NORTH SOUTH UNIVERSITY

NAME: MAHMUDA AKTER MARZIA

ID- 2014151649
COURSE NAME: PHR121; SECTION: 03
SUBMITTED BY: MAHMUDA AKTER MARZIA
SUBMITTED TO: TAHMINA YASMIN

FINAL ASSIGNMENT

QUESTION 01: Describe the process of urine from action in our body?

Answer: The kidneys clear out undesirable materials from the blood and convey urine to
excrete them. There are 3 most important steps of urine formation. These methods make
sure that handiest waste and extra water are eliminated from the body. Waste is excreted
from the human body, in particular with inside the shape of urine. Our kidneys play a
chief function with the system of excretion. Constituents of regular human urine
encompass ninety five percentage water and five percentage strong wastes. It is produced
with inside the nephron that is the structural and practical unit of the kidney. Urine
formation consists of 3 processes: (1) Ultrafiltration, (2) Selective reabsorption, (3)
Selective Secretion.
(1) Ultrafiltration: It is filtration which takes place beneath neath excessive blood stress.
The afferent arteriole materials blood to glomerulus and efferent arteriole collects blood
from glomerulus. Therefore, the blood stress in glomerulus will become seventy five mm
of Hg. The smaller molecules of glucose, water, salts, ammonia etc. diffuse from
glomerulus to Bowman's pill and this method is referred to as ultrafiltration. About 1.5-
2.5% of water and solutes are eliminated from the blood plasma that flows thru
glomerulus. The amount of glomerular filtrate fashioned every mines in all nephrons of
each kidneys is referred to as the glomerular filtration price. In an everyday person, the
glomerular filtration price is set 125ml. consistent with minute.
(2) Selective reabsorption: As the filtrate travels along the length of the nephron, the cells
lining the tubule selectively, and often actively, take substances from the filtrate and
move them out of the tubule into the blood. Recall that the glomerulus is simply a filter
 and anything suspended in the plasma that can fit through the holes in the filtration
membrane can end up in the filtrate. This includes very physiologically important
molecules such as water, sodium, chloride, and bicarbonate (along with many others) as
well as molecules that the digestive system used a lot of energy to absorb, such as
glucose and amino acids. These molecules would be lost in the urine if not reclaimed by
the tubule cells. These cells are so efficient that they can reclaim all of the glucose and
amino acids and up to 99% of the water and important ions lost due to glomerular
filtration. The filtrate that is not reabsorbed becomes urine at the base of the collecting
duct.
(3) Selective secretion: The metabolic waste products like ammonia, hip uric acid,
creatinine, H+ ions etc., present in the blood diffuses into DCT. This process is called
selective secretion. It changes the complete composition of glomerular filtrate which is
now called urine.

