phys Flashcards
(200 cards)
1
Q
what keeps the visceral and the parietral together to keep the lung attached to the rib cage
A
negative pressure(relative to atmospheric) exists within the pleural cavity, hence keeping the lung inflated at stuck to the cage
2
Q
what is the pressure within the lungs
A
the same as the atmospheric pressure
3
Q
boyles law
A
says that within a closed system an increase in volume decreases pressure and a decrease in volume increases pressure
4
Q
how does boyles law apply to inhalation and exhalation
A
1) inhalation,increase lung volume causes a lower pressure hence the air moves from a high pressure in the atmosphere to a low pressure in the lungs
vice versa for exhalation
5
Q
intrapulmonary pressure
A
pressure of air in lungs(also known as alveolar pressure)- 0mmHg at rest
6
Q
intrapleural pressure
A
pressure in pleural space
at rest= -4 mmHg
7
Q
transpulmonary space
A
pressure difference between intrapleural and intrapulmonary pressure
8
Q
describe the inspiration and expiration process
A
1) chest expands
2)intrapulmonary/alveolar and intrapleural pressure decreases
3)gases rush INTO lungs to equalise pressure to 0mmHg(inspiration)
4)as diaphragm relaxes along with the chest, lung volume decreases
5)intrapulmoary/alveolar pressure increases to approx 4 mmHg
6)gases rush out of the lungs to equlaise pressure to 0mmHg(expiration
9
Q
what is lung compliance
A
the ability for the lung to inflate
10
Q
what are the two main factors of lung compliance
A
elastic force
surfactant surface tension
11
Q
what are elastic force and surfactant surface tension affected by
A
lung elasticity
muscles vs resistance
surfacant surface tension
12
Q
what is surfactant surface tension
A
surfactants(absorbed and produced),decreases surface tensio by 7-40% preventing the water from sticking together and causes the aveoli from collapsing(lung collapse)
13
Q
surfactants in babies
A
production of surfactants doesn’t begin until 6-7 months and hence can result in respiratory diseases- cortisol given to stimulate this production
14
Q
lung elasticity
A
stretching of parenchyma(connective tissue) of lungs- tissue fibrosis decreases lung compliance
15
Q
muscles vs resistance
A
the abiltiy of respiratory muscles to overcome the resistance of the chest wall,lungs and airways in order to inflate- fibrosis, thickening and scoliosis(stiff chest walls) decrease compliance
16
Q
what happens to airflow resistance as one goes down the order of bronchi
A
decreases( not exactly but still)
17
Q
does airway length or radius have a greater affect on resistance
A
radius has a greater affect
18
Q
which size of bronchi have the greatest resistance
A
medium sized
19
Q
factors affecting resistance
A
airway radius
nervous system affects(bronchomotor control
20
Q
bronchomotor control
A
vagal afferent nerves(bronchoconstriction)
inhaled stimuli like dust(bronchostriction reflex)
sympathetic nerve supply(bronchodilation)
circulating catecholomines(bronchodilation)
21
Q
whats commonly used to measure lung capacity
A
spirometer
Tidal volume (Vt): during quiet breathing
Vital capacity: volume of maximum breathe
22
Q
what is used to measure air flow rate
A
spirometer
FVC: forced vital capacity
FEV1:amount of air expired in first 1 second
FEV1/FVC= 75% in a healthy person
COPD and asthma –> a decrease in FEV1 (obstructive)
23
Q
obstructive lung disease
A
asthma + COPD –> decrease in FEV1
24
Q
restrictive lung disease
A
fibrosis–> decrease in both FEV1 and FVC usually normal looking ratio
25
5 factors which impact diffusion
partial pressure of gases on each side of the membrane
thickness of aveoli of membrane
area of lungs for diffusion
solubiltiy of gas
matching of ventilation and perfusion
26
what is oxygen driving pressure and CO2's
60 and 4
this can change with different altitudes resulting in a lower oxygen driving force( if high alt) and increasing drivinf force of O2 (if low alt)
27
features of aveoli which help diffusion
thin membrane and large SA
28
what can affect aveoli thickness
fibrosis and edema and emphesyma(damaging wall causing them to rupture decreasing SA)
29
how to measure oxygen diffusion
oximeter --> which measures the amount of O2 fixed to heamaglobin
