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Urinary (Semester 3) > Controlling Volume > Flashcards

Flashcards in Controlling Volume Deck (23)
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1
Q

What cardiac factors influence BP?

A

The total volume of blood from the L ventricle (CO) and the peripheral resistance - which increases the BP

2
Q

How does viscosity and elasticity influence BP?

A

Viscosity: Increased blood viscosity means more resistance and higher pressure, can increase when the % of blood composed of cells increases

Elasticity: less stretch means systolic pressure goes up

3
Q

What is the role of baroreceptors?

A

Short term decrease of BP:

Sense (through stretching) the increased arterial pressure in the carotid sinus and the aortic arch, then send messages to the medulla to induce bradycardia and vasodilate in order to lower arterial BP

4
Q

What can the lowering of arterial BP induce?

A

A sympathetic response: which re-increases the heart rate, secretes renin and constricts bloodflow in non-vital areas

5
Q

What determines long term BP?

A

Blood volume, determined by drinking and the amount of solute

6
Q

What causes edema? Name 4 likely places on the body where one is likely to occur

A

Edema is caused by too much interstitial fluid, fluid is distributed largely by gravity and can accumulate in the:

  1. abdomen (ascites)
  2. legs
  3. ankles
  4. lower back
7
Q

What is the principal solute in the ECF? Which major ion must be controlled to maintain volume?

A

Sodium chloride, sodium is the main ion that needs to be recovered

8
Q

Which channel is in all basolateral membranes? What differs on the apical/luminal membrane?

A

All basolateral membranes have a Na-K-ATPase, but the sodium transporters will differ on the luminal membrane

9
Q

What do diuretics do?

A

Increase sodium and water secretion

10
Q

Name 4 targets for diuretics and which diuretic you would prescribe depending on the target

A
  1. ENaC channels: amiloride
  2. Na/K/Cl co transporter: loop diuretics
  3. Na/Cl transporter: thiazides
  4. Aldosterone receptors: aldosterone antagonists
11
Q

Which channels are specialized for K+ transport into the lumen in the thick ascending LOH/early DCT? Why is it vital that this channel be active?

What type of diuretic can target this process?

A

The ROMK channel transports K+ into the filtrate. It is vital as alongside ROMK on the luminal membrane is the Na-Cl-K cotransporter pumping Na, Cl and K+ into the cell and ROMK must pump K+ back into the filtrate to drive this gradient.

Loop diuretics such as furosemide target this; as they target the Na-2Cl-K cotransporter, without this channel you K+ will not accumulate in the cell and ROMK cannot pump out any K+ into the filtrate.

12
Q

Which channel resorbs Na and Cl from the filtrate in the DCT? Which diuretic targets this?

A

Apical NCC channels, sensitive to thiazide diuretics

13
Q

What channel is present in principle cells that drives the resorption of Na+ in the DCT? What diuretic can target this?

A

ENac channels pump Na+ into the cell due to the Na-K ATPase channel pumping Na+ out of the cell. This can be targeted by Amiloride

14
Q

What is the primary role of alpha intercalated cells?

A

Acid-base balance, they secrete H+ into the urine and can resorb more HCO3-

15
Q

Explain the RAAS system

A

RAAS is used as an effector to alter sodium excretion and intake

Macula densa cells sense the amount of Na+ in the DCT. If they sense it’s low, the macula densa sends prostaglandins to the JG cells (and lacis cells) to secrete renin: an enzyme that converts angiotensinogen (created by the liver and floating inactive in the blood) – angiotensin 1. Angiotensin 1 is converted to angiotensin 2 by ACE (produced in the lungs).

Angiotensin II triggers:

  1. Vasoconstriction of smooth muscle cells - increasing the resistance
  2. Acts on the adrenal gland to secrete aldosterone: increases na+ and water resorption.

Overall: increase BP

16
Q

What are the 3 triggers for renin?

A
  1. Low BP
  2. Low Na+ in the DCT
  3. Sympathetic response
17
Q

What is a sodium appetite, which population is it prevalent in?

A

A physiological mechanism to get salt back into the body if the sodium conc in the ECF is low. Prevalent in elderly with dementia

18
Q

What hormone does the opposite to renin?

A

If the BP is already high… atrial cells in the heart will detect this AND venous pressure will increase causing their walls to stretch: So atrial cells release ANH: atrial natriuretic hormone which stimulates more Na+ and water to be excreted in the urine

19
Q

Explain the brief cycle that occurs when a healthy person ingests salts?

A

The osmolarity of their ECF will increase, and so will the BP. More solutes stimulate more thirst, which also increases the volume. RAAS is inhibited and ANP is released, sodium and extra water may be excreted

20
Q

What is the consequence of having renal artery stenosis?

A

Renal artery stenosis means the perfusion to the kidney decreases. The kidney then mistakenly interprets this as a sign that the BP in the body is low, and triggers RAAS. This only increases BP and puts more pressure on the renal artery and the heart

21
Q

What is Conn’s syndrome?

A

When the adrenal gland secretes excessive aldosterone, too much Na+ and water is resorbed

22
Q

What is a consequence of chronically high BP?

A

Damages the endothelium, causing them to be more prone to an atheroma. This decreases perfusion to important areas, which can increase the tendency for kidney failure, heart problems (MI) and eye problems.

23
Q

Name 4 types of drugs you might prescribe to treat hypertension

A
  1. ACE inhibitor: prevents angiotensin II
  2. Angiotensin 2 antagonist
  3. Diuretics; excrete more fluid
  4. Calcium channel antagonists promote vasodilation and reduce the TPR