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Year 1 Medicine Newcastle > Case 3 > Flashcards

Case 3 Flashcards

1
Q

What is the peritoneum

A

A thin, serous membrane that covers all the organs and lines the abdominal cavity

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2
Q

What are the two layers of the peritoneum and where are they

A

The visceral peritoneum covers the abdominal viscera and organs
The parietal peritoneum lines the abdominal cavity

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3
Q

How would you describe and organ if it is completely surrounded in peritoneum

A

intraperitoneal

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4
Q

What are retorperitoneal organs

A

they only have peritoneum on their anterior surface

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5
Q

What organs and viscera are intraperitoneal (6)

A 
Liver
Gall Bladder
Spleen
Stomach
Small intestine (most of)
Large intestine (some of)
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6
Q

What organs and viscera are retroperitoneal

A 
S uprarenal glands
A orta & IVC
D uodenum (most of)
P ancreas (most of)
U reters
C olon
K idneys
O esophagus
R ectum
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7
Q

What is the mesentery

A

It’s an organ that attaches the intestines to the abdominal wall and it allows nerves to communicate between the viscera and the abdominal wall
It is double layered

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8
Q

What is an omentum

A

The connections between viscera and other viscera

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9
Q

What are ligaments with regards to the peritoneum

A

These are between viscera and other viscera or viscera and the abdominal wall

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10
Q

Where is the lesser omentum between

A

The liver and stomach/duodenum

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11
Q

What ligaments are in the lesser omentum

A

Hepatogastric ligament and heptatoduodenal ligament

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12
Q

What structures are found within the hepatoduodenal ligament

A

The bile duct, hepatic vein and hepatic artery

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13
Q

Where is the greater omentum between

A

The stomach down to the transverse colon

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14
Q

How many layers does the greater omentum contain?

A

4

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15
Q

Where is the phrenicolic ligament between

A

The colon and diaphragm

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16
Q

Where is the lienorenal ligament between

A

The spleen and kidney

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17
Q

What are mesentery reflections

A

Reflections of two layers of visceral peritoneal lying on top of each other and connect to the abdominal wall

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18
Q

What do the lesser and greater sac communicate and pass fluid through

A

The omental foramen

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19
Q

Where can the omental foramen be found (what ligament is it behind)

A

The hepatogastric ligament

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20
Q

What three layers can be found within the greater sac

A

The supracolic, infracolic and pelvic areas

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21
Q

What are recesses in the abdomen

A

Small places that fluid can congregate

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22
Q

What recesses can be found in the infracolic region of the greater sac and what is their function

A

The paracolic gutters (either side of the left intestine)

Any fluid that accumulates in the infracolic region can settle in these gutters

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23
Q

What recess can be found in the pelvis in males

A

The vesicorectal pouch

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24
Q

What recesses can be found in the pelvis in female

A

Vesicouterine and rectouterine pouches

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25
Q

What is a problem if infectious fluid builds up within one peritoneal reflection

A

It may spread across the whole peritoneum as the spaces are consistent with one another

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26
Q

What can cause a build up of infectious fluid in peritoneal reflections and cavities?

A

Bacterial contamination during abdominal surgery
Rupture of the gut as a result fo infection/inflammation
When an ulcer in the stomach or duodenum perforates through the wall of an organ

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27
Q

What is the disadvantage of the paracolic gutters being linked with other recesses

A

They are able to spread infectious fluid or cancerous cells throughout the peritoneal organs

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28
Q

What is the role of the transversus abdominis muscle

A

It contains transverse fibres that support the viscera and rotates and flexes the trunk

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29
Q

What does the quadratus lumborum muscle do

A

Stavilises the 12th rib

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30
Q

What do the muscles psoas major/minor/iliacus do

A

They work with the hip flexor

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31
Q

Where is the lumbar plexus

A

This is from the anterior rami of spinal nerves T12-L4

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32
Q

What is the crossover of lumbar and sacral nerves known as and what is its function

A

the lumbosacral trunk

it allows the passage of information between the two sections

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33
Q

What is the word for something related to the ureter

A

ureteric

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34
Q

What is the word for something related to the urethra

A

urethral

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35
Q

What is the word for something related to the uterus

A

uterine

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36
Q

Are the kidneys intra or retro peritoneal

A

retroperitoneal

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37
Q

What level of vertebrae are the kidneys found at

A

T12-L3

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38
Q

Which kidney is lower than the other

A

The right is lower than the left

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39
Q

What is the renal hilum

A

Found on the medial surface fo the kidney and it is where the main blood vessels and transport systems in and out of the kidney are found

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40
Q

What structures are anterior to the right kidney

A

The liver and parts of the small intestine

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41
Q

What retroperitoneal structures are attached to the right kidney

A

The right colic flexure (large intestine)
Descending part of the duodenum
the suprarenal gland

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42
Q

What intraperitoneal structures lie on the left kidney

A

The spleen
Stomach
Small intestine

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43
Q

What retroperitoneal structures lie on the left kidney

A

Pancreas
Left colic flexure (large intestine)
Descending colon

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44
Q

what is the renal capsule

A

A tough fibrous layer that protects the kidneys

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45
Q

What is the perirenal fat

A

Its a fatty capsule that surrounds the kidney to keep it protected, a layer within the renal capsule