arterial blood sample---> partial pressure of O2= 100 and CO2=46
TLCO and DLCO = measure gas transfer from air to blood
30
why in DLCO use CO
diffuses easily across alveolar surfaces
highly soluble and high affinity to Hb
not present in plasma so easy to measure when in plasma
31
how to use DCLO
inhale CO and Helium hold for 10 seconds
exhale into bag and then measure the bag contents
normal= 25ml
32
ficks law
A/T x D x (P1-P2)
P1-P2= O2 and CO2 gradient
A/T= structural elements
D=constant for properties of the gases
33
importance of ventilation-perfusion
for effecient effusion there must be a match between the perfusion of each area of the lung and the ventilation to that part of the lung, measured with V/Q ratio= close to 1(normal=0.8)
34
V in ventilation
flow of air in and out of aveoli
35
Q for perfusion is
flow of blood to alveolar capilaries
36
V-P differing how in aveoli
like slinky the aveoli at the bottom have a higher V/Q since they are kinda stacked more closely
37
shunting
reduced ventilation hence ratio < 0.8 (pneumonia,asthma
38
dead space and V-P
dead space- reduced perfusion hence ratio is >0.8(pulmonary embelism)
39
V-P scan
radioactive tracers to evaluate circulation of air and blood
second part measures how well air gets to all parts of lungs(ventilation)
40
two ways in which oxygen can be transported
dissolve in plasma
through Hb(majority)
41
oxygen saturation
percentage of Hb occupied by oxygen
42
what is the ICU(hypoxic) point
at 60 mmHg which gives a reading of 90
43
during circulation what does O2 drop down to
from 100% to 75% leaving leftover just incase there is a big drop (eg. excersize)
44
factors shifting O2 dissociation left
this causes greater affinity to O2(eg. in excersize)
increased PCO2
increased temp
decrease ph(acidic)
increase in 2,3 DPG. FIX
45
factors shifting O2 dissociation right
this causes less affinity to O2
decrease PCO2
decrease temp
increase pH(basic)
decrease 2,3 DPG
46
ways in which CO2 are diffused
-plasma + RBC cytoplasm
-bound to Hb(20%)
-HCO3- in plasma(75%)
47
solubulity difference between O2 and CO2
CO2 is 20 times more soluble
48
how quick does CO2 diffused
0.25 of a second(to reach equilibrium)
49
two ways in which breathing is controlled
neural control-automatic rythm and modulation
chemical by )2 and CO2 receptors
-modulation of rythm
50
Pre-Botzinger complex
ventral respiratory group(VRG) in the medulla which regulates unconscious breathing
51
what does the VRG do
-modulated by corotoid bodies,stretch receptors,chemo and mechanoreceptors
-suppressed by opiotes causing respiratory arrest
-also innervates internal intercostals
52
what is the role of the DRG
signals from dorsal respiratory group(DRG) go to the diaphragm to signal it to inspire -also innervates external intercostals
53
pons neumotaxic area role
cessation of breathing(by the apneustic area)
54
what is a part of chemical control of breathing
central chemoreceptors
periphearal chemoreceptors
55
central chemoreceptors
located in medulla
monitor CO2 via H+ conc
slower speed but greater effect(70% greator than peripheral
ph receptors at CO2
56
periphereal receptors
located in cortacoid bodies and aortic arch
monitors O2,CO2 and H+
faster speed but smaller effect
respond to
decrease in PO2
PCO2 and increase in H+
57
what do central chemoreceptors respond to if not CO2
H+(which does not cross blood-brain barrier)
58
SPO2 level which casues unconciousness
<40%
59
what are the three main layers of the gut
mucosa, submucosal layer, muscular propria
60
layers of the mucosa
mucosal layer
muscular layer
61
layers of submucosal layer
submucosal plexus
62
layers of muscular propia
longitudinal muscle
circular muscle
63
what is the epithelial type in the mucosal layer of the oesophagus
stratified squamous
64
what is the epithelial type in the mucosal layer of the stomach
simple columnar with gastric pits and parietal cells
65
what is the epithelial type in the mucosal layer of the small intestine
simple columnar with microvilli
66
what is the epithelial type in the mucosal layer of the large colon
simple columnar with goblet cells
67
what is the epithelial type in the mucosal layer of the rectum
simple columnar--> stratified squamous
68
effects of Act
promotes digestion