QUESTION 02: Describe the mechanisms of blood pressure regulation in our body?
Answer: In general, an individual’s “blood strain,” or systemic arterial strain, refers back to the
strain measured inside huge arteries with the systemic circulation. This wide variety splits into
systolic blood strain and diastolic blood strain. Blood strain is historically measured the usage of
auscultation with a mercury-tube sphygmomanometer. It is measured in millimeters of mercury
and expressed in phrases of systolic strain over diastolic strain. Systolic strain refers back to the
most strain in the huge arteries whilst the coronary heart muscle contracts to propel blood via the
frame. Diastolic strain describes the bottom strain in the huge arteries for the duration of
coronary heart muscle rest among beating.
Arterial strain without delay corresponds to cardiac output, arterial elasticity, and peripheral
vascular resistance. Blood strain is remarkably clean to modify and may be suffering from many
activities. Maintaining blood strain inside ordinary limits is essential. A blood strain among
140/eighty mmHg to 159/ninety nine mmHg is classed to as degree 1 high blood pressure.[1]
Categorization of Stage 2 high blood pressure is a strain among 160/one hundred mmHg to
179/109 mmHg.[2] Hypertensive urgency describes a blood strain more than 180/one hundred
twenty mmHg and hypertensive emergency refers to a completely excessive blood strain that
outcomes in doubtlessly life-threatening signs and symptoms and end-organ damage.[3]
Hypotension, on the opposite hand, is a blood strain much less than 90/60 mmHg.[4] It is vital
for the frame for you to alter to acute adjustments in blood strain and for the affected person to
acquire scientific remedy or life-style modifications for continual variations.
There are numerous mechanisms via which the frame regulates arterial strain.
Mechanism:
Baroreceptor Reflex:
In reaction to acute adjustments in blood strain, the frame responds via the baroreceptors placed
inside blood vessels. Baroreceptors are a shape of mechanoreceptor that emerge as activated with
the aid of using the stretching of the vessel. This sensory facts is conveyed to the critical
apprehensive machine and used to persuade peripheral vascular resistance and cardiac output.
There are two types of baroreceptors.
High-Pressure Baroreceptors:
Two baroreceptors are placed in the excessive-strain arterial machine. 1. The carotid
baroreceptor responds to each will increase and reduces in blood strain and sends afferent
indicators thru the glossopharyngeal nerve (CN IX). 2. The aortic arch baroreceptor responds
handiest to will increase in blood strain, sending its indicators via the vagus nerve (CN X).
These each ship indicators in reaction to the bodily distortion of the vessel. The stretch of the
vessel results in an growth in movement capacity relayed from the sensory endings placed in the
tunica adventitia of the artery. These movement potentials get transmitted to the solitary nucleus
that indicators to autonomic neurons secrete hormones to have an effect on the cardiovascular
machine. Activation of the aortic baroreceptor for the duration of will increase in blood strain
efficiently inhibits the efferent sympathetic nerve reaction.[5] On the opposite hand, if an
individual’s blood strain had been to fall consisting of in hypovolemic shock, the price of
movement capacity from the baroreceptors might be reduced because of decreased
depolarization; this will cause decreased inhibition of sympathetic activity, ensuing in a reflex to

