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year 1 flash cards > renal strand > Flashcards

renal strand Flashcards

1
Q

what are 3 functions of the kidneys

A
  • remove toxins, excess water and waste products
  • vital role in BP
  • activate vitamin D
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2
Q

what things put individuals at risk of chronic kidney disease/CKD

A
  • diabetes
  • high BP
  • heart and circulatory disease
  • family history of CKD
  • black/ asian minority
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3
Q

what is a nephron

A

a filtering unit

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4
Q

what is the outer area of the kidney called

A

the cortex

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5
Q

what is the middle region of the kidney called

A

the medulla

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6
Q

what is the blood supply to the kidney

A

renal vein and renal artery

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7
Q

where do we usually get collection of stones in the kidney

A

ureter - causing narrowing

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8
Q

list the journey the blood would take as it enters the kidney via the renal artery and leave via the renal vein

A

renal artery –> afferent arteriole –> bowman capsule –> glomerulus –> efferent arteriole —> peritubular capillaries —> vasa recta –> renal vien

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9
Q

where is the fluid leaked out of the blood supply and into the filtration system in the nephrons ? what blood vessles are involved here

A

fluid leaked out when the blood enters the glomerus into the bowmans space of the bowmen capsule
via the fenestrated capillaries and the basement membrane

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10
Q

highlight the steps the flitrate flows through in the kidneys

A

bowmans capsule –> bowmans space –> proximal tubule –> ascending loop of Henle –> descending loop of Henle –> distal tubule –> collecting duct

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11
Q

how are the nephrons arranged in the kidney

A

placed horizontally end to end

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12
Q

what are the 2 broad functions of the kidney

A
  • homeostasis (maintenance of internal environment)

- hormone secretion (endocrine function)

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13
Q

how does the kidney maintain fluid and electrolyte balance ? what electrolytes does it control the levels of

A

maintains

  • volume status : regulates the fluid balance through urine
  • electrolyte levels: Na+, K+, Urea and creatinine
  • osmolarity (conc of particles excepting an osmotic pressure)
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14
Q

how does the kidney regulate the acid base balance

A

maintains the optmimum pH for cellular function through bicarbonate regeneration in the proximal tubule

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15
Q

what small molecules does the kidney reabsorb

A

sugars and AA

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16
Q

what does the presence of sugars in the urine indicate

A

diabetes

tubular disorders

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17
Q

what does the presence of AA in the urine indicate

A

disease of the primal tubule

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18
Q

what does the kidney excrete

A

waste products

drugs

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19
Q

what are waste products produced by the kidney

A

nitrogenous waste products from protein metabolism:

urea and creatinine

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20
Q

what is creatine related from? why are its levels measured in the blood

A

muscle

used to measure kidney function

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21
Q

what kind of drugs can accumulate in the kidneys in kidney disease

A
  • antibiotics (eg. penicilin)
  • digoxin
  • opiates
  • lithium
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22
Q

how does the kidney stimulate RBC production / erythropoiesis ? what do patients with kidney disease develop

A

release erythropoietin which stimulates production off RBC

patients with kidney disease develop anaemia

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23
Q

what stimulates the production of RBC in the kidneys

A

hypoxia

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24
Q

why do athletes train at high altitudes

A

because hypoxia stimulates the release of

erythropoietin in the kidneys and so stimulates RBC production

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25
Q

what does the kidney release in order to maintain calcium phosphate balance

A

activated from of vitamin D

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26
Q

what is the activated form of vitamin D called

A

1,25 dihydroxy cholecalciferol

form calciterol

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27
Q

where does the first and second stage of hydroxylation of vit D happen

A

first stage happened on the liver

second stage happens in the kidneys

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28
Q

where do calcium and phosphate get absorbed and excreted

A

absorbed form the gut/small intestine and excreted by the kidneys

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29
Q

what does calciterol induce

A

increases the absorption of calcium and phosphorus in the gut and the release of calcium and phosphorus in the bone

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30
Q

what gland detects low calcium levels and how does it respond

A

parathyroid gland detects low calcium levels and responds by releaseing PTH/ parathyroid hormone

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31
Q

what can low levels of calciterol cause

A

bone disease

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32
Q

in chronic kidney disease there is a decreased

A
  • activation of vit D

- level of calcium

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33
Q

levels of which hormone is increased in CKD? what can this lead to and why is this dangerous?

