Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
31 Cards in this Set
- Front
- Back
|
Water excretion =
|
pressure diuresis
The effect of pressure to increase water excretion is called pressure diuresis. |
|
|
Salt excretion =
|
naturesis
The effect of pressure to increase Na excretion is called pressure natriuresis |
|
|
Renal System for Arterial Pressure Control
|
Art pressure elevated by transfusing in 400 ml blood
Plays a dominant role in long term pressure control. As extracellular fluid volume increases arterial pressure increases. The increase in arterial pressure causes the kidneys to lose Na and water which returns extracellular fluid volume to normal. |
|
|
The major determinants of long-term arterial pressure control.
|
Based on renal function curve
Salt and water intake line |
|
|
Long term arterial pressure determined by:
|
Degree of the pressure shift for water and salt output
Level of water and salt intake |
|
|
vit B deficiency, vaso dilation
|
beriberi
|
|
|
elevated osteoclastic activity
|
Paget’s –
|
|
|
Failure of Total Peripheral Resistance to Elevate Long-term Arterial Pressure
|
Cardiac output and art. Pressure vary greatly from normal, and long term resistance increases, but renal salt and water excretion remains constant
And overall art pressure is ‘normal’ Changes in TPR does not affect long-term arterial pressure level. One must alter the renal function curve in order to have long-term changes in arterial pressure. Changing renal vascular resistance does lead to long-term changes in arterial pressure . |
|
|
_______ is a Major Determinant of ECFV
|
Sodium
(much more than H2O intake) |
|
|
As Na intake is increased; Na stimulates drinking, increased Na concentration stimulates thirst and ADH secretion.
|
.......
|
|
|
Changes in Na intake leads to changes in _________ fluid volume
|
extracellular (ECFV).
|
|
|
ECFV is determined by the balance of
|
Na intake and output
|
|
|
Salt
|
Higher salt in tissues (and hypothalamus) causes thirst stimulus.
To reset tissue osmolarity to normal, water is retained to dilute salt conc. Tissue saltiness in posterior pituitary causes release of ADH, saves water in kidneys & concentrates urine salt Resultant increases in ECF volume increases blood pressure more so, and for a longer period than, increases in blood volume. |
|
|
Chronic Hypertension
|
Mean art pressure stays above normal.
Results in: Excess cardiac workload Vascular damage and cerebral ‘events’ Kidney damage |
|
|
Renin-Angiotensin System
|
Renin is synthesized and stored in modified smooth muscle (JG) cells in afferent arterioles of the kidney.
Renin is released in response to a fall in art. pressure. Renin acts on a substance called angiotensinogen to form a peptide called angiotensin I. (10 a.a.s) A-I is converted to A-II (8a.a.s) by a converting enzyme located in the endothelial cells in the pulmonary circulation. Powerful vasoconstrictor |
|
|
______ is released in response to a fall in art. pressure.
|
Renin
|
|
|
Renin Angiotensin System
|
Causes vasoconstriction
Causes Na retention by direct and indirect acts on the kidney- so water is also retained. It works directly on the kidneys to save water and salt (constrict renal art flow & increases renal tubular resorption of salt & water) It cause aldosterone release from the adrenals that affect distal kidney tubules to save water and salt Causes shift in renal function curve to right Important response to sudden blood loss |
|
|
Renin Angiotensin System Effect of Na Intake
|
RAS is important in maintaining a normal Art. Press. during changes in Na intake.
As Na intake is increased renin levels fall to near 0. As Na intake is decreased renin levels increase significantly. Eating pizza is O.K.. |
|
|
Primary (essential) Hypertension
|
Hereditary
Weight gain, non-active lifestyle C.O. is increased sympathetic activity is increased Angiotensin II and aldosterone are increased (d.t. increased symp. effect on kidneys) Impaired renal natriuresis Treat with life style changes, vasodilators and natriuretic and diuretic drugs, ACE inhibitors |
|
|
_________ lower arteriolar resistance and increase venous capacitance; increase cardiac output and cardiac index, stroke work and volume, lower renovascular resistance, and lead to increased natriuresis (excretion of sodium in the urine).
|
ACE inhibitors
|
|
|
ACE inhibitors
|
ACE inhibitors lower arteriolar resistance and increase venous capacitance; increase cardiac output and cardiac index, stroke work and volume, lower renovascular resistance, and lead to increased natriuresis (excretion of sodium in the urine).
Normally, angiotensin II will have the following effects: - vasoconstriction (narrowing of blood vessels) - cardiac hypertrophy - stimulate the adrenal cortex to release aldosterone, a hormone which acts on kidney tubules to retain sodium and chloride ions and excrete potassium. Sodium is a "water-holding" molecule, so water is also retained. This leads to increased blood volume, hence an increase in blood pressure. - stimulate the posterior pituitary into releasing vasopressin (ADH) which also acts on the kidneys to increase water retention. With ACE inhibitor use, the effects of angiotensin II are prevented, leading to decreased blood pressure. |
|
|
Epidemiological and clinical studies have shown that ACE inhibitors reduce the progress of _________ independently from their blood pressure-lowering effect.
|
diabetic nephropathy
This action of ACE inhibitors is utilized in the prevention of diabetic renal failure. |
|
|
Hypertension involving Angiotensin II
|
From tumors of the JG cells – secreting high levels of renin and forming high levels of Angiotensin II.
Which causes vasoconstriction and salt & water retention From Kidneys responding to restricted flow into them from the renal artery – Goldblatt one and two kidney preps – put out more renin. |
|
|
Angiotensin – dependant hypertension
|
From diseased kidneys that secrete renin chronically (renal hypertension)
Ischemic sections in damaged kidneys constrict blood flow, or limit blood flow, into normal areas of the kidney that read ‘impaired flow” and produce more renin that begins the hypertensive cascade. Common in older patients with kidney damage |
|
|
Hypertension from volume load & vasoconstriction
|
Coarctation of the aorta – malformed aorta. Lower aorta divides into multiple vessels and resistance is higher and flow is lower to the kidneys. They produce renin….pressure rises in the upper body until the kidneys reach normal pressures.
Extremities have normal pressures, because they are locally controlled. |
|
|
Other hypertensions
|
Toxemia of pregnancy-preeclampsia
Caused by ischemia of the placenta which releases toxic cellular products and raises maternal pressures Damage to the carotid bodies or Solitary Nucleus |
|
|
Factors Which Decrease Renal Excretory Function and Increase Blood Pressure
|
Angiotensin II
Aldosterone Sympathetic nervous activity Endothelin In a healthy individual, a delicate balance between vasoconstriction and vasodilation is maintained by endothelin, calcitonin and other vasoconstrictors on the one hand and nitric oxide, prostacyclin and other vasodilators on the other |
|
|
Factors Which Increase Renal Excretory Function and Reduce Blood Pressure
|
Atrial natriuretic peptide
Nitric oxide Dopamine |
|
|
Different Forms of Hypertension
|
Primary or Essential hypertension
Renovascular Hypertension Neurogenic-Sleep Apnea – along with obesity Chronic Renal Disease Hyperaldosteronism Pheochromocytoma (adrenal medulla tumor) – elevated epinephrine levels Pregnancy-induced Hypertension (preeclampsia) Exogenous substances (alcohol, steroids, sympathomimetics) |
|
|
Drugs which affect renal blood flow to tx HTN:
|
Inhibition of sympathetic nervous system
Angiotensin Converting Enzyme inhibitors – ACE inhibitors Dilators |
|
|
Drugs that inhibit Na reabsorption to tx HTN:
|
- Diuretics & natriuretics
|