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46
Q

What is between the two fat layers within the kidney

A

renal fascia

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47
Q

What is the layer of fat closest to the kidney called

A

pararenal fat

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48
Q

What five vessels are in the renal hilum

A 
From anterior to posterior
Renal vein
Renal artery
Ureter
Renal pelvis 
Lymphatics and sympathetics
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49
Q

Where does urine drain into after exiting a nephron

A

minor calyces

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50
Q

What do minor calyces join together and where do these subsequently go

A

These join to form a major calyx which join to the renal pelvis and then ureter

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51
Q

Where does the ureter join the bladder

A

The ureteropelvic junction

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52
Q

How does the urine move down the ureters

A

Peristalsis

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53
Q

Where are the main constrictions in the ureters (3)

A

renal pelvis, pelvic brim and ureteric orifice

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54
Q

In what cavity is the bladder found

A

The pelvic cavity

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55
Q

What are the muscles in the bladder walls called

A

The detrusor muscle

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56
Q

What is the function of the internal urethral sphincter in males

A

To prevent ejaculatory reflux of semen into the bladder

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57
Q

Why are females more at risk of UTIs

A

They have a much shorter urethra

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58
Q

What are the four parts of the male urethra from bladder to penis end

A

Preprostatic
Prostatic
Membranous
Spongy

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59
Q

Where does urethral obstruction result in a calculus forming in males

A

The external meatus

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60
Q

What do you locate first on females in order to catheterise them

A

the external urethral meatus

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61
Q

Why is catheterisation more difficult with males

A

The penis has two angles and it is longer

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62
Q

If catheterisation doesn’t work with regards to through the urethra what can be done

A

You can catheterise a patient through the anterior abdominal wall, just above the pubic symphis

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63
Q

What are the first two stages of kidney development, what is the functionality of each stage and when do they develop

A

Pronephros- no functionality
Mesonephros- limited functionality
3-4 weeks

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64
Q

What is the final stage of kidney development and when does it become functional

A

Metanephros- develops at 5 weeks but becomes functional at 12

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65
Q

When does urine production first occur and how does it work

A

It begins at the 12th week as the foetus takes on amniotic fluid, filters it through the kidney and then excretes it back into the amniotic cavity

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66
Q

What are the two definitive structures the kidney is formed from

A

The metanephric mesoderm and ureteric bud

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67
Q

When does the ureteric bud begin to branch and what does it branch into

A

6 weeks- it branches within the metanephric mass to form the major calyx, minor calyx and renal pelvis

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68
Q

What is the role of the mesonephric duct in males

A

It forms the male genital tract- it degenerates in females

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69
Q

By what stage do the kidneys need a blood supply and what is this supplied through

A

6 weeks- the transient renal vessels that are connected to the abdominal aorta

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70
Q

When do the kidneys move cranially, whilst the ureters are still attached

A

7 weeks

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71
Q

What replaces the transient renal vessels after complete kidney translocation

A

The renal vessels

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72
Q

What is renal agenesis and hypoplasia

A

When the kidneys fail to develop and grow

this can be unilateral or bilateral (fatal)

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73
Q

What is supernumerary renal vessels and what complications may arise

A

This is when the transient renal vessels don’t regress and stay attached
These may trap the ureter with the vessels which leads to hydronephrosis (a build-up of urine)

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74
Q

What is renal ectopia

A

When the kidneys fail to migrate so a kidney may remain in the pelvis or migrate to the wrong side
There also may be abnormal rotation where the hilum faces ventrally

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75
Q

What is a horseshoe kidney

A

This is when the caudal ends of the kidney migrate close together to eventually fuse

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76
Q

What is the order of structures the fluid flows through in a single nephron

A

Bowmans capsule> proximal convoluted tubule> descending limb> loop of Henle> ascending limb>distal convoluted tubule> collecting duct> minor calyx

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77
Q

How does the renal artery branch into a nephron

A

Reanl artery> interlobar arteries> interlobular arteries> afferent arteriole>glomerulus

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78
Q

How do the blood vessels link after the glomerulus

A

Glomerulus> efferent arteriole> peritubular plexus> arcuate veins

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79
Q

What are vasa recta

A

Small arteries associated with the Loop of Henle

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80
Q

What percentage of nephrons cross the cortex and medulla and what are these nephrons called

A

20%, most are cortical nephrons- juxtamedullary nephrons

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81
Q

What is the name of the tissue between glomerular capillaries and how is it adapted to its function

A

It’s called the mesangium and contains fenestrated endothelium that contains small spaces within it

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82
Q

What are podocytes

A

Cells that wrap around the mesangium and capillaries through an interlocking process

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83
Q

What layer is between the podocytes and mesangium in glomerular capillaries

A

A three layered basement membrane

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84
Q

What cells in the kidney secrete renin

A

Juxtaglomerular cells

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85
Q

What cells line the inside of the ureters and bladder and how is it adapted to it’s function

A

Urothelium- it is impenetrable to urine, even when it is stretched as it is made of stratified endothelium and contains umbrella cells on the surface

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86
Q

How is the body fluid split between intra and extracellular fluid (plasma and interstitial)

A

Intracellular fluid is about 25L~40% of body weight

Interstitial fluid is about 80% of ECF- 12L

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87
Q

What is sensible fluid loss and what are examples of it

A

Sensible is easy to meausure fluid loss such as
sweat (100ml/day)
Faeces (100ml/day)
Urine (1.5L/day)