A

levels of parathyroid hormone increase

can lead to secondary hyperparathyroidism= increases release of calcium from bone = bone disease

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34
Q

what disease is associated with CKD and why

A

renal osteodystrophy - increased risk of fractures and anemia due to fibrosis of the bone

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35
Q

how does the kidney control BP

A

through renin secretion

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36
Q

do patents with CKD have high or low BP

A

often have high BP due to damage of kidney (angiotensin 2 released due to low blood flow through kidney)

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37
Q

what blood test investigations do we do in someone with CKD

A
  • urea and electrolytes
  • bicarbonate
  • chloride
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38
Q

what do you test for in a urea and electrolyte test

A
  • Na
  • K
  • urea
  • creatine
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39
Q

what is the normal range for Na levels in a urea and electrolyte test

A

133-146 mol/L

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40
Q

what is the normal range for K levels in a urea and electrolyte test

A

3.5-5.3 mmol/L

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41
Q

what is the normal range for urea levels in a urea and electrolyte test

A

2.3-7.5 mmol/L

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42
Q

what is the normal range for creatine levels in a urea and electrolyte test - remember this varies in males and females

A

male: 64-104 mol/L
female: 60-93 mol/L

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43
Q

why are normal levels for creatine lower in females than males

A

because males have an increased muscle mass in comparison to females

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44
Q

what is the normal range for bicarbonate in a blood test

A

22-29 mmol/L

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45
Q

what is the normal range for chloride in a blood test

A

95-108 mmol/L

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46
Q

what does a failure in bicarbonate regeneration of the kidneys lead to

A

decreased bicarbonate can lead to the patient becoming acidemic which effects cellular function

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47
Q

what can increased levels of urea in CKD lead to

A

pericarditis (inflammation of heart)
seizures
confusion

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48
Q

what do we check for in a urinalysis (urine test, the test strip ones )? what does their presence suggest?

A 
pH 
haematuria - not normal
proteinuria - not normal
Glucose - diabetes 
Nitrates - infection
Leucocytes - infection
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49
Q

what is specific gravity a measure of

A

whether someone can conc their urine

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50
Q

what do we see in a urinalysis of someone with a UTI

A
  • Blood trace
  • nitrogen postive
  • leukocyte positive
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51
Q

what do we see in a urinalysis of someone with a glomeritus (inflammation of the kidney)

A
  • blood

- protein

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52
Q

what do we check for in an actual 2ml urine sample (ie. not the strip/urinalysis)

A
  • protein/creatinine ratio
  • albumin/creatine ratio
  • midstream urine
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53
Q

what are normal levels for protein/creatine ratio

A

<13.0 mg/mmoL

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54
Q

what are normal levels for albumin/creatine ratio

A

<3.0 mg/mmoL

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55
Q

what is midstream urine

A

clean catch of urine - sent if suspected UTI

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56
Q

what do we check in an ultrasound of the kidney

A
  • check the size of the kidney (small kidneys indicate CKD- scarred)
  • any obstruction in the kidney
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57
Q

why would we perform a kidney biopsy

A

to diagnose some forms of kidney disease - guided by ultrasound

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58
Q

what are the complications of performing a kidney biopsy

A

risk of bleeding (1 in 100)

risk of losing a kidney (1 in 1000)

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59
Q

what would we observe in a histological biopsy of someone with focal segmental glomeruloscelerosis (a diseased kidney)

A
  • diseased glomerluous recognised by deposition of fibrotic material in the glomerulus
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60
Q

what does the glomerular filtration rate measure

A

how much blood your kidneys filter per min

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61
Q

what is the normal glomerular filtration rate

A

100-120 mls/min

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62
Q

why is it hard to get an accurate measure of glomerular filtration rate

A

time consuming and requires the injection of a radioactive catheter

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63
Q

what is creatine clearance

A

an estimation of globular filtration rate

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64
Q

which is more accurate, creatine Clarence or glomerular filtration rate

A

glomerular filtration rate is more accurate than creatine clearance

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65
Q

how do you obtain the measure for creatine clearance

A

a blood test and 24 hour urine collection

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66
Q

what is creatine released by

A

muscle

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67
Q

what is creatine filtered and removed by

A

the kidneys - additional removal of creatinine is by secretion into the filtrate by the proximal tubule of the kidneys

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68
Q

what are the normal ranges for male and female serum creatine levels

A

64-104 mol/l - male

60-93 mol/L - female

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69
Q

when do serum creatine levels increase

A

kidney disease

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70
Q

in what case do we get a delay in rise of serum creatine levels

A

following acute kidney injury

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71
Q

is serum creatine specific or non specific

A

not specific for the site of injury

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72
Q

what is the estimated glomerular filtration rate measured by - eGFR

A

Automatically calculated by laboroties

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73
Q

what variables are used to calculate eGFR

A
  • age of patient (kidney function declines with age)
  • sex of patient (males have higher average muscle mass)
  • serum creatinine
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74
Q

what is a correction factor which is used in the calculation of eGFR? in who and why do we use it

