Trigger 6 Flashcards

(53 cards)

1
Q

Blood pressure equation

A

Bp = Q x TPR

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2
Q

what is the mean arterial pressure regaulated by

A

baroreceptors

renin-angiotensin system

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3
Q

what is the effect of baroreceptors

A

fast neuronal response
M2AchR = decrease Q
B1AR = increase Q
a1AR = increase vasoconstriction = increase TPR

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4
Q

outline the renin angiotensin pathway

A

plasma angiotesnionogen - cleaved be renin
= angiotensin I - cleaved by ACE (in the lungs)
= angiotensin II

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5
Q

what does angiotensin II stimulate

A

release of aldosterone
release of ADH
release of ANP
vasoconstriction

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6
Q

what is the effect of aldosterone

A

released from the adrenal cortex
increase Na2+ and fluid retention (distal convulted and collecting duct)
loss K+ and H+ in the urine

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7
Q

what is the effect of ADH

A
released from the posterior pituitray 
increases fluid retention 
aquaporins in collecting duct 
V2R (Gs) stimulates aquaporins
stimulates Na2+ K+ 2Cl- cotransporter
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8
Q

effect of angiotensin on smooth muscle contraction

A

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

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9
Q

what is ANP

A

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

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10
Q

what is the glomerus filtration rate

A

rate of fluid filtered through the kidneys

estimates how much blood passes through the glomeruli each minute

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11
Q

normal GFR rates

A

males - 125ml/min

females - 105ml/min

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12
Q

GFR equation

A

urine conc x urine flow/plasma conc

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13
Q

what is urine flow

A

amount of urine produced in a given time

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14
Q

what is plasma conc

A

conc of urine in blood after a IV injection

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15
Q

how is the GFR regulated

A

intrinsic mechanisms
- renal autoregualtion - vasocontrsiction/dilation

extrinsic mechaisms

  • neural/endocrine control - ANP = increase GFR
  • tubulogolmular feedback - specialised cells within the distal tubule monitor Na2+
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16
Q

what happens if K+ conc decreases

A

if it reduces by a 1/3 leads to paralysis as nerves unable to generate AP

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17
Q

what happens if Ca2+ conc decrease

A

if it reduces by 1/2 leads to tetanic skeletal muscle contractions

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18
Q

what are the 3 types of dehydration

A

hypotonic/hyponatremic - primarily loss of electrolytes
hypertonic/hypernatremic - primarily loss of water
isotonic/isonatremic - equal loss of water and electrolytes

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19
Q

where is Na largely loacted

A

extracellularly

primary determinent of extracellular fluid volume

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20
Q

where is K+ largely located

A

intracellularly

primary determinent of extracellular fluid volume

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21
Q

what is hypokalemia and why does it occur

A

low K+
caused by directics, diarrhoea
leads to intracellular hyperpolarization
RMP further from resting membrane potential

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22
Q

what is hyperkalemia and why does it occur

A

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

23
Q

role of principle cells

A

secrets K+

exchanger with Na2+

24
Q

what stimulates principle cells

A

aldosterone
K+ increase
alkalosis

25
role of intercalacted cells
reabsorbs K+ | exchanger with H+
26
what stimulates intercalated cells
acidiosis | K+ decrease
27
what is the bodys pH range
6.8-8
28
what is the pH of acidosis and the result
pH < 7.35 results in depression of the CNS - increase in H+ secretions and excitation
29
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
30
risk factors for UTIs
females - poor hygine, unprotected sex, diaphragm and spermicide use, antibiotics anatomincal structure and functional abnormalities
31
what are the different classifications of UTIs
Urethritis - infection of urthera Cystisis - infection of the bladder Acute pyelonephritis - baterical infection of the kidney parenchyma
32
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 ```
33
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
34
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
35
where is the thyroid gland
located in the neck just below the layrnx and in front of the trechea
36
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
37
how are T3 and T4 made
tyrosine molecules are iodinased
38
role of T3
responsible for almost all thyroid activity | half life - 1 day
39
role of T4
largely converted to T3 intracellulary | half life - 7 days
40
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
41
effect of thyroid hormones on the mitochondria
direct action to increase oxidative phosphorylation | stimulates mitochondiral DNA transcription
42
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
43
thyroid hormones act to enchance
basal metabolism cardiac muscle activity sympathetic NS activity protein synthesis and growth
44
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
45
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
46
pituitary gland
size of a pea, situated in a bony hollow just behind the bridge of your nose controls several other hormones glands
47
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
48
thyroid abnormalities
hypothroidism - not enough thyroxine is produced | hyperthroidism - too much thyroxine produced
49
what is hyperaldosterone
excessive levels of aldosterone which may be independant of the RAAS axis (primary) or due to high renin levels (secondary)
50
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
51
levels for primary hyperaldosterone
aldosterone - high renin - low cortisol - normal
52
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
53
levels for secondary hyperaldosterone
aldosterone - high renin - high cortisol - normal