promotes peristalsis
sphincter relaxation
69
effects of NA
impairs digestion
impairs peristalsis
sphincter constriction
70
what are the major gut secretions
saliva, stomach acid, bile, cholecystokinin, secretin, pancreatic secretions
71
what is saliva produced by
3 pairs of extrinsic salivary glands and 100+ intrinsic buccal salivary glands
72
what is saliva made of
mostly water: drug absorption, taste sensation
ions: calcium phosphate to prevent demineralisation of teeth
salivary amylase(pytalin)
mucin: lubricates food
immunoglobulins
73
what is the distal trigger of salivation
-approach, presence or taste of food promotes
-sleep/fear reduces
74
what is the proximal trigger of salivation
parasympathetic stimulation increases salivation ( and other gut secretions) via afferent/efferent pathways.
75
what are the steps in swalllowing
buccal/voluntary
pharyngeal
oesophageal
76
what happens in the buccal/voluntary stage of swallowing
movement: oral cavity --> pharynx
innervation: somatic motor(skeletal) from cereberal cortex
77
what happens in the pharyngeal stage of swallowing
movement: pharynx --> oesophagus
innervation: parasympathetic(autonomic) and somatic motor (skeletal) from swallowing center in the medulla/brainstem via vagus nerve
78
what happens in the oesophageal stage of swallowing
movement: oesophagus --> stomach
innervation:
parasympathetic(autonomic) and somatic motor (skeletal) from swallowing center in the medulla/brainstem via vagus nerve
79
what is dysohagia
refers to difficulty swallowing
80
aetiology of dysphagia
mouth, tongue, or salivary glands
neuromuscular disorders
outpouchings of pharynx or oesophagus
secondary to stroke or parkinson's
81
treatment of dysphagia
treat underlying pathology
surgical repair
self resolving
82
what secretes HCL in stomach
parietal cells in stomach lumen secrete HCL
83
function of stomach acid
activates pepsinogen, a precursor to pepsin, a digestive enzyme for proteins
kills pathogens in ingested food
breaks down cellulose
84
what are the different triggers for production of stomach acid
PROMOTE
cephalic= approach or presence of food
gastric= stomach distension
acetylcholine
REDUCES
intestinal= duodenal distension, protein digestion products, acidity
85
function of parietal cells
secretes stomach acid( HCL)
secretes intrinsic factor used for absorption of vitamin B12
86
what causes pernicious anaemia
deficiency of intrinsic factor ( intrinsic factor secreted by parietal cells)
87
outline the entire cellular process of stomach acid production
1) G cells(gastrin), ECL Cells(histamine), Muscarinic receptor(acetylcholine) are receptors present on parietal cell
2)receptors signal to H+/K+ ATPase protein pump to release HCL into gastric lumen
3) H+ taken up from H2CO3 in blood H2CO3 --> HCO3- + H+
88
what is GORD
gastro-oesophageal reflux disease
89
how can stomach acid be inhibited
most efficient to inhibit H+/K+ protein pump via PPIs
eg. esomeprazole
90
what is esomeprazole used for
stomach acid inhibition
91
issues when it comes to fat digestion that the body must tackle
fat is hydrophobic
acidic( enzymes dont work)
big molecules
92
what are pancreatic duct cells function in fat digestion
secretes HCO3- to neutralise the acid
hormone=secretin
93
hepatocytes role in tackling issue of fat digestion
they emulsify fat into droplets through bile salts and phospholipids through the hormone CCK
comes from the liver
94
what are the two triggers for acid
chyme released from stomach is full of H+ ions
decrease in pH(acid) in small intestine( results in sphincter of oddi to relax
95
outline the mechanism of bile
hepatocytes --> bile duct --> common bile duct --> sphincter of oddi --> Small intestine
96
what does the gal bladder store between meals
bile
97
effect from too much fat in duodenum on response by CCK from the small intestine
1) gall bladder contracts
2)sphincter of oddi opens
3) pancreas releases lipase
4) pyloric sphincter closes
5) stomach stops peristaltic movement
98
what is the sphincter of oddi
The sphincter of Oddi is a muscular valve that controls the flow of bile and pancreatic juices from the liver and pancreas into the small intestine (duodenum)
99
outline the events in the break down of triglycerides