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88
Q

What is insensible fluid loss and what are some examples

A

Hard to measure fluid loss
Evaporation from skin (300-400ml/day)
Humidification during respiration (300-400ml/day)

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89
Q

If a cells volume increases and starts to swell what regulatory response will it take to decrease volume

A

It will lose solutes such as taurine

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90
Q

If theres a decrease in water content of cells what does the cell do to counteract this

A

It tries to gain osmotically active particles such as KCl

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91
Q

How do the kidneys regulate plasma volume

e.g. if there is a decrease in blood plasma volume how would the kidneys react

A

The kidneys use stretch receptors in the body to sense this and then will release renin
This initiates the RAA system that acts to maintain Na+ balance within the body

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92
Q

How is plasma osmolality maintained by the kidneys (e.g. a decrease)

A

If there is a decrease in plasma osmolality then this is detected by osmoreceptors in the hypothalamus
This leads to the release of ADH down to the kidney byt he posterior pituitary gland and more water is reabsorbed
there is also increased vasoconstriction

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93
Q

What is isotonic dehydration

A

this is when there is an equal amount of water and solutes lost so the extracellular volume decreases but the osmolality stays the same

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94
Q

What causes isotonic dehydration

A

vomiting, diarrhoea, haemmorhage and/or burns

It may also be caused by an internal effusion

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95
Q

How do you treat isotonic dehydration

A

By replacements fluids such as an isotonic NCl solution

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96
Q

What is hypo-osmotic dehydration

A

this is when the fluid that is lost contains more NCl than water and therefore the fluid volume and osmolality decreases
because there is balancing out between intr and extracellular environments this can result in an increase in cell volume as fluid moves down its concentration gradient, into cells

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97
Q

What causes hypo-osmotic dehydration

A

Addisons disease or rare cases of vomiting

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98
Q

What is hyper-osmotic dehydration

A

This is when more water is lost than salt levels

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99
Q

What causes hyper-osmotic dehydration

A

Osmotic diuresis, increased ADH secretion, high fever, heat stroke and diarrhoea

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100
Q

How is hyperosmotic dehydration treated

A

Slow water replacement

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101
Q

How is the release of renin stimulated and when

A

It is stimulated by the sympathetic nervous system in response to a fall in plasma volume or increase in Na+ concentrations

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102
Q

Where is erythropoietin produced

A

In the kidney by the peritubular interstitium and cells of the inner cortex

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103
Q

What does erythropoietin do

A

It acts on erythrocyte cells in the bone marrow and stimulates erythrocyte production

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104
Q

What stimulates the release of erythropoietin

A

hypoxia, anaemia or renal ischaemia

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105
Q

Where is vitamin D synthesised from in the external environment and where is it hydrolysed in our body

A

It’s synthesised from the sun and is hydrolysed in our liver and then kidney

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106
Q

What is the role of vitamin D in the body

A

It’s for the mineralisation of bones and it maintains calcium and phosphate homeostasis by promoting absorption form the gut

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107
Q

What is anomalous about glomerular capillaries when compared with other capillaries (3)

A

They have a relatively constant pressure throughout them
a lot higher pressure than systemic capillaries
Also arranged in a two capillary network with peritubular capillaries

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108
Q

What does vasoconstriction of the afferent arteriole mean for glomerular blood flow and pressure

A

Reduced blood flow and pressure

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109
Q

What does vasoconstriction of the efferent arteriole mean for glomerular blood flow and pressure

A

Increased blood flow and pressure

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110
Q

What causes vasoconstriction or dilation of glomerular arterioles

A

A sympathetic response will initiate the release of renin
Hormones and autacoids such as adrenaline
Autoregulation

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111
Q

What are the macula densa cells and where are they found (3)

A

These are cells found in direct contact with the afferent and efferent arteriole
They, upon sensing a change in Na+ and Cl- concentration, release paracrines that decrease afferent arteriole diameter

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112
Q

How can you measure renal blood flow

A

Using a renal arteriography or angiography- uses injection dyes
A flow probe however can be invasive
Ultrasound- only produce 2D image so overlapping organs difficult to distinguish

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113
Q

What is the glycolax and why is it charged

A

The glycolax is the luminal surface of endothelial cells in the glomerular filtration barrier and is negatively charged in order to repel negatively charged proteins

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114
Q

What are fenestrae

A

The openings between endothelial cells that allow water and small molecules to pass through

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115
Q

Where is the glomerular basement membrane found and what is its function

A

It is in the glomerular filtration barrier and acts as a negatively charged barrier to filtration

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116
Q

What is between podocyte cells

A

filtration slits

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117
Q

What is clearance with regard to glomerular filtration

A

This is how quickly something in the blood plasma is filtered into the kidney and removed through urine

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118
Q

Why is it hard to estimate GFR

A

Very few substances meet all the criteria that are required in order to be useful at estimating GFR

119
Q

What is the gold standard substance for GFR measurements but what is its limitation

A

Inulin is a plant polysaccharide however it needs to be injected

120
Q

What natural body waste product is commonly used to estimate GFR and why is it not perfect

A

Creatinine- there is some tubular secretion of it so it tends to overestimate GFR

121
Q

How can we calculate the GFR hen given the urinary and plasma concentration of our substance and the urine volume

A

GFR= (U x V)/P

122
Q

What is the most important trait of a substance in order to measure renal blood flow

A

The substance must be completely cleared of the kidney on first pass

123
Q

What substance is a good measure of renal blood flow but by how much does it underestimate it?