growth strain.
Low-Pressure Baroreceptors:
These baroreceptors are gift the low-strain venous gadget. They exist inside huge veins,
pulmonary vessels, and the partitions of the proper atrium and ventricle. The venous gadget has
compliance about 30 instances extra than that of the arterial gadget [6]. Changes in extent in
large part have an effect on the baroreceptors with the venous gadget. Decreased frequency in
motion potentials in low-strain eventualities ends in the secretion of antidiuretic hormone, renin,
and aldosterone. These cause a downstream impact to alter arterial strain.
Antidiuretic Hormone:
Antidiuretic hormone (ADH), additionally referred to as vasopressin, is a hormone synthesize in
the magnocellular neurosecretory cells with inside the periventricular nucleus and supraoptic
nucleus of the hypothalamus. ADH is synthesized and launched in reaction to a couple of
triggers which are:
1. High serum osmolarity, which acts on osmoreceptors with the hypothalamus.
2. Low blood extent reasons a reduced stretch inside the low-strain baroreceptors, main to the
manufacturing of ADH.
3. Decreased blood strain reasons reduced stretch with the excessive-strain baroreceptors,
additionally main to the manufacturing of ADH.
4. Angiotensin II.
The antidiuretic hormone produced with the hypothalamus makes its manner down the pituitary
stalk to the posterior pituitary wherein it's far stored in reserve for launch in reaction to the
above-indexed triggers. ADH particularly features to growth unfastened water reabsorption with
the amassing duct of the nephrons with inside the kidney, inflicting a growth in plasma extent
and arterial strain. ADH in excessive concentrations has additionally been proven to purpose
mild vasoconstriction, growing peripheral resistance, and arterial strain.[7][8]
Renin-Angiotensin-Aldosterone System (RAAS):
The renin-angiotensin-aldosterone gadget is an important regulator of arterial blood strain. The
gadget is based on numerous hormones that act to growth blood extent and peripheral resistance.
It starts with the manufacturing and launch of renin from juxtaglomerular cells of the kidney.
They reply to reduce blood strain, sympathetic frightened gadget activity, and decreased sodium
degrees with the distal convoluted tubules of the nephrons. In reaction to those triggers, renin is
launched from the juxtaglomerular cells and enters the blood wherein it comes in touch with
angiotensinogen that's produced constantly through the liver. The angiotensinogen is transformed
into angiotensin I through renin. The angiotensin I then make its manner to the pulmonary
vessels, wherein the endothelium produces the angiotensin-changing enzyme (ACE).
Angiotensin I is then transformed to angiotensin II through ACE. Angiotensin II has many
features to growth arterial strain, including: 1.Potent constriction of arterioles throughout the
body. 2. Vasoconstriction of the centrifugal arterioles at intervals the capillary vessel of the
excretory organ, leading to the upkeep of capillary vessel filtration rate. 3. Increased metallic
element biological process at intervals the excretory organ tubules - the increased metallic
element biological process from the excretory organ tubules leads to passive biological process
of water through osmosis; this causes a rise in blood volume and blood pressure. 4. The
unharness of vasoconstrictor (ADH) release from the gland. 5. The release of mineralocorticoid
from the zone glomerulus of the cortex at intervals the ductless gland-
1. Aldosterone functions to extend the blood pressure through the up regulation of Na+/K+
pumps of the distal convoluted tube-shaped structure and aggregation duct at intervals the tubule.
2. This activity is that the distal convoluted tube-shaped structure results in increased biological
process of metallic element, moreover as increased secretion of K. 3. The increase in metallic
element biological process results in passive biological process of water and a rise in vital sign.
Clinical Significance:
The role of blood pressure regulation is to keep up a high enough pressure that enables for
correct introduction of body tissue and organs; however not therefore high on cause bodily hurt.
Once the body enters a state of acute cardiovascular disease, the bar reflex perform makes an
attempt to come back blood pressure to its stable state to permit continuous introduction. [9] The
body might enter a state of chronic high blood pressure, however most frequently there's not
associate degree distinctive cause however rather a consequence of the interaction between
multiple risk factors. The term for this condition is important high blood pressure. It represents
some ninety fifth of patients with high blood pressure.[10][11] Treating high blood pressure is
crucial as a result of it may end up in cerebral, cardiac, and excretory organ complications. Initial
line medications to treat hypertension embrace metal channel blockers, ACE inhibitors,
vasoconstrictor receptor blockers, and diuretic drug diuretics.

