Trigger 6 Flashcards
Blood pressure equation
Bp = Q x TPR
what is the mean arterial pressure regaulated by
baroreceptors
renin-angiotensin system
what is the effect of baroreceptors
fast neuronal response
M2AchR = decrease Q
B1AR = increase Q
a1AR = increase vasoconstriction = increase TPR
outline the renin angiotensin pathway
plasma angiotesnionogen - cleaved be renin
= angiotensin I - cleaved by ACE (in the lungs)
= angiotensin II
what does angiotensin II stimulate
release of aldosterone
release of ADH
release of ANP
vasoconstriction
what is the effect of aldosterone
released from the adrenal cortex
increase Na2+ and fluid retention (distal convulted and collecting duct)
loss K+ and H+ in the urine
what is the effect of ADH
released from the posterior pituitray increases fluid retention aquaporins in collecting duct V2R (Gs) stimulates aquaporins stimulates Na2+ K+ 2Cl- cotransporter
effect of angiotensin on smooth muscle contraction
angiotensin II At receptor is a Gs and leads to Ca2+ release
increase in intracellular Ca2+ leads to calmodulin activating the MLC kinase which phosophorylates MLC leading to contraction
Gs - leads to cAMP, which inhibts MLC leading to relaxtion
what is ANP
released from the atria
due to stretch/distension
binds to natriuetic peptide receptor resulting in guanylate cyclase activity - increase cAMP
smooth muscle relaxation, vasodilation of affertent
causes a decrease in renin and subsequently angiotensin and aldostrone
what is the glomerus filtration rate
rate of fluid filtered through the kidneys
estimates how much blood passes through the glomeruli each minute
normal GFR rates
males - 125ml/min
females - 105ml/min
GFR equation
urine conc x urine flow/plasma conc
what is urine flow
amount of urine produced in a given time
what is plasma conc
conc of urine in blood after a IV injection
how is the GFR regulated
intrinsic mechanisms
- renal autoregualtion - vasocontrsiction/dilation
extrinsic mechaisms
- neural/endocrine control - ANP = increase GFR
- tubulogolmular feedback - specialised cells within the distal tubule monitor Na2+
what happens if K+ conc decreases
if it reduces by a 1/3 leads to paralysis as nerves unable to generate AP
what happens if Ca2+ conc decrease
if it reduces by 1/2 leads to tetanic skeletal muscle contractions
what are the 3 types of dehydration
hypotonic/hyponatremic - primarily loss of electrolytes
hypertonic/hypernatremic - primarily loss of water
isotonic/isonatremic - equal loss of water and electrolytes
where is Na largely loacted
extracellularly
primary determinent of extracellular fluid volume
where is K+ largely located
intracellularly
primary determinent of extracellular fluid volume
what is hypokalemia and why does it occur
low K+
caused by directics, diarrhoea
leads to intracellular hyperpolarization
RMP further from resting membrane potential
what is hyperkalemia and why does it occur
caused by renal failure, tissue damage and acidosis
depolarisation of excitable cells - high K+ outside
causes an increase in voltage gated Na channel opening in the first instance, which depolarises the cell, then the channels are inactivated once it reaches a certain voltage leading to overall inhibition of the cell
role of principle cells
secrets K+
exchanger with Na2+
what stimulates principle cells
aldosterone
K+ increase
alkalosis
role of intercalacted cells
reabsorbs K+
exchanger with H+
what stimulates intercalated cells
acidiosis
K+ decrease
what is the bodys pH range
6.8-8
what is the pH of acidosis and the result
pH < 7.35
results in depression of the CNS
- increase in H+ secretions and excitation
what is the pH of alkasis and the result
pH >7.45
overexcitabilty of the CNS and PNS
- sensory neurones fire in absence of stimuli
- motor neurons casues muscle twitches/spasm
- decrease in H+ secretion and excrtion
risk factors for UTIs
females - poor hygine, unprotected sex, diaphragm and spermicide use, antibiotics
anatomincal structure and functional abnormalities
what are the different classifications of UTIs
Urethritis - infection of urthera
Cystisis - infection of the bladder
Acute pyelonephritis - baterical infection of the kidney parenchyma
describe the follcular phase
O and P levels low = signals to piturtary gland to produce FSH FSH = maturing folicle levels of FSH start to decrease casues folicle to produce more O suppress development of other follicles postive feeback lasts about 14 days
descirbe the ovulation phase
increased O causes an LH surge
ovulation
stimulated enzymes in the follicel release an egg
ovulatiory phases lasts about 16-32 hours
eggs travels down the fallopian tube
decribe the luteal phases
corpus lutem secretes large amount of O&P prepares uterus for fertilsation P causes - endothelium to thicken - fill with fluid and nutrients - mucus in the cervix to thicken - slight increase in body temp
LH & FSH fall
if the eggs is not fertilised the corpus lutem shrinks an degenerates, unfertlised egg dies
O&P levels fall
uterus lining is shed
where is the thyroid gland
located in the neck just below the layrnx and in front of the trechea
structure of the thyroid
bufferfly shaped with two lobes connected by the isthmus
made up of many sphericle thyroid follicles
follicles contain colloid, which stores the glycoprotien = thryrogloblin
how are T3 and T4 made
tyrosine molecules are iodinased
role of T3
responsible for almost all thyroid activity
half life - 1 day
role of T4
largely converted to T3 intracellulary
half life - 7 days
effect of thyroid hormones on the nucleus
stimulate nuclear receptors to activate DNA transcritpion
receptors are normally occupied by inhibitory repressors which are displaced by T3 to start activation
effect of thyroid hormones on the mitochondria
direct action to increase oxidative phosphorylation
stimulates mitochondiral DNA transcription
effect of thyroid hormones on the cell membrane
may also be a cell surface GPCR receptor which has an indirect function to stimulate nuclear DNA transcription
thyroid hormones act to enchance
basal metabolism
cardiac muscle activity
sympathetic NS activity
protein synthesis and growth
hypothalmus location and role
part of the dicephalon
between the cerebral hemisphere and brain stem
ventral to the thalamus
regulates
- body temp
- food intake
- water balance
endocrine gland location and role
releases hormones into hypophysical portal blood that causes release or inhibition of hormones from the anterior pituitary
also contains cell bodies of neurones of the posterior pituitary
pituitary gland
size of a pea, situated in a bony hollow just behind the bridge of your nose
controls several other hormones glands
anterior pituitray gland
surronded by a capillary network which extends from the hypothalamus
the hypophyseal portal system allows hormoes prodcued by the thalamus to be carried directly to the posterior pituitray without entering the blood
thyroid abnormalities
hypothroidism - not enough thyroxine is produced
hyperthroidism - too much thyroxine produced
what is hyperaldosterone
excessive levels of aldosterone which may be independant of the RAAS axis (primary) or due to high renin levels (secondary)
primary hyperaldosterone
at the gland
renin independant increase in the secretion of aldosterone
disease of adult hood
causes
- adrenal adenoma
- usually benign encapsulated adenoma
- tumours
levels for primary hyperaldosterone
aldosterone - high
renin - low
cortisol - normal
secondary hyperaldosterone
occurs at the previous site or further up the system
occurs in the kidney decrease in - blood flow - blood pressure - Na2+ levels in the blood
more renin, more signals to adrenal gland so more aldosterone
levels for secondary hyperaldosterone
aldosterone - high
renin - high
cortisol - normal