A

used for increased muscle mass based on race

a correction factor of x1.2 for black people is used based on average increased muscle mass

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75
Q

what does eGFR estimate

A

the % kidney function - which is useful when discussing with patients

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76
Q

does eGFR decrease with age

A

yes - goes to about 90 in 40-59 its and about 75 in older than 75

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77
Q

at what level of eGFR will patients need to carry out dialysis

A

<10 mls/min/1.73m2

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78
Q

at what level of creatine is 50% of kidney function lost

A

by the time the creatine level rises above 104 mol/L in male

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79
Q

what is the function of the convoluted tubule

A

recovers 70% of glomerular filtrate

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80
Q

what kind of things are recovered by the proximal convoluted tubule

A
  • water - by aquaporins
  • electrolytes
  • glucose
  • AA
  • and recovery and re-generation of bicarbonate (to maintain acid-base balance)
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81
Q

what enzyme is the regernation of bicarbonate dependent on in the proximal convoluted tubule

A

carbonic anhydrase - combines CO2 and H20 to form H2CO3 and into HCO3-

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82
Q

what drug inhibits the action of carbonic anhydrase ? what is this drug used for

A

acetazolamide - used in altitude sickness : hypoxia, hyperventilation, respiratory alkalosis

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83
Q

what are the 2 types of kidney disease we can have

A

acute and chronic

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84
Q

how is the function of the proximal convoluted tubule effected by kidney disease

A

failure to regenerate bicarb can lead to academia (metabolic)

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85
Q

what happens in the ascending limb oh Henle

A

uptake of:

  • Na+
  • K+
  • 2CL-
  • H20
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86
Q

on what part of the nephron and how do the loop diuretics work?

A

work of the ascending limb of Henle
act to remove the fluid form the patient but inhibiting co-transporter uptake which results in the loss of electrolytes and water

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87
Q

what kind of patents receive loop diuretics

A
  • heart failure
  • CKD
  • nephrotic syndrome
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88
Q

what happens in the cortical collecting duct

A

site of reabsorption of Na+ (with water and Cl) in exchange for K+

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89
Q

what hormone controls the reabsorption in the collecting duct

A

aldosterone

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90
Q

how is the action of the cortical collecting duct inhibited

A

by spironolactone - diuretic

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91
Q

what can problems in the cortical collecting duct lead to

A

heart failure
acscites
so use dirurectics (spironolactone) to treat

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92
Q

what part of the nephron is in the medulla of the kidney

A

loop of hence and medullary collecting duct

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93
Q

what happens in the medullary collecting duct

A

site of urinary conc

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94
Q

what hormone controls the action of the medullary collecting duct

A

ADH - increases water reabsorption through aquaporins

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95
Q

why would we get an increased secretion in the medullary collecting duct

A

due to fluid loss through:

  • haemorrahage
  • burns
  • vommitng and diarrhoea
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96
Q

what is osmolality

A

number of particles of solute per kg of convent

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97
Q

what is molecules effect osmolality

A

Na
urea
glucose

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98
Q

how is osmolality calculated

A

(2 x Na+) + glucose + urea

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99
Q

what is plasma osmolaty normally maintained at

A

275-290 mOsm/Kg

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100
Q

what does rising osmolity trigger

A

thist

ADH secretion

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101
Q

what is the normal range for urine osmolality

A

500-850 mOsm/Kg

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102
Q

what is the normal daily output of urine

A

1.5-2 L

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103
Q

why do the kidneys concentrate urine at times of decreased fluid uptake

A

to conserve salt and water

to maintain circulating volume and BP

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104
Q

what does the counter current mechanism refer to

A

establishing a high conc gradient in the medulla

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105
Q

what does the counter current mehcnsim allow fro

A

eagles reabsorption of water from filtrate in the proximal tubule and collecting duct

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106
Q

in states of fluid loss how is the haemodynamic stability maintained though hormones? what do they do

A
  • increased secretion of ADH = inserts more aquaporins into collecting duct = more absorption of water = conc urine with high osmolity
  • renin : increase Na reabsorption and vasoconstriction
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107
Q

what does insensible loss refer to

A
  • sweating
  • faeces
  • respiration
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108
Q

what is the best measure of fluid balance

A

taking a daily weight

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109
Q

What does the paraxial mesoderm go on to form?

A

The majority of the skeletal muscles, skeleton and dermis of the skin

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110
Q

What does the intermediate mesoderm go on to form?

A

The gonads, internal reproductive tract and kidneys

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111
Q

What does the lateral plate mesoderm go on to form?

A

The lining of the body cavities

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112
Q

When does kidney development begin?

A

Week 4

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113
Q

What are the three nephric structures?

A
  • pronephros
  • mesonephros
  • metanephros
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114
Q

What is the pronephros?