CCK --> pancreatic lipase release from acinar cells
lipase breaks triglycerides--> monoglycerides + fatty acids
fatty acids join micelles( tiny droplets of emulsified fats)
fatty acids are then absorbed into the intestinal epithelial cells
100
how does the body deal with issue of most proteolytic enzymes being in an inactive state w/n pancreas
convert enzymes into active state
101
outline the mechanism of trypsinogen
inactive enzyme that is converted to active trypsin by enterokinase(membrane bound protein w/n epithelial intestinal cells)
102
how does the body deal with polysaccharides being to big of a molecule
they break them down through amylase which operates well in normative pH of small intestine (not in stomach)
-breaks them into glucose+ fructose
103
what is acute pancreatis
inflammation of pancreas (eg. from blockage or chronic stress)
104
causes of acute pancreatis
alcohol, hypertriglyceridemia, gallstones
105
effect acute pancreatis
digestive enzymes begin to activate within the pancreas --> self digestion
-decreases duct + acinar cell function
-malabsorption of fat
-abdominal pain
-weight loss
106
how is acute pancreatis treatment
electrolytes
analgesia
107
what is the small bowel consitent of
duodenum, jejunum and ileum
extends from pyloric sphincter to the ileocaecal sphincter
108
what occurs in the small bowel
chemical digestion and nutrient absorption
109
what are the two types of contractions
mixing and segmenting contractions
migrating myeolectric complex( peristaltic contractions of several adjacent segments from stomach to large intestine)
110
definition of constipation and causes
stools <2 weeks
straining > 25% of time
causes:
-pregnancy
-IBS
-Iron, antidepressants
-spinal cord lesions
-depression, anorexia nervosa
-intestinal obstruction, colonic disease
-rectal prolapse
-diabetes, hypercalcaemia, hypothyrodism
111
diarrhoea definition
rapid moving poooo
112
cholesterol
precursor to bile salts
113
bile salts
helps emulsify fat in SB
114
lecithin
forms micelles with bile salts derived from phospholipids
115
electrolytes
HCO3- to neutralise
116
water
exists
117
bile pigments
produced from hem breakdown
118
what's the rate limiting enzyme of bile acid synthesis
7a-hydroxylase
119
how is bile acid synthesis
Farnesoid X receptor (FXR) and retinoid X receptor (RXR) are activated by bile acids to inhibit production
120
describe the enterohepatic circulation
bile enters into duodenum, emulsify fat and then be reabsorbed
- 95% reabsorbed through portal venous circulation
- 5% excreted as secondary bile acids
-lost bile is synthesised
121
formation of bilirubin
broken down hem --> biliverdin--> bilirubin
122
what is the major bile pigment
bilirubin
123
roles of bilirubin in liver
become stercobilin and be excreted via faeces, providing colour
recirculate
become urobilin and be excreted via urine
124
definition of jaundice
yellow appearance of skin, sclera and mucous membranes caused by excess of bilirubin in blood
icterus
clinically detectable when serum bilirubin> 50 micro mol or 3mg/dl
(normal is 17 and 1)
125
clinically detectable jaundice numbers
when serum bilirubin >50 micro mol or 3mg/dl
126
normal serum bilirubin levels
<17 micro mol/litre or 1mg/dL
127
how is unconjugated bilirubin formed
breakdown of hemme from RBC's mainly in the spleen forms unconjugated bilirubin
128
breakdown of where bilirubin is derived from
80% derived from Hb while remainder from other hemoproteins or free hem
129
how is unconjugated bilirubin transported to liver
it is bound to albumin as unconjugated bilirubin is water insoluble
130
how is bilirubin conjugated
liver hepatocytes conjugate it with glucoronic acid to form the conjugated bilirubin
131
what percent of bilirubin is recycled back
95% of secreted bilirubin is reabsorbed by a terminal ileum and portal circulation via the enter hepatic circulation
132
what happens to the remaining 5% bilirubin which remains and isn't reabsorbed
hydrolysed by the intestinal flora and reduced to form urobilinogen, which colourless and water soluble
133
what is pre-haptic jaundice
occurs due to a fault somewhere upstream or proximal to bilirubin conjugation
-unconjugated bilirubin is produced but is not converted properly in the liver