A

Para-aminohippuric acid (PAH) however it underestimates it by about 10%

124
Q

What do you need to take into account when measuring renal blood flow from renal plasma flow and how is this done

A

Haematocrit- the proportion of blood that is composed of RBCs
RBF= RPF/(1-HTC)

125
Q

What are the differences between Starling’s forces across a glomerular capillary when compared with an extra-renal capillary (6)

A

The hydrostatic pressure is constant across a glomerular capillary
Glomerular capillaries are less permeable to proteins so the oncotic pressure in the Bowman’s capsule is lower than the interstitium
Plasma oncotic pressure rises along a glomerular capillary whilst it is constant normally
Hydrostatic pressure in the Bowman’s capsule is greater than the interstitium of other tissues
ultrafiltration pressure is greater in glomerular capillaries
There is a net movement out of the glomerular capillaries as the gradient is always down with regards to oncotic and hydrostatic pressure

126
Q

What is ureas role in the body and what percentage is reabsorbed by the kidney and why

A

Urea has an important role in nitrogen excretion with 50% being reabsorbed in order to maintain a good concentration gradient to reabsorb water

127
Q

What are the two size limits for GFR from uninhibited filtration to barely any

A

7kDa and under have uninhibited filtration whilst molecules over 70kDa barely filter

128
Q

what percentage of glucose is reabsorbed by the early proximal convoluted tubule and by what transporters

A

98% by GLUT2 and SGLT2 transporters

129
Q

Where is the final 2% of glucose reabsorbed

A

The late proximal convoluted tubule

130
Q

How does the kidney assist in a compensatory mechanism to metabolic acidosis

A

It produces ammonium that is excreted in the urine in order to facilitate the excretion of acid and bicarbonate to counter the acidosis effect

131
Q

hat percentage of glucose production does renal gluconeogensis account for

A

20-25%

132
Q

What is Tm or transport maximum- in the kidney

A

This is the point at which an increased concentration of a substance does not result in increased movement of that substance- this is the point no more is absorbed or secreted in the kidney due to transport channels being saturated

133
Q

Why does diabetes mellitus produce glucose in the urine

A

The Tm of glucose is reached as there is high plasma glucose concentration so no more is absorbed and it is excreted in the urine

134
Q

What is the role of secretion in the kidney (3)

A

It acts to eliminate exogenous solutes such as drugs and toxins, metabolic byproducts and delivers autacoids and drugs to distal nephron

135
Q

What is plasma threshold with regards to renal function

A

Plasma threshold is the concentration of a substance in the plasma required in order for that substance to not be reabsorbed anymore

136
Q

hat can lead to the overriding of renal blood flow autoreglation and why

A

Shock, trauma, haemorrhage and extreme exercise

This results in greater efferent arteriole constriction in order to preserve BP

137
Q

What is nephritic syndrome

A

This is an inflammatory response in the kidney that increases the permeability of the filtration membrane which can lead to proteinuria, haematuria and hypertension

138
Q

What is nephrotic syndrome and how is it different to nephritic syndrome

A

This also increases permeability of the filtration membrane however it doesnt lead to haematuria- nor does it affect renal function

139
Q

What is a positive Na+ balance and when would this happen

A

when you are taking on more Na+ than is being excreted- this occurs when there is a sudden dietary or IV influx of Na+ and resultantly more Na+ will be excreted as the ECF volume signals this

140
Q

What does aldosterone do in response to a decrease in ECF

A

It acts in the kidney to increase the activity of ENaC and the number of Na/K pumps in principal cells (the cells in the collecting duct and distal tubule epithelium)
This increases Na+ and thus water reabsorption but results in increased K+ and H+ secretion

141
Q

How does an increase in AGII result in a decrease in BP

A

It acts as a vasoconstrictor but also stimulates ADH secretion to increase DCT permeability

142
Q

Where is aldosterone produced in the adrenal gland and what receptors does it act on

A

The zona glomerulosa- mineralocorticoid receptors

143
Q

How does AGII effect the afferent and efferent arterioles (3)

A

It constricts them both however the efferent slightly more in order to decrease Starling’s forces by decreasing HP
It increases oncotic pressure so more Na+ is reabsorbed

144
Q

What happens if you decrease vasa recta blood flow

A

This decreases solute washout and less urea is moved away from the Loop of Henle
Therefore there is a higher concentration gradient for NaCl reabsorption

145
Q

What are the two different mechanisms of GFR control mechanisms and when are they utilised

A

Spontaneous GFR control prevents effects from postural changes in blood pressure
Compensatory GFR changes modulate GFRs to combat excess in dietary sodium intake

146
Q

How does atrial natriuretic peptide affect the renal system

A

It suppresses the sympathetic nervous system
This dilates the afferent arteriole
This increases GFR
Inhibits renin
Increases vasa recta blood flow to decrease Na reabsorption

147
Q

What is the oncotic pressure like in the efferent arteriole and peritubular capillaries in comparison to the filtrate and intersitium