A

Nephric structure denied from mesoderm in central region. This is a rudimental structure with no function and regresses.

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115
Q

What is the mesonephros?

A

A nephric structure in the lumbar region. It has a short period of function, but is remodelled and regresses.

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116
Q

What is the metanephros?

A

Forms the derivative kidney

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117
Q

Describe the formation of the pronephros

A

Occurs in the 4th week of development

  • non-functional
  • intermediate mesoderm in the cervical region condenses and reorganises
  • forms a number of epithelial buds
  • regresses around day 25
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118
Q

Describe the formation of the mesonephros

A
  • week 4
  • derived from the intermediate mesoderm in upper thoracic to the lumbar regions
  • this is induced to epithiliase forming a solid duct.- mesonephric duct
  • develops caudally and fuses with the walls of the cloaca at day 26
  • canalisation comenses from the caudal end at day 26
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119
Q

What does canalisation of the nephric duct induce?

A

Formation of the mesonephric buds

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120
Q

Describe the formation of the mesonephric ducts

A

Tubules are formed in a craniocaudal fashion

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121
Q

Describe the formation of the Bowman’s capsule

A

The mesonephric tubules differentiate and
lengthen rapidly to form an S- shape and
Bowman’s capsule

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122
Q

Describe how the Glomerulus is formed

A

The tuft of the capillaries at the end of the elongated, differentiated mesonephric tubules forms the glomerulus

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123
Q

What forms the rudimentary excretory units?

A

The renal corpuscle

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124
Q

How do the mesonephric tubules regress?

A 
6/7 Cranial-most  tubules
fuse with mesonephric
duct
• Function between weeks
6-10 to produce small
amounts of urine
• Mesonephric ducts then
regress.
• Male -> develop into
reproductive structures • Female -> regress
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125
Q

What is the urogenital ridge?

A

Where gonadal development takes place (on the medial aspect)

Sometimes is referred to as the mesonephric ridge

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126
Q

When does the metanephros develop?

A

28 days

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127
Q

Describe the metanephros

A
  • forms the definitive kidney

- has dual origin - the collecting and excretory portion

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128
Q

Describe the collecting portion of the metanephros

A
  • collecting ducts
  • major and minor calyces
  • renal pelvis
  • ureter
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129
Q

Describe the excretory portion of the metanephros?

A
  • Bowman’s capsule
  • Proximal consulted tubule
  • Loop of Henle
  • Distal convoluted tubule
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130
Q

What is the collecting portion of the metanephros called?

A

Uretic bud

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131
Q

What is the excretory portion of the metanephros called?

A

The metanephric mesenchyme

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132
Q

Describe the development of the metanephros

A
  • Starts with the formation of the ureteric buds at the caudal end of the mesonephric duct
  • by day 32 the steric buds penetrate the metanephric mesenchme
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133
Q

In short, what is the metanephros?

A

The collecting system

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134
Q

Describe development of the metanephros

A

The uteric bud penetrates the mesenchyme and branches

Renal pelvis -> Major calyces -> Minor calyces -> Collecting Tubules

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135
Q

What covers a newly formed collecting tubule of the metanephros?

A

A metanephric tissue cap

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136
Q

What does interaction between the tubule and the metanephric cap cause?

A
  1. Specific branching of the tubule
  2. Differentiation of cells in the metanephric cap to form renal vesicle
  3. Renal vesicle expands to form S-shape tubule and Bowman’s capsule
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137
Q

What makes up the nephron (a secretory unit)?

A

renal corpuscle
tubule
collecting tubule

138
Q

Describe duplication of the Ureter

A
  • premature bifurcation of the uteric bud
  • bifurcation can be partial or complete
  • bifid ureter
  • ectopic ureter
  • present in approximately 5% of the population
139
Q

What causes renal agenesis?

A

early degeneration of ureteric bud or failed interaction between ureteric
bud and metanephric tissue cap

140
Q

What are symptoms of renal agenesis?

A
  • Generally asymptomatic

* Hypertrophy of remaining kidney

141
Q

Why is bilateral renal agenesis not compatible with life?

A

Leads to Oligohydraminos (decreased volume amniotic fluid causing the fetus to present with
Potter sequence). Therefore, the foetus cannot develop respiratory muscles

142
Q

What causes congenital cystic kidney disease?