134
common causes of pre-haptic jaundice (haemolysis)
haemolysis--> faster than normal breakdown of red blood cells( increased--> increased unconjugated bilirubin--> too. much for liver to handle)
135
common causes of pre-haptic jaundice (congenital)
defects in liver uptake or transport system (issue with transport to liver or liver cannot convert unconjugated bilirubin
136
common causes of prehaptic jaundice (physiological)
developing babies in first week have neonatal jaundice
137
what's the result of excess unconjugated bilirubin
increase conjugated bilirubin production:
-results in excess urobilinogen in the gut
--> excess urobillinogen detected in urine
colourless but detectable in urine by dipstick
138
what is intrahepatic jaundice
liver hepatocyte lose ability to conjugate bilirubin and cirrhosis can affect bile ducts
139
common causes of intrahepatic jaundice
viral hepatitis, alcohol, non-alcoholic steatosis hepatitis (NASH)--> liver inflammation due to accumulated fat in the liver
140
what makes intrahepatic jaundice different
as cirrhosis develops the intra hepatic parts of biliary tree are compressed ( hence predominantly have conjugated hyperbilirubinanaemia)
141
what is post-hepatic jaundice
occurs due to a fault somewhere downstream or distal to bilirubin conjugation
142
common causes of post hepatic jaundice (intra luminal)
gallstones blocking the billary tree
143
common causes of post hepatic jaundice(mural)
cholangiocarcinoma, intrahepatic cholestasis( multiple small blockages within the liver itself) eg. structures or drug induced cholestasis
144
common causes of post hepatic jaundice(extra-mural )
head of pancreas cancer abdominal masses or pregnancy
145
reason for dark urine during post hepatic jaundice
conjugated bilirubin from the liver can't get to the gut
it spills into the bloodstream and since it is water-soluble, it passes via the glomerulus into the urine, producing dark urine( water-soluble)
reduced bilirubin in gut--> little to no urobiligen--> no urobiligen in the urine(causes dark urine) --> little stercobilin made --> pale stools (sterocobilin makes it brown)
146
what does sterocobilin do
by product of bilirubin when it is broken down in the intestine
-bilirubin to sterocibilin
gives stool the brown appearance
147
symptomatic characterisation of pre hepatic jaundice
no change in colour (colourless urine)
absence of bilirubin(unconjugated bilirubin= not water soluble so it can't be present in urine)
- increase urobiligen
148
symptomatic characteristics of intra hepatic jaundice
maybe darker urine
presence of conjugated bilirubin in urine
149
symptomatic characteristics of post hepatic
darker colour urine
presence of conjugated bilirubin in urine(water soluble--> leaks out of hepatocytes into urine)
absence of urinary urobiligen(cholestasis- cant enter small intestine
150
liver function test biliary enzymes
biliary enzymes(cholestatic enzymes) - detect interrupted bile flow
151
liver function test ALP
alkaline phosphatase
produced by epithelial cells lining the bile canaliculi
increase in intra or extra hepatic obstruction
152
liver function test Gamma-GT
Gamma-glutamyl transferase
produced by epithelial cells lining lining bile canaliculi
increase inter hepatic ie mixed enzyme induction by alocohol or drugs
153
liver function test ALT + AST
aspartate amino transferase(AST) and alanine aminotransferase(ALT)
contained within the hepatocytes--> hepatitis
ALT- more specific for liver damage
abdominal ultrasound
154
likelihood ratios
pre test prob= prob of disease before taking test
(sensitivity/1- specificity)
post test prob=prob disease after taking test
1- sens/ specificity
155
what is the renal corpuscle made of
Glomerulus: afferent + efferent arteriole + arterial bundle
Bowman’s capsule: the ‘cup’ of the nephron, which filters blood through its walls. The filtrates end up in the bowman’s space, which is continuous with the nephron tubule
Mesangium: matrix of connective tissue and mesangial cells between arterioles and bowman’s capsule
Urinary Pole: where bowman’s space meets PCT
156
Juxtaglomerular Apparatus
(JGA) role
These cells are responsible for controlling renin release to regulate blood pressure - more on this later.
