angiotensin II can also directly lead to sodium reabsorption
angiotensin II also results in constriction at the efferent arteriole which leads to increase in hydrostatic pressure > increase GFR

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12
Q

What are the 2 factors that lead to the increase in aldosterone levels?

A

1) angiotensin II secretion stimulating adrenal cortex to produce aldosterone

2) when there is an increase in potassium levels in the blood (hyperkalemia)

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13
Q

pharmacological manipulation of RAAS

A

1) beta blocker to reduce sympathetic activity
2) NSAIDs to reduce prostaglandins
3) ACE blockers/inhibitors
4) angiotensin II receptor blocker
5) aldosterone antagonist

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14
Q

describe ANP (atrial natriuretic peptide) and its MOA

A

when there is a decrease in ECF volume, the body would reduce ANP when there is an increase in ECF volume

ANP is produce by cardiac muscle fibers
it regulated the ECF volume and sodium levels by doing the opposite of RAAS

instead of stimulating increase in reabsorption of sodium and water, it would stimulate increase in excretion of sodium and water.

increase in ECF volume > stretch of atria > release of ANP by cardiac muscle fiber > dilates the afferent arterioles > reduce renin secretion and angiotensin II formation > increase in sodium and water excretion

15
Q

micturition control (the act of passing urine) is controlled by?

A

2 sphincters
1) internal urethral sphincter
- involuntary control
- made up of smooth muscle

2) external urethral sphincter
- voluntary control
- made up of skeletal muscle

16
Q

innervation of bladder (sympathetic and parasympathetic activation)

A

sympathetic activation > detrusor muscle to inhibit and relax the internal sphincter > urinary bladder relaxes > allow for urine to fill up urinary bladder

parasympathetic activation > detrusor muscle to inhibit and contraction of the internal sphincter muscle > urinary bladder contracts > emptying of the bladder

17
Q

During micturition
what allows for urination and what does not allow for urination

A

the external sphincter is controlled by the motor nerve, as long as it is activated the sphincter would remain close to prevent urine excretion

when the urine fills up the bladder, this would activate the stretch receptors on the walls of the bladder to inhibit the motor nerve activity, parasympathetic activation would result in the contraction of the bladder allowing for urination to occur

18
Q

what are the 5 common diseases in the urinary system?

A

1) glomerulonephrtitis
2) kidney stones
3) urinary tract obstruction
4) acute kidney injury
5) chronic kidney disease

19
Q

what happens in kidney failure?

A

1) failure to excrete metabolic waste and get rid of toxic chemical substances > accumulation results in toxic and harmful effects
2) failure to synthesize active vitamin D3, px with kidney failure > low blood calcium levels
3) increase in water retention
4) increase in blood potassium levels (hyperkalemia)
5) kidney acidosis (failure in secreting excess H+)
6) anemia (low blood count)

20
Q

why does kidney failure lead to anemia?

A

because kidney helps to synthesize erythropoietin (EPO), EPO is a glycoprotein and its functions include stimulating the stem cells in the bone marrow to undergo blood cell production, with a decrease in EPO this would lead to low blood cell production = anemia

can be treated by giving synthetic EPO

21
Q

how can we treat kidney failure? (control disease progression)

A

1) adjust diet, reduce protein and sodium intake (both of which would increase GFR)
2) decrease water intake (since kidney is unable to get rid of excess water as efficiently)

serious cases: kidney transplant/dialysis

hemodialysis - passing blood through a filter to extract metabolic waste products and toxic chemicals before returning blood back into the circulation
peritoneal dialysis - infusing fluid into peritoneal cavity allow for equilibration and this would help with the removal of waste substances