A
  • genetic factors
  • Failure of induction between ureteric bud
    and metanephric caps
  • Nephrons fail to develop and ureteric bud
    fails to branch
143
Q

Describe autosomal recessive congenital cystic kidney disease

A
  • 1 in 5000 births

- cysts form in the collecting duct

144
Q

Describe autosmal dominant congenital cystic kidney disease

A
  • 1 in 500 to 1 in 1000 births
  • Cysts form from all parts of the nephron
  • Less progressive and usually presents in
    adulthood
145
Q

Describe relocation of the kidneys

A 
• Kidneys develop in the pelvic region but
reside in a more cranial position in the
adult
• ‘Ascent’ of the kidneys caused by
growth and elongation of developing
fetus
• As the kidney ascends it establishes a
new blood supply more cranially. The
original lower vessels normally
degenerate
• Attain adult position by week 9
146
Q

Describe horseshoe kidney

A
  • occurs in 1/600 people
  • inferior poles of kidney fuse
  • resides in the lower lumbar region
  • usually asymptomatic
147
Q

Describe formation of the bladder

A 
- In weeks 4-7, the cloaca divides into
• Urogenital sinus
• Anal canal
-  Separated by urorectal septum –
mesoderm derivative
148
Q

What are the three divisions of the urogenital sinus?

A
  • Upper part: presumptive urinary bladder
  • Pelvic part: Urethra
  • Phallic part: Penile urethra (m) or vestibule (f)
149
Q

With what structure is the bladder initially continuous with?

A

The allantois

150
Q

What does the allantois obliterate to form?

A

The urachus that connects the apex of the bladder with the umbilicus in the adult

151
Q

what is acute kidney injury also known as

A

acute renal failure

152
Q

what is the general definition of acute kidney injury, include the time frame over which this occurs

A

rapid reduction in kidney function - occurs over hours or days

153
Q

what rises and what normally decreases in acute kidney injury

A

creatinine

decreases in urine output (but not all forms usually have this association)

154
Q

what are the risk factors for acute kidney injury

A
  • > 75 yrs
  • pre existing CKD
  • previous episode of AKI
  • debility and dementia
  • heart failure
  • liver disease
  • diabetes
  • hypotension
  • sepsis
  • hypovalemia
155
Q

what are the pre renal causes for acute kidney injury

A
  • sepsis
  • hypotension
  • hepatorenal syndrome
  • renal artery syndrome
156
Q

what are the post renal causes for acute kidney injury

A
  • kidney stones
  • prostatic hypertrophy
  • tumours
  • retroperitoneal fibrosis
157
Q

what are the intrinsic causes for acute kidney injury

A
  • prolonged pre-renal

- nephrotoxins

158
Q

name some nephrotoxins

A
  • gentamicin (used to treat bacterial infections)
  • IV contrast
  • NSAIDs
  • rhabdomylosis
  • haemoglobinuria
159
Q

what is the most common form of acute kidney injury? what is this due to

A

ischaemia-reperfusion injury :

- due to a decrease in BP and reduction in perfusion

160
Q

which position of the nephron does acute kidney injury normally occur

A

the proximal straight tubule - just after the proximal convoluted tubule

161
Q

how does ischemia and reperfusion effect the epithelium of the proximal tubule in AKI

A

causes a loss of polarity of the brush border —> breakdown of the cellular membrane —> necrosis and apoptosis of the membrane cells —>leads to sloughing of viable and dead cells with luminal obstruction

162
Q

normally after ischemia and reperfusion in AKI do we get repair of the membrane ? if so how?

A

yes we normally get complete repair
we get migration and differentiation of the viable cells leading to proliferation of the viable cells = reestablishing the polarity of the membrane

163
Q

what 3 things occur if the membrane doesn’t fully recover ? what is the overall effect of this

A
  • sustained loss of capillary density = decreased blood flow = hypertension
  • immune response = activation of macrophages = inflammation
  • tubular defect in proliferation = tubular apoptosis/senescene

= chronic fibrosis and scarring of tissue

164
Q

what is the clinical presentation of AKI

A
  • normally a silent disease
  • few symptoms
  • secondary to other illness
165
Q

what kind of risk factors in patients lead us to suspect AKI

A
  • hypovolaemia
  • hypotension
  • fever
  • sepsis
  • nausea, vomitting, diarrhoea
  • high soma output
  • haemorrhage : trauma
  • burns
166
Q

what investigations would we carry out for someone with AKI

A
  • full blood count (high/low WBC with infection)
  • U&Es and bicarbonate (good marker for previous kidney infection)
  • C reactive protein
  • Liver function tests
  • calcium and phosphate
  • immunological screen
  • creatine kinase
  • urinalysis
  • ultrasound of renal tract within 24 hours if : obstruction suspected, rare cause suspected requiring biopsy
167
Q

what do we check in a U&Es test in AKI

A
  • electrolyte abnormalities (hyperkalaemia)
  • uraemia
  • raised creatinine
168
Q

what levels are dangerous in CRP for AKI

A

when they are elevated = signal infection and inflammation

169
Q

why do we test for calcium in AKI

A

high calcium signals myeloma (bone marrow cancer)