157
What cells make up the JGA?
Macula densa cells (DCT) - detect Na
Juxtaglomerular cells/Granular cells (afferent arteriole) - store + release renin
Mesangial cells - selective vasoconstriction/dilation of afferent/efferent arteries
158
Where are the JGA located?
Between the Distal convoluted tubule and the glomerulus - juxtaglomerular
159
What happens if there are changes in GFR?
↑ GFR → inadequate reabsorption (less time for reabsorption) → substances lost in urine
↓ GFR → reabsorption increased (more time for reabsorption) → wastes not excreted
Therefore, maintaining a relatively constant GFR is important for homeostasis
160
what is auto regulation
Autoregulation = The ability of an organ to maintain its blood flow nearly constant despite changes in arterial pressure.
161
what issue with autoregulation with gfr and urine
-urine is not auto regulated and is directly proportional to blood pressure h/w gfr is
162
special circumstance of pressure < 80 or >180
Autoregulation doesn't occur at arterial pressures below 80 mmHg and above 180 mmHg as it is not preferred in these circumstances:
If pressure too low (below 80mmHg) then filtration needs to be reduced to conserve blood volume
If pressure too high (above 180mmHg) then filtration needs to be increased to reduce blood volume
Hence we want changes in RBF and GFR occur at pressures above or below these values
163
myogenic mechanism in afferent arterioles
An increase in blood pressure will lead to ↑RBF and ↑GFR
-this will put stress on the arteriole walls, causing stretch receptors in the vascular smooth muscle cells (VSMC) to initiate vasodilation --> decrease rbf and gfr
opposite for decrease in blood pressure
164
lap laces law
When the VSMCs sense a change in pressure (due to increased stretch), this leads to calcium channels opening, an influx of calcium into the cell, and therefore constriction to reduce tension
If there is decreased stretch, the calcium channels will close, preventing calcium from entering the cell and causing dilation to increase tension
165
Tubuloglomerular feedback
Macula densa senses changes in flow rate or the amount of sodium in the filtrate as it comes back and touches its own glomerulus
166
Tubuloglomerular feedback process of GFR increase and GFR decrease
If GFR increases:
Flow through the tubules (proximal, loop of Henle, distal) increases
Flow past the macula densa increases
The macula densa cells senses this increased flow rate, increases the release of adenosine, which causes constriction of the afferent arteriole and reduces the release of renin, which causes dilation of the efferent arteriole
Juxtaglomerular cells secrete renin
This will decrease PGC (due to increased resistance)
As a result, GFR, filtration rate and flow rate will all decrease (back to normal)
If GFR decreases (due to dehydration/blood loss):
Flow through the tubules (proximal, loop of Henle, distal) decreases
Flow past the macula densa decreases
The macula densa cells senses this decreased flow rate, reduces the release of adenosine, which dilates the afferent arteriole and increases the release of renin, which constricts the efferent arterioles
This will increase PGC (due to increased resistance)
As a result, GFR, filtration rate and flow rate will all increase (back to normal)
167
Aldosterone ( what is it, where produced, how diffuses, and role in Na+ reabsorption)
A steroid hormone (mineralocorticoid) that:
Is produced by the outer section (zona glomerulosa) of the adrenal cortex in the adrenal glands
Diffuses freely into the tubular endothelium
Aldosterone is the most important controller of Na+ reabsorption
By changes in [aldosterone]plasma, Na+ reabsorption can be finely controlled
168
Aldesterone role in the nephron( distal convoluted tubule and the collecting duct)
-Aldosterone increases sodium reabsorption in the late distal tubule and collecting duct segments of the nephron by binding to the cytoplasmic mineralocorticoid receptor.