A

Much Higher

148
Q

What cells are on the inner lumen of the PCT

A

Brush boarder cells

149
Q

How are brush boarder cells adapted for their function

A

They have microvilli on their apical surface

150
Q

What channels is water reabsorbed through

A

Aquaporin AQP1 channels

151
Q

What is the process of a substance moving up it’s concentration through the assistance of another substance acting as a power generator by moving down its concentration gradient

A

Secondary active transport

152
Q

Where is secondary active transport seen in the PCT

A

Through the movement of Na and many other substances acting as the secondary molecule

153
Q

How is a low Na concentration maintained in the brush boarder cells

A

There are many Na/K pumps that pump Na out of these cells , into the interstitium and thus capillaries

154
Q

What is paracellular transport

A

The movement of molecules between the leaky junctions of cells

155
Q

What results in paracellular backflow of Na into the early PCT

A

There is a net negative charge as Na moves out due to the high concentration of Cl- ions in the PCT- not many are absorbed at these times- and thus Na+ flows back into the lumen

156
Q

Why is there no paracellular backflow in the late PCT

A

Chloride ions are also absorbed alongside Na+ ions at this stage so there is no charge imbalance pulling them back

157
Q

What do free H+ ions form with after being exchanged with Na+ in the brush boarder cells

A

They form Carbonic acid, H2CO3 with HCO3-

158
Q

What reaction does carbonic acid catalyse and where

A

It catalyses the breakdown of H2CO3 in the apical border to H2O and CO2 so these products can move freely across the apical surface into the brush boarder cells

159
Q

What carbonic anhydrase substrate reforms H2O and CO2 into H2CO3 in the brush boarder cells

A

Carbonic anhydrase type 2

160
Q

Through what route is the HCO3- absorbed into the peritubular capillaries

A

Through the Na=/HCO3- cotransporter

161
Q

What is osmolarity

A

The concentration of solute particles

162
Q

What is the coritco-papillary gradient

A

The increase in osmolarity as you go from the cortex to the papilla- down the Loop of Henle

163
Q

What is water reabsorption dependent on in the DCT

A

ADH levels

164
Q

What is the descending limbs permeability to water and ions respectively

A

It contains AQP1 channels and has a lo permeability to ions

165
Q

What is the ascending limbs permeability to water and ions respectively

A

It is impermeable to water and has a high permeability to ions with an Na/K ATPase pump

166
Q

At which point of the descending limb is the water movement out by osmosis at its highest and why

A

At the base of it as the interstitium gets increasingly salty and osmolar so more water moves out due to the increase in concentration gradient

167
Q

How does Na+ move out of the thin ascending limb

A

Through passive diffusion

168
Q

How does Na+ move out in the thick ascending limb and why does water not follow it

A

It is actively pumped out by the many Na/K ATPase pumps

Water doesn’t follow it as there are no aquaporins to channel through

169
Q

What is the trend of osmolarity of the filtrate as you go up the ascending limb

A

It becomes increasingly dilute as ions are moving out and water cannot follow

170
Q

How do chloride ions move out of the thin ascending limb

A

Passively through chloride channels

171
Q

How do we transport K and Cl back into the thick ascending limb lumen in order to create concentrated urine

A

Through Na/K/2Cl transporter as Na+ moves down its concentration gradient into the lumen and transports the other two by secondary active transport
This concentration gradient is maintained by the Na/K ATPase pumps pumping Na out of the lumen

172
Q

Is the vasa recta permeable to solutes and water?

A

Yes

173
Q

How does the vasa recta maintain the hyperosmotic interstitial gradient set up

A

As it bypasses the ascending limb it releases water down its concentration gradient and into the interstitium whilst salt is reabsorbed down its concentration gradient into the vasa recta
When it bypasses the descending limb it reabsorbs water but gives out salt to maintain the gradient and continue with the Loop of Henle

174
Q

What is the permeability of the DCT and collecting duct changed by

A

The activation of ADH

175
Q

As the filtrate moves down the descending Loop of Henle, what direction does the net movement of urea go in

A

More goes into the Loop as you go down as there is a higher concentration of urea in the interstitium, the further you go down towards to papillary

176
Q

Is the ascending Loop permeable to urea and how does this help

A

No- this means there is a high concentration of urea in the DCT to increase the osmolarity of the filtrate and this results in more water moving out

177
Q

Ho does ADH assist the movement of urea

A

It implants a urea transporter in the late collecting duct so urea moves out into the interstitium so it can be recycled back and maintain a cortico-papillary gradient

178
Q

How does Na move out of the early DCT

A

There are Na/Cl cotransporters that allow Na to move down its concentration gradient and transport Cl- via secondary active transport

179
Q

How is Na+ reabsorbed in the late DCT and collecting duct

A

Through ENaC channels

180
Q

What are osmoreceptors and what do they do

A

These are specialised cells found in the anterior hypothalamus that sense the osmolarity of extracellular fluid through AQP4 channels in their apical surface

181
Q

How do the osmoreceptors respond to an increased osmolarity in the bloodstream

A

If there is an increased osmolarity water will move out of the osmoreceptors, through the APQ4 channels
this will cause them to shrink and in turn release action potentials that trigger the ‘thirst response’

182
Q

What does the thirst response do

A

It activates the posterior pituitary gland to release ADH and retain water from the kidney

183
Q

How do the juxtaglomerular cells initiate a thirst response

A

They detect a low blood volume and secrete renin to initiate the RAAS
AGII converges on the hypothalamus to trigger a thirst response