170
Q

why do we do an immunological screen in AKI

A

vasculitis

171
Q

why do we test for creaitine kinase in AKI

A

rhabdomyolysis

172
Q

why would we do a urinalysis

A
  • exclude infection

- blood and protein - vasculitis

173
Q

how do we manage AKI

A
  • depends on diagnosis
  • majority of cases supportive
  • treatment of underlying cause : sepsis, hypvolaemia
  • stop/avoid toxins
  • kidney replacement kidney
  • rarer cases: refer to renal team, specific therapy
174
Q

what does STOP AKI stand for

A

S- sepsis (treat)
T- toxins (avoid)
O- optimise BP/ volume status
P- prevent harm (identity cause, treat complications, review medication doses, review fluid prescription)

175
Q

what is sepsis caused by

A

the way body responds to an infection - body overreacts to infection

176
Q

what can sepsis lead to

A

increased capillary permeability:

  • vasodilation and hypotension
  • shock
  • multiple organ failure
  • CV collapse (Sevre hypotension)
  • death
177
Q

what is sepsis

A

life threatening organ dysfunction caused by dysregualted host reposes to infection

178
Q

what is SOFA

A

Sepsis-related Organ failure assessment

179
Q

what SOFA score is concerning

A

> 2

180
Q

what are the factors of SOFA

A
  • respiratory rate > 22/min
  • altered mentation (mental state)
  • systolic blood pressure <100mm Hg
181
Q

what is septic shock

A

subset of sepsis

- profound circulatory, cellular and metabolic abnormalities

182
Q

how does sepsis lead to multi organ failure

A
  • endothelial dysfunction –> capillary leakage
  • coagulopathy —> disseminated intravascular coagulation –> reduced tissue perfusion
  • cellular dysfunction –> catabolic state –> reduced cellular energy consumption
  • CV dysfunction –> L ventricular dilation –> hypotension
183
Q

what can acute organ failure lead to

A
  • acute lung injury
  • CV instability (hypotension)
  • AKI
  • GI mucosal injury (translocation of bacteria from bowel to bloodstream)
  • liver dysfunction
184
Q

what are the risk factors for sepsis

A
  • <1 year and >75 yrs
  • very frail people
  • recent trauma or surgery or invasive procedure
  • impaired immunity due to illness or drugs (steroids, chemotherapy, immunosuppressants)
  • indwelling lines/catheters
  • IV drug misusers
  • any breach of skin integrity : cuts, burns, blisters, skin infections
185
Q

do people with sepsis always have specific symptoms

A

may have non-specific symptoms and non-localising presentations (eg. feeling v unwell)

186
Q

what are the high risk criteria for sepsis

A
  • respiratory rate : >25 breaths per min
  • new need for oxygen :
  • heart rate >130 beats per min
  • systolic BP < 90
  • not passed urine in previous 18 hours
  • mottled or ashen appearance
  • cyanosis of skin, lips or tongue
  • non-blanching rash of skin
187
Q

when should treatment for sepsis ideally begin

A

within the first hour

188
Q

how do we treat for sepsis (think of the acronym)

A

BUFALO

  • B: blood cultures
  • U- urine output (monitor hourly - urine cultures, U & E)
  • F: fluid resuscitation
  • A- antibiotics (IV)
  • Lactate measurement - from arterial or venous gas
  • Oxygen - correct hypoxia
189
Q

why do we prescribe resuscitation fluids in AKI or sepsis

A

to correct hypovolaemia - restore the BP and perfusion pressure to organs

190
Q

what are the 2 types of hypokalaemia we can get

A
  • true hypovolaemia

- relative hypovolaemia

191
Q

what is true hypovolaemia ? how do we get it

A 
when the rate of fluid loss of extra cellular fluid exceeds net intake 
eg:
- haemorrhage 
- vomitting 
- diarrhoea
192
Q

what is relative hypovolaemia ? how do we get it

A

when there is a decrease in the effective circulating volume
eg: sepsis

193
Q

how do resuscitation fluids correct hypovolaemia

A
  • restore the circulating volume by:
  • rapidly expanding the intravascular space
  • restoring the BP and organ perfusion
194
Q

what are the main resuscitation fluids we use

A

crystalloids:

  • 500mls Hartman’s solution
  • 500mls 0.9% sodium chloride salt
195
Q

if a patient presents with sepsis and is taking diuretics and ACEi do we stop them? how long for and why

A

yes we would stop them for a while due to fluid resuscitation management (to increase amount of fluid), however resume once patient has recovered