-On binding, the receptor complex migrates to the nucleus, where it induces gene transcription.
-Taken together, the activation of multiple sodium transport mechanisms leads to augmented sodium and water reabsorption by the kidney.
169
P1-P4 of how expression of proteins that stimulate reabsorption are enhanced
-basolateral
-ATP production
-NA channels
-luminal membrane to K+
Increasing sodium-potassium ATPase protein and activity at basolateral membranes of distal nephron segments. (P2)
Increasing the production of ATP to be used as an energy source for the sodium-potassium ATPase pump. (P3)
Increasing the expression and activation of epithelial sodium channels, which enhances sodium entry into the cell. (P1)
Increasing the permeability of the luminal membrane to potassium, which drives the sodium-potassium ATPase pump. (P4)
170
what are the two ways in which substances can be absorbed tubularly in the nephron
+ how
Paracellular (through tight junctions)
Transcellular (through the tubular epithelial cells)
active( with ATP) or passive
171
what is transport maximum (mg/min)
the maximum amount of a substance which can be transported actively
there is a limit to the rate the solute can be transported (back into the peritubular capillaries)
This is caused by the saturation of carrier proteins (all being used)
If there is too much of a substance coming into glomerular capillaries, the carrier proteins will be saturated, leading to the excess substance being excreted through urine
172
what percent of water+ H2O, and HCO3- is absorbed at the proximal convoluted tubule
Majority of stuff is reabsorbed here (e.g 65% Na+ and water, 95% HCO3-)
173
where are the NA+/K+ ATPase on the PCT
-baso-
Na+/K+ ATPase is on the basolateral surface
Secondary active transport
174
role of the loop of henle descending and ascending + how thick and thin
Thin descending limb
Water is reabsorbed from the tubule due to highly concentrated interstitium
Forms HYPERtonic urine
Thick ascending limb
Solutes are reabsorbed into the interstitium using ATP
175
through what properties and how does the ascending limb create a concentrated interstituim
Not permeable to water
Allows for solutes to be pumped into the interstitium to raise the interstitial concentration
The descending limb is more concentrated than the ascending limb
176
which hormone in the DCT helps for the reabsorption of calcium
parathyroid hormone
177
what are aquaporins and role in dehydration and where are they found
Allows water to be reabsorbed to concentrate urine
Antidiuretic hormone (ADH/vasopressin) increase the number of aquaporins--> can be released when dehydrated
COLLECTING DUCT
178
what is present within the collecting duct hormonally
antidiuretic hormone--> aquaporins
aldosterone= Na+ reuptake--> K+ secretion
179
how is acidosis and alkalosis fought in the collecting duct
1. ALPHA INTERCALATED CELLS
Secretes acid, reabsorbs bicarb
CO2 passively diffuses into cell and becomes HCO3- and H+
2. BETA INTERCALATED CELLSSecretes bicarb, reabsorbs H+
CO2 entering cell from interstitium to become HCO3- and H+
180
how many litres in fluid compartments in your body
ECF
ICF
intracellular - ⅔ (28L)
Extracellular - ⅓ (14L)
181
what is osmotic pressure
Normally, osmotic pressure in ICF = ECF = 280 mOsm/L
182
where is ADH produced and what is its role
Released by the posterior pituitary
Triggers binding of aquaporins to membrane in DT and CD
Allows water to escape from tubules to plasma
183
list the kidney functions AWETBED
Kidney Functions: A WET BED
A - Acid-Base balance
W - Water balance
E - Electrolyte balance
T - Toxin removal
B - Blood pressure
E - Erythropoietin production
D - Vitamin D activation
184
what is renal failure
Renal failure occurs when there is kidney disease that obliterates or diminishes some or all of these functions.