184
Q

What channels does ADH indirectly promote the binding of after a signaling cascade

A

AQP2 channels after ADH binds to V2 receptors on the basolateral membrane of principal cells

185
Q

What is hyponatremia and at what value is it considered

A

This is a deficiency of sodium and is at <135mM

186
Q

What is hypernatremia and at what value is it considered

A

An excess of sodium >145mM

187
Q

What are the major causes of hyponatremia (3)

A

A net loss of Na (hypoaldostrenism, thiazides, bodily functions)
Disturbances of water input (voluntary or mental illness water intoxication)
Disturbances of water output (increased ADH secretion)

188
Q

What are the causes of hypernatremia

A

A net gain of Na (dietary, Iv, hyperaldostrenism)
Disturbances of H2O input (unconscious patient, lack of water access, voimiting)
Disturbances of H2O output (increased insensible losses, vomiting, diarrhoea)
Diabetes insipidus results in non functional ADH that means excessive water loss

189
Q

What is neurogenic diabetes insipidus

A

The failure of ADH secretion as a result of a lesion in the hypothalamus or posterior pituitary gland and is treated with synthetic ADH

190
Q

What is nephrogenic diabetes insipidus

A

the failure of the principal cells to respond to ADH caused by a V2 receptor mutation

191
Q

What do thiazides inhibit

A

The Na/Cl cotransporter in the DCT

192
Q

How do Loop diuretics work

A

They work on th eLoop of Henle by inhibiting the Na/K/2Cl cotransporter in the thick ascending loop

193
Q

How do aldosterone antagonists work

A

They don’t allow aldosterone to bind with its mineralocorticoid receptors so it cannot translocate to the nucleus and transcribe the ENaC channels
It also inhibits the generation of K channels so less K is excreted out and the Na/K channels work less effectively

194
Q

What is specific about potassium sparing diuretics

A

They antagonise the ENaC channels in the principal cells of the late collecting duct as well
This spares K from being transported into the urine because the function of Na/K pumps is greatly reduced

195
Q

How does inhibiting the RAAS help to retain sodium

A

Decrease in ADH to release dilute urine
Reduced Na reabsorption in the PCT and Loop of Henle (increased vasa recta washout so decreased gradient)
There’s decreased sympathetic activity so more arteriole dilation and more Na in filtrate
Decreased binding of Na/H exchanger in PCT

196
Q

What is the normal body pH

A

7.4

197
Q

Why is a constant pH important

A

To maintain enzymes, receptors and transporters

198
Q

What is the main reaction in the bicarbonate buffer system to neutralise protons

A

HCO3- + H+ —> H2CO3

199
Q

What does H2CO3 dissociate into and what catalyses this reaction

A

It dissociates into H2O and CO2 by the enzyme carbonic anhydrase

200
Q

How do protons react with phosphate

A

2H+ + PO4(2-) –> H2PO4

201
Q

What do protons and proteins form as part of our internal buffer system

A

Protonated proteins

202
Q

How does haemoglobin combine with protons as part of our internal buffer system

A

It forms haemoglobinic acid

203
Q

What is the biggest contributor to a potentially acidic pH in our blood and how is this combated

A

The partial pressure of CO2

It is combated by the bicarbonate system

204
Q

How can we calculate the pH of the blood using CO2 partial pressure and HCO3- concentration

A

Pk’ (6.1) +log( {HCO3-}/{dissolved CO2}

205
Q

Why re endogenous acids dangerous

A

They are not contributed by CO2 and thus cannot be lost through the lungs

206
Q

Ho do we normally lose alkali substances

A

Through stools from the GI tract

207
Q

What is the rapid response due to a decrease in pH and what takes longer out of the respiratory and renal methods

A

The respiratory is a rapid response whilst the renal response is a lot slower

208
Q

What is the main outcome of the renal response to acidosis with regards to the movements of molecules

A

The kidney removes protons and increases the reabsorption of HCO3-

209
Q

What main pump releases protons into the tubular lumen

A

The Na/H pump

210
Q

What stimulates an increase in HCO3- reabsorption and by what channels are they reabsorbed

A

A decrease in cell Ph

HCO3- reabsorbed by Na/3HCO3 or Cl/HCO3 pump

211
Q

Where do the kidneys generate bicarbonate ions and how does this occur (3)

A

The kidneys generate bicarbonate ions in the PCT
This can occur through gluconeogensis, triggered by the excretion of ammonium salts as bicarbonates are a biproduct of this process
it may also occur through activation of the phosphate buffer system as bicarbonates are generated as acid is removed

212
Q

Where are alpha intercalated cells found and what is their function

A

These are found in the collecting duct and they generate a small amount of HCO3- in response to a low pH

213
Q

Where are alpha intercalated cells found and what is their function

A

These are in the collecting duct and they respond to a high pH by secreting bicarbonate into the lumen to extrude H+ into the ECF

214
Q

What is respiratory acidosis and what causes it

A

This is when the retention of CO2 occurs and is usually down to respiratory problems such as hyperventilating or lung disease
It results in a decrease of Ph and increase of p.p of CO2

215
Q

How does the body compensate respiratory acidosis

A

it signals the kidney to retain HCO3- and shift the equilibrium of the bicarbonate dissociation equation back to the middle, increasing pH