196
Q

what is hyperkalemia? is it dangerous and why

A

high potassium

medical emergency - risk of cardiac arrest

197
Q

what happens of an ECG of hyperkalaemia

A
  • a tented T wave is presented (T wave is more raised and spiked)
  • loss of the P wave
198
Q

how do we manage hyperkalaemia

A
  • calcium glutinate (shifts K+ into cell and protects cardiomyocytes)
  • glucose and soluble insulin (facilitates uptake of glucose into the cell and thereby K+)
  • stop drugs causing increased K+
  • salbutamol nebulisers (push K+ intracellular)
199
Q

in severe cases of hyperkalemia how would we mange it

A

kidney replacement therapy

200
Q

if someone presents with pulmonary oedema how do we approach it (ie. treatment methods)

A
  • sit up
  • O2 high flow via reservoir mask
  • high dose furosemide (loop diuretic)
  • IV nitrates
  • kidney replacement therapy
201
Q

why would we give a high dose of furosemide to someone suffering from pulmonary oedema? in what case would we persist its use

A
  • only if volume replete (v full)

- do not persist if unresponsive

202
Q

what drugs are removed by the kidneys

A
  • antibiotics : penicilin
  • opioids : morphine
  • metformin
  • digoxin
203
Q

what can an accumulation of penicillin cause

A

seizures

204
Q

what can an accumulation of morphine lead to

A
  • pinpoint pupils

- respiratory depression

205
Q

what can an accumulation of metformin lead to

A

lactic acidosis

206
Q

what can an accumulation of digoxin lead to

A

cardiac toxicity

207
Q

what drugs can lead to nephrotoxity

A
  • aminoglycosides: gentamicin

- NSAIDS (ibuprofen)

208
Q

name indications where we would perform kidney replacement therapy

A
  • hyperkalaemia unresponsive to medical therapy
  • pulmonary oedema unrepsocive to medical therapy
  • sevre acidaemia
  • uraemia complications (increased urea)
209
Q

name 2 uraemic complications

A
  • encephalopathy (disease of the brain)

- pericarditis (friction rub= bleed = cardiac arrest)

210
Q

what is the function of the Bowmans capsule

A

collects what is filtered through the glomerulus

211
Q

what is the function of the proximal conciliated tubule

A
  • reabsorbs 65% filtrate volume (glucose, AA, Na, Bicarb, water)
  • secretes toxins (ammonia, creatinine, organic acids, some drugs)
  • adjusts filtrate pH
212
Q

what is the function of the descending loop of henle

A

water reabsorption

213
Q

what is the function of the ascending loop of henle

A

reabsorbs Na/Cl

urea secreted

214
Q

what is the function of the distal convolated tubule (hormone control)

A
  • aldosterone: reabsorb Na and so Cl follows
  • secrete K
  • reabsorb Ca
  • reabsorb bicarb and water
  • synthesises bicarb
215
Q

what is the function of the collecting duct

A
  • ADH: reabsorb water

- reabsorb various ions (sodium, potassium, hydrogen ions, bicarb)

216
Q

what does the glomerular filtration rate refer to

A

ultrafiltration of the plasma across the glomerulus into the urinary space

217
Q

what is the glomerular filtration rate calculated from

A
  • serum creatinine
  • sex
  • age
218
Q

what is the normal value of GFR in healthy people

A

> 90mL/min/1.73m2

219
Q

what is chronic kidney disease

A
  • abnormalities of kidney structure or function which lead to decreased kidney function
220
Q

is chronic kidney disease reversible

A

reversal is unlikely

221
Q

what is the most common cause of CKD

A

diabetes

222
Q

over what time frame does CKD present

A

present on at least 2 occasions > 3 months apart (long standing)

223
Q

is eGFR of >60 normal? in what cases is it not

A

yes it is normal unless there are signs of kidney disease:

  • urinary abnormalities
  • electrolyte and other abnormalities due to tubular disorders
  • structural abnormalities
  • histological abnormalities
  • genetic disease
  • kidney transplantation
224
Q

is CKD a silent disease

A

yes that’s why need to check the risk in that population (eg. black minority groups)

225
Q

what are the causes of CKD

A
  • diabetes (leads to diabetic nephropahty)
  • glomerular disease (glomerulonephritis)
  • obstruction
  • inherited disorders
  • renovascualr disease
  • AKI
  • reflux nephropathy
  • interstitial disease
226
Q

what inherited diseases can cause CKD

A
  • autosomal dominant polycystic kidney disease

- Alport syndrome (x linked)