185
what are indicators of the renal failure + why is creatinine used+ other indicator other than creatinine
Defined as:
Increase in serum creatinine by ≥0.3 mg/dL from baseline (≥26.5 mcmol/L) within 48 hours, or
Increase in serum creatinine to ≥1.5 times baseline within the prior seven days, or
Urine volume ≤0.5 mL/kg/hour for six hours
Serum creatinine is totally excreted by the kidneys, so levels of serum creatinine are highly reflective of renal function.
Similarly, the kidneys produce urine, hence reductions in urine output may be reflective of kidney injury.
186
why may acute kidney injury symptoms not manifest
Remember, as you have two kidneys, these clinical manifestations may not occur unless both kidneys are affected. This is particularly important when discussing post-renal AKIs.
187
how is pre-renal AKI defined as
The lesion occurs at a level that precedes the kidney causes a reduction in renal blood flow, reducing the glomerular filtration pressure and GFR as a consequence
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how is intra-renal AKI defined
Damage occurs to the renal parenchyma, either the vasculature within the kidneys, glomeruli, tubules, or the intersitium, and sometimes a combination.
Most commonly a result of prolonged renal hypoperfusion (a prerenal cause of AKI). ( hypo perfusion is insufficient blood)
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how is post-renal AKI defined
Damage occurs somewhere that proceeds the kidney i.e., the urinary tract, that causes backflow and increases pressure within the nephron to prevent glomerular filtration.
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5 causes of pre-renal AKI
Hypovolaemia
Redistribution of Fluid / Third Spacing
Decreased Cardiac Output
Renal Vasoconstriction
Renal Arterial Obstruction
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3 causes of intra-renal AKI
Acute Tubular Necrosis
Acute Interstitial Nephritis
Glomerulonephritis
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3 causes of post-renal AKI
Upper Tract Obstruction
Vesicoureteric Junction Obstruction
Bladder Outlet Obstruction
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3 treatments for AKI
Treat the underlying cause and stop any nephrotoxic drugs.
Supportive therapy and close monitoring of volume status (e.g., dehydration, urine output, weight…) and electrolyte balance.
In some cases, renal replacement therapy (RRT) may be necessary.
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define chronic kidney disease
Presence of kidney damage or decreased kidney function for three or more months, irrespective of the cause.
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CKD causes
Causes of CKD include:
Poorly controlled diabetes mellitus,
Hypertension,
Glomerulonephritis,
Polycystic kidney disease
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why are early stages of CKD asymptomatic
Early stages of CKD are asymptomatic.
This is due to our renal reserve: we have more kidney function than is strictly necessary, and normal homeostasis can be maintained with only 1 kidney.
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CKD symptoms
Symptoms of CKD only begin to manifest when significant kidney damage has occurred and they include:
Fatigue,
Urinary symptoms (oliguria, frothy urine (due to proteinuria), haematuria),
Fluid overload (bloating, orthopnoea, pedal oedema),
Persistent pruritus,
Chest pain (due to uraemic pericarditis),
Resistant hypertension…
198
what are the 4 tests which can help Identify CKD
However, CKD can be detected while asymptomatic through tests such as:
serum creatinine (elevated),
estimated glomerular filtration rate (eGFR; reduced),
urinalysis (abnormal),
ultrasound (small and echogenic (more dense), or large and cystic (PCKD)...
199
what are some main complications of hypertension
heart failure
CKD
stroke
vascular disease
200
what are the risk factors for hypertension:
SNAP-W:
SNAP-W:
smoking
nutrition
alcohol
physical activity
weight