216
Q

What is respiratory alkalosis and what causes it

A

This is an excessive loss of CO2 generally caused by hyperventilation
This decreases the p.p. of CO2 and the carbonic acid equation shifts to the left to accommodate this, increasing pH

217
Q

What is the compensatory response to respiratory alkalosis

A

there is a net loss of bicarbonate by the kidney in order to return to a normal pH and shift equilibrium of the carbonic acid equation back to the right

218
Q

What is the carbonic acid equilibrium

A

CO2 +H2O H2CO3 H+ + HCO3-

219
Q

What is metabolic acidosis and how is it caused

A

It increases the H+ concentration in the body and is caused by diabetes, heart failure, renal failure and diarrhoea
It shifts the equilibrium of the carbonic acid equation to the left

220
Q

What is the compensatory response to metabolic acidosis

A

The lungs blow off more CO2 to decrease p.p. of CO2 and shift the carbonic acid equilibrium to the left to decrease {H+}

221
Q

What is metabolic alkalosis and what causes it

A

It’s a net loss of H+ caused by things such as vomiting

This raises pH as the equilibrium is shifted to the right

222
Q

What compensatory response occurs in reaction to metabolic alkalosis

A

The lungs blow off less CO2 by hypoventilation

223
Q

What is the role of potassium in the body (6)

A

Regulating cell volume
Regulating intracellular pH
Synthesising DNA and proteins for growth
Cellular enzyme function
Maintaining a resting membrane potential
Cardiac and neuromuscular activities and BP

224
Q

What body function problems can arise during hypokalaemia (<4mM)

A

Cells become more negative and less sensitive to depolarisation
muscle weakness can lead to paralysis
Abnormal neural conduction leads to confusion and eventually comas
Increased cardiac excitability

225
Q

What problems can arise due to hyperkalaemia (>5mM)

A

Cardiac arrhythmia and risk of cardiac arrest

Abnormal neural conduct

226
Q

What are major sources of K+ in the diet

A

Meat, fruit and fruit juice

227
Q

What occurs to potassium as soon as it is ingested

A

It is distributed around cells in the body and then sloly let out into the ECF until the next meal

228
Q

What is the uptake of potassium stimulated by

A

Insulin and adrenaline and aldosterone

229
Q

How does a build up of plasma protons result in hyperkalaemia

A

When there is an excess of protons in the plasma they are absorbed into cell through a K/H pump so a build up of K+ can occur in the bloodstream as these are exchanged

230
Q

How is K+ reabsorption controlled by the kidney

A

If a person has a high K+ diet less K+ is reabsorbed in the DCT and collecting duct and some may even be secreted into the DCT and collecting duct

231
Q

How is K+ reabsorbed into the late proximal tubule

A

The K+ is reabsorbed paracellularly as the lumen is positive so it is driven by a potential difference

232
Q

How is K+ reabsorbed in the thick ascending Loop of Henle

A

The Na/K/2CL cotransporter

233
Q

How do the principal cells drive increased K+ secretion due to an excess in the blood plasma

A

They contain many Na/K ATPase pumps and as a result reabsorb more Na in exchange for K
This is stimulated aldosterone that is released independently of the RAAS

234
Q

What bodily state increases K+ secretion- alkalosis or acidosis and why

A

Alkalosis as it increases Na/K pump activity and increases the number of K+ channels

235
Q

What are the main symptoms of UTIs (7)

A 
Change in urinary frequency
Dysuria (painful urination)
Passing of only small amounts of urine
Haematuria
Pyuria (foul smelling or cloudy urine)
Urgency
Urinary incontinence
236
Q

What symptoms of UTIs are specific to upper UTIs (kidneys) (3)

A

Upper back and flank pain
Shaking and chills
High fever

237
Q

What are severe symptoms of UTIs

A

Rigors (feeling weak dizzy and uneasy)
Pyrexia (high temp.)
Nausea and vomiting
Acute confusional state

238
Q

What is bacteriuria

A

Bacteria being present in the urine

239
Q

What is a relapse with regards to bacteriuria

A

This is when a patient becomes reinfected with the same bacterium they were infected with before

240
Q

What is urethritis

A

Infection of the urethra

241
Q

What is cystitis

A

Infection of the bladder

242
Q

What is pyelonephritis

A

Infection of the kidney

243
Q

What is the trend of UTI frequency with increasing age

A

As age increases so does the frequency of UTIs

244
Q

What are the main risk factors to contracting a UTI

A 
Female gender
Increasing age
Recent antibiotic use
Recent sexual activity 
New sexual partner
Diabetes
Presence of catheter
Pregnancy
245
Q

What are uncomplicated UTIs

A

These are infections in a structurally and neurologically normal urinary tract and persistent infection can lead to kidney problems

246
Q

What are complicated UTIs

A 
infections of the urinary tract with abnormalities such as 
Diabetes 
Kidney stones
Blockages
Developmental abnormalities
247
Q

What are the three conditions for a bacteria to cause a UTI

A

Get into the urinary tract
Adhere to the epithelial surface
Multiply and elicit an inflammatory response

248
Q

What are the two routes for a bacteria to enter the urinary tract

A

The ascending route as the bacteria ascend the UT by bowel flora
The haematogenous route is by blood borne bacteria and is mainly due to infection of the renal parenchyma