227
Q

what are the complications of diabetes

A
  • retinopathy
  • neuropathy
  • albuminuria/proteinuria
228
Q

does glomerular disease effect one or both kidneys

A

immune mediated and effects both kidneys

229
Q

what is the clinical presentation of glomerular disease

A
  • nephrotic syndrome (leak large amounts of protein into urine)
  • nephritic syndrome (inflammation of the kidneys)
230
Q

what would we see in the urinalysis of glomerular disease

A
  • haematuria

- proteinuria

231
Q

what investigations would we carry out for someone with glomerular disease

A
  • immunological investigations
  • ultrasound
  • kidney biopsy
232
Q

what is the clinical presentation of nephrotic syndrome

A
  • oedema
  • hypoalbuminuria
  • proteinuria
233
Q

what is the clinical presentation of nephritic syndrome

A
  • AKI
  • haematuria
  • proteinuria
  • hypertension
234
Q

what occurs in autosomal dominant polycystic kidney disease (ADPKD), include clinical presentation

A
  • Development of multiple cysts
  • hypertension
  • cardiac abnormalities
  • berry aneurysms
235
Q

where do the cysts in ADPKD occur

A

kidneys
liver
pancreas

236
Q

what chromosomes do ADPKD effect

A

chromosome 16 and 4

237
Q

what’s the pahtophysiology associated with ADPKD

A
  • Raised intra-glomerular pressure
  • glomerulosclerosis
  • tubulointersitial fibrosis
  • loss of renal cortex
  • shrunken kidneys
238
Q

what is gloneruloscelrosis

A

expansion of glomerular mesangium and deposition of EC matrix

239
Q

what happens in tubulointerstitial fibrosis

A

tubular atrophy
interstitial inflammatory cell infiltrate
deposition of EC matrix in intersitium

240
Q

what are the signs and symptoms of CKD

A

silent disease

may not maifest until significant decrease of kidney function

241
Q

what are the clinical manifestations of CKD

A
  • Aches and pains
  • loss of lean body mass
  • reduced UO
  • salt and water retention
  • loss of appetite/ nausea
  • sleep disturbance
  • vomiting
  • bleeding/bruising
242
Q

what are the consequences of uraemia

A
  • kidney failure (very high urea)
  • pericarditis ( risk of cardiac tamponade- fluid increase in pericardium = press on heart)
  • encephalopathy
  • uraemia frost
243
Q

what are the sings of encephalopathy

A
  • reduced conscious level
  • impaired cognition
  • confusion
  • coma
  • seizures
244
Q

what is uraemia frost

A

urea and urate deposits on the skin

245
Q

which individuals are at high risk of CKD

A
  • diabetes
  • hypertension
  • AKI
  • CV disease
  • structural renal tract disease
  • multi system diseases with potential kidney involvement (eg.myeloma)
246
Q

what are the initial screening of CKD

A
  • blood eGFR
  • urinalysis (blood/protein)
  • BP
247
Q

what further investigations would you carry out for CKD

A
  • distinguish between AKI and CKD : baseline serum creatinine value and compare
  • features to favour CKD:
    anaemia
    low calcium
    high phosphate
    elevated PTH
    ultrasound appearances (scared/shrunken kidneys)
248
Q

how would you manage CKD

A
  • fluid balace (salt and water retention ) - loop diuretics
  • hypocalcaemia (vit D analogues)
  • tertiary hyperparathyroidism ( inhibit PTH secretion: calcimimetics)
  • dose adjustments of drugs
  • dietary advice : reduce K+ and phosphate
249
Q

what specific therapy would we use for ADPKD

A

tolvaptan - vasopressin V2 receptor antagonists :

  • inhibit cyst growth
  • slow the decline of kidney function
250
Q

before resulting to kidney replacement therapy what options do we have

A
  • haemodialysis
  • peritoneal dialysis (uses persons peritoneum to transfer dissolved substances)
  • transplantation
251
Q

what is the basic principle of the dialysis machines

A

blood with toxins moves into dialysis and toxins are removed from blood and put back into the blood

252
Q

what kind of membrane inside the dialysis allows for toxins to be filtered out

A

semipermeable membrane

253
Q

how many times a week and for how long do you carry out harm-dialysis

A

3 times a week for 3-4 hours

254
Q

how Is peritoneal dialysis inserted

A

catheter is pushed through the skin and peritoneal membrane into the peritoneal space of the abdomen near the bladder - dialysis is carried out in this peritoneal space

255
Q

hw does glucose concentration affect peritoneal dialysis

A

the higher the glucose concentration in the peritoneal dialyse the more ultrafiltration is achieved

256
Q

when do you do an automated peritoneal dialysis

A

machine performs exchanges overnight

257
Q

how does a continuous ambulatory Peritoneal dialysis work

A

manual exchange 3-4 times each day

1-3 L in each exchange

258
Q

what are the (+) of haemodialysis

A
  • less protein loss
  • shorter treatment times
  • social network at dialysis centