Urinary L5.1 Flashcards
1) What are the two major components of extracellular fluid (ECF)?
2) What can too much interstitial fluid in the body lead to?
1) Intravascular volume and interstitial fluid.
2) Edema in ankles, lower bacl, abdomen
1) Why is most of the blood contained in the veins?
2) What is venous return?
3) Describe the relationship between volume and venous pressure
4) How does an increase in venous pressure lead to an increase in CO?
1) Veins have larger vascular capacity - high ability to expand, high compliance
2) amount of blood returning to the heart through the veins.
3) ↑ Volume (more blood) → ↑ Venous Pressure.
↓ Volume (less blood) → ↓ Venous Pressure.
4) Higher venous pressure increases venous return, which boosts the amount of blood available for the heart to pump.
This increase in venous return results in an increased cardiac output (CO)
1) What is blood pressure?
2) What is blood pressure influenced by?
1) the force exerted by blood against vessel walls
1) How is mean arterial pressure (MAP) calculated? (MAP is a measure of blood pressure)
2) What is total peripheral resistance?
3) Describe the impact of cardiac output on blood pressure
4) How do tissue autoregulate blood flow?
5) What happens when peripheral resistance increases?
1) MAP = Cardiac Output (CO) x Total Peripheral Resistance (TPR).
2) resistance of blood flow through the body’s vascular system.
3) TPR is constant, an increase in cardiac output (CO) will result in an increase in arterial pressure.
This happens even if the demand for blood flow by tissues does not increase.
4) When tissues do not need extra blood flow despite increased arterial pressure, they autoregulate blood flow.
Mechanism:
Tissues regulate blood flow by increasing peripheral resistance. This is done by increasing arteriolar resistance, which restricts the blood flow.
5) As peripheral resistance increases due to arteriolar constriction, this leads to further increases in arterial pressure.
Describe Frank-Starling Law of the Heart
Heart pumps out more blood when more blood enters it.
CO (Cardiac Output) = SV (Stroke Volume) × HR (Heart Rate).
Stroke volume (SV) is determined by:
EDV (End-Diastolic Volume): The amount of blood in the ventricles before contraction. ESV (End-Systolic Volume): The amount of blood remaining in the ventricles after contraction. SV=EDV−ESVSV=EDV−ESV.
State and explain 5 factors affecting blood pressure
1) Cardiac factors: vol of blood ejected from left ventricle
2) Peripheral resistance: Arteriolar diameter
3) Blood volume (total vol of blood circulating in both, cells + plasma)If blood volume ↓ BP ↓
4) Viscocity: thickness of blood. Increase in viscocoty, greater resistance to flow, therefore, incresed arterial pressure
5) Arterial elasticity, refers to elasticity of larger arteries (aorta). Reduced elasticity, increasses BP
1) Why is it important for the kidneys to have a stable MAP?
2) What can happen when we have a decreased and increased GFR?
3) What is the role of autoregulation of blood flow in maintaining GFR?
4) What are the limits of autoregulation?
5) What range of MAP is autoregulation effective in?
To maintain adequate GFR (glomerular filtration rate), essential for filtering blood + forming urine.
Constant GFR important to maintain renal function + prevent renal damage
2) Reduced waste removal
3) Maintains stable GFR across a range of BPs
Autoregulation mediated by afferent and efferent arterioles.
4)
5) 80-180 mmHg
1) What is the mechanism involved in short-term regulation of blood pressure?
2) Location of baroreceptors
3) What is the mechanism involved in long-term regulation of blood pressure?
1) ANS. Baroreceptor reflex (specialised stretch receptor) (rapid adjustments in BP). High BP, baroreceptors detect STRETCH in vessel, signal sent to brain. BP then decreased, less stretch detcetd, reduceing baroreceptor signal
2) Aotric arch, carotid sinuses
3) Control of BP over hours/days by regulation of blood volume + hormones
Increase ECF vol = increase blood vol = increase venous return = cardiac output = increase BP. Hormonal: RAAS
1) What affects ECF volume ?
2) What is the relationship between long term and short term BP control?
1) Total amount of osmotically active solutes (Na+) in ECF. (UNDERSTANDING: solutes draw water to maintain osmolarity)
2) Long-tern: baseline control of BP
Short-term: Short-term control mechanisms SUPERIMPOSED (work on top of) long term ones. Because short term allows for rapid adjustments
Sodium consumption
How is sodium reabsorbed in the kidneys?
- Sodium reabsoroption in PCT
-obligatory reabsorption of sodium (65%)
- Basolateral Na+/K+/ATPase pumps actively transport N
What are the three sensors involved in regulating ECF volume?
1) JGA
- located in kidneys
- granular cells within JGA release renin in response to low BP
- renin initiates RAAS
2) Atria
- detect high ECF vol (therefore, increase blood vol)
- release ANP (ATRIAL NATRIURETIC PEPTIDE)
-promotes sodium excretion (natriueresis), decreases sodium + water reabsorption. Therefore, reduced blood vol, blood pressure
3) Carotid sinus
-baroreceptor in carotid artery, senses change in BP
-low blood pressure, low blood bol (hypovolemia), carotid sinus sends signal to brain to activate sympathetic nervous system
-triggers ADH release from posterior pituitary
-ADH promotes water reabsorption in kidneys, increasing blood vol + blood pressure
1) Which cells release renin?
2) When is renin produced?
3) How is renin formed?
4) What is Renin’s primary role?
1) Granular cells in JGA, located around afferent arteriole in kidneys
2) An enzyme produced in response to low BP
3) Granular cells form precursor: prorenin. When bp drops, prorenin clreaved to form active enzyme renin
4) Initiate RAAS. It cleaves agiotensionogen (protein produced by liver) to produce angiotensin I (inactive precursor). Angiotensin I converted to angiotensin II by angiotensin-converting enzyme (ACE) in lungs. Angiotensin II is a vascoconstrictor, stimulates alodosterone release.
What are three ways renin secretion is stimulated?
- Low BP (sensed by cariopulmonary baroreceptors). Triggers sympathetic stimulation, therefore, catecholamine release, stimulates β1 receptors in
the JGA. - Low BP (sensed by afferent arteriole baroreceptors) triggers local release of prostaglandins. Prostaglandins act on JGA
- Increased sympathetic activity via renal nerves: Direct stimulation of β1 receptors on the JGA.
What are the three ways renin secretion are inhibited?
1) Increased Na+/Cl- reabsorption by macula densa cells of early distal tubule
2) High BP in (sensed by afferent arteriole baroreceptors) afferent arteriole
3) Angiotensin II (-ve feedback)
4) Vasopressin
Describe the RAAS System
Renin-angiotensin-alodtserone system
Aldosterone released from adrenal cortex (ZONA GLOMERULOSA). Agiotensin II triggers aldosterone release.
What happens if blood pressure increases?
Which cells secreete ANP?
Blood pressure increases because ECF vol increases
Causes atria to stretch, due to heart vol expanstion, stretch of atria causes release OF anp
Atrial natriuretic peptide(ANP) inhibits expression of ENaC channels in principal ce..s
Reduces Na+ reabsorption from collecting ducct, reduces ECF vol and therefore BP
Heart arterial cells