249
Q

What is the main causative organism in UTIs

A

UPEC- uro-pathogen E.coli

250
Q

Why can catheters lead to increased risk of UTIs

A

in catheters the urine is not washed away properly by the flow of excreting urine and this gives a chance for bacteria to colonise and develop

251
Q

What lab tests can be run to clinically diagnose UTIs

A

Urine microscopy can show leukocytes which indicate the presence of infection
Dipstick analysis of urine
Urine culture

252
Q

What drugs can be used to treat a lower UTI

A

Trimethoprim or Nitrofurantoin

253
Q

with which drugs can you treat pyelonephritis

A

Cefalexin

254
Q

What is microscopic haematuria

A

When blood is present in the urine but not enough to be visible to the naked eye

255
Q

What is proteinuria

A

When there is protein in the urine

256
Q

What is glycosuria

A

When there is glucose in the urine

257
Q

What enzyme tests for the presence of leukocytes

A

leukocyte esterase

258
Q

What does increased leukocytes in the urine suggest

A

infection in the kidneys or urinary tracts

259
Q

What does a positive nitrites result in the urine suggest

A

it may indicate a UTI as gram negative bacteria converts to nitrites in the bladder

260
Q

What does increased urobilinogen suggest

A

Liver cell damage or increased bilirubin excretion to intestines

261
Q

What does protein in the urine suggest

A

Kidney disease

262
Q

What does acidic urine suggest

A

kidney disease or diet

263
Q

What does blood in the urine suggest

A

Infection or disease in the kidney or bladder

264
Q

What does increased ketones suggest

A

Diabetes, low carb diet or starvation

265
Q

What does increased bilirubin concentration suggest

A

liver damage

266
Q

What does glucose in the urine suggest

A

Diabetes mellitus

267
Q

What factors increase the likelihood of an individual having a kidney stone

A 
Structural abnormalities affecting urine flow (e.g. horseshoe kidney)
Loop Diuretics 
Relative dehydration 
Diet high in purines 
Hypercalcaemia 
Metabolic disorders
increasing oxalate levels 
consequence of necrosis following AKI
History of renal calculi or recurrence
268
Q

How can hyperparathyroidism lead to hypercalcaemia

A

hyperparathyroidism results in an increase in parathyroid gland and this increases bone reabsorption which releases calcium

269
Q

What does cystinuria cause an excess of to be released into the urine

A

Amino acids

270
Q

What is the most common type of kidney stone

A

Calcium oxalate stones- approximately 60% of stones

271
Q

What are the main symptoms of kidney stones

A 
loin to groin pain 
sweating
nausea
vomiting 
dysuria 
haematuria
272
Q

Where will stones high up in the kidney cause pain

A

In the flank

273
Q

What is the character of the loin to groin pain caused by lower down kidney stones

A

It has spasms of sharp pain due to dilation of the ureter and small periods of relief but a persistent dull ache

274
Q

What investigations should take place upon the potential for a kidney stone

A

An x-ray as 90% of kidney stones are opaque however the gold standard is CT-KUB (kidney ureter bladder)
Ultrasound is used when radiation should be avoided

275
Q

When should you consider hospital admissions upon the presence of kidney stones

A 
Fever
Solitary kidney function 
Inadequate pain or persistent pain 
Inability to take adequate fluids
Anuria 
Pregnancy
276
Q

What drugs can be used to reduce ureteric spasm and help stones pass

A

Alpha blockers and calcium channel blockers

277
Q

What technique can be used to break down stones into smaller crystals so they can pass

A

Extracorporeal shockwave therapy

278
Q

What is ureteroscopy

A

This is the insertion of a ureterscope into the ureter via the external meatus to the stone under general anesthesia

279
Q

What is percutaneous nephrolithotomy

A

This is the use of keyhole access through the skin in the flank directly into the kidney under anaesthesia

280
Q

What is a case control study

A

This is when exposure and outcome have already occurred
It proceeds backwards form effect to cause
It uses a control group to compare

281
Q

What is a cohort study

A

two or more groups are selected on the basis of their differences of exposure to a particular agent
these groups are then followed
this can be used to study incidence, causation and prognosis

282
Q

What is a cross-sectional study

A

Looks at data on a population at a specific point in time to provide a snapshot
it’s observational so you can’t draw cause and effect conclusions from it
these are inexpensive and fast studies that provide a basis for further research

283
Q

What are randomised control trials

A

Aim to compare doses or treatments on two or more groups

The participants are randomly assigned to groups and then these groups are followed up and analysed over time

284
Q

What are systematic reviews

A

Overviews of primary literature that focus on a research question

285
Q

What is meta analysis

A

This is presenting a balanced summary of all existing research
this is to be done on a quantitative basis

286
Q

What is fabrication

A

The making up or manipulation of data

287
Q

What is improper analysis

A

using the wrong statistical test

288
Q

What is selective reporting

A

This is only including the data that supports the hypothesis the author is after

289
Q

What is epidemiology

A

The study of how often diseases occur in different groups of people and why

290
Q

What is absolute risk

A

The risk of a patient developing a condition over a given period of time

291
Q

What is relative risk

A

This is the comparison of two groups of people and how likely they are to develop a disease

292
Q

What is the odds ratio

A

The association between an exposure and an outcome

293
Q

What is attributable risk

A

A measure of the proportion of the disease occurrence that can be attributed to a certain exposure

Year 1 Medicine Newcastle (8 decks)

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