References:
1. Whelton PK, Carey RM, Aronow WS, Casey DE, Collins KJ, Dennison Himmelfarb C,
DePalma SM, Gidding S, Jamerson KA, Jones DW, MacLaughlin EJ, Muntner P,
Ovbiagele B, Smith SC, Spencer CC, Stafford RS, Taler SJ, Thomas RJ, Williams KA,
Williamson JD, Wright JT. 2017
ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the
Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A
Report of the American College of Cardiology/American Heart Association Task Force on
Clinical Practice Guidelines. J Am Coll Cardiol. 2018 May 15;71(19):e127-e248. [PubMed]
2. Reboussin DM, Allen NB, Griswold ME, Guallar E, Hong Y, Lackland DT, Miller EPR,
Polonsky T, Thompson-Paul AM, Vupputuri S. Systematic Review for the 2017
ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the
Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A
Report of the American College of Cardiology/American Heart Association Task Force on
Clinical Practice Guidelines. Circulation. 2018 Oct 23;138(17):e595-e616. [PubMed]
3. Aronow WS. Treatment of hypertensive emergencies. Ann Transl Med. 2017
May;5(Suppl 1):S5. [PMC free article] [PubMed]
4. Brzezinski WA. Blood Pressure. In: Walker HK, Hall WD, Hurst JW, editors. Clinical
Methods: The History, Physical, and Laboratory Examinations. 3rd ed. Butterworths;
Boston: 1990. [PubMed]
5. Sanders JS, Mark AL, Ferguson DW. Importance of aortic baroreflex in regulation of
sympathetic responses during hypotension. Evidence from direct sympathetic nerve
recordings in humans. Circulation. 1989 Jan;79(1):83-92. [PubMed]
6. Gelman S. Venous function and central venous pressure: a physiologic
story. Anesthesiology. 2008 Apr;108(4):735-48. [PubMed]
7. McClure JM, Rossi NF, Chen H, O'Leary DS, Scislo TJ. Vasopressin is a major
vasoconstrictor involved in hindlimb vascular responses to stimulation of adenosine A(1)
receptors in the nucleus of the solitary tract. Am J Physiol Heart Circ Physiol. 2009
Nov;297(5):H1661-72. [PMC free article] [PubMed]
8. Henderson KK, Byron KL. Vasopressin-induced vasoconstriction: two concentration-
dependent signaling pathways. J Appl Physiol (1985). 2007 Apr;102(4):1402-9. [PMC free
article] [PubMed]
9. Zhang R, Behbehani K, Crandall CG, Zuckerman JH, Levine BD. Dynamic regulation of
heart rate during acute hypotension: new insight into baroreflex function. Am J Physiol
Heart Circ Physiol. 2001 Jan;280(1):H407-19. [PubMed]
10. Carretero OA, Oparil S. Essential hypertension. Part I: definition and
etiology. Circulation. 2000 Jan 25;101(3):329-35. [PubMed]
11. Oparil S, Zaman MA, Calhoun DA. Pathogenesis of hypertension. Ann Intern
Med. 2003 Nov 04;139(9):761-76. [PubMed]
QUESION 03: When valves (all 4) of heart open and close? Explain the mechanism?
Answer: The heart consists of 4 chambers, 2 atria (upper chambers) and a combine of ventricles
(lower chambers). There’s a valve through that blood passes before deed every chamber of the
center. The valves stop the backward flow of blood. These valves unit actual flaps that unit
assault every finish of the 2 ventricles (lower chambers of the heart). They act as unifacial inlets
of blood on one aspect of a ventricle and unifacial shops of blood on the choice aspect of a
ventricle. Ancient valves have 3 flaps, except the valve, that has 2 flaps. The four heart valves
embrace the following:
Tricuspid valve: set between the right atrium so the middle ventricle.
Pulmonary valve: set between the right ventricle so the artery.
Mitral valve: set between the atrium of the middle so the middle ventricle.
Aortic valve: set between the middle ventricle so the vessel.
As the animal tissue contracts and relaxes, the valves open and shut, belongings blood flow into
the ventricles and atria at alternate times. the subsequent is additionally a piecemeal illustration
of however the valves operate usually at intervals the left ventricle: After the middle ventricle
contracts, the guts valve closes so the valve opens, to permit blood to result the atrium of the
middle into the middle ventricle. As the atrium of the middle contracts, lots of blood flows into
the middle ventricle. When the middle ventricle contracts, the valve closes so the guts valve
opens, therefore blood flows into the vessel. Heart valves will have one in all 2 malfunctions:
regurgitation (or run of the valve): The valve(s) doesn't shut fully, inflicting the blood to flow
backward through the valve. This finally lands up in run of blood back to the atria from the
ventricles (in the case of the mitral and angulate valves) or run of blood into the ventricles (in the
case of the artery and organ valves). Stenosis (or narrowing of the valve): The valve(s) gap
becomes narrowed or valves become broken or scarred (stiff), inhibiting the flow of blood out of
the ventricles or atria. The center is forced to pump blood with magnified force therefore on
maneuver blood through the narrowed or stiff (steno tic) valve(s). Heart valves will have each
malfunctions at an identical time (regurgitation and stenosis). Also, over one heart valve is
affected at an identical time. Once heart valves fail to open and shut properly, the implications
for the center is serious, presumably hampering the heart's ability to pump blood adequately
through the body. Heart valve issues unit one rationalization for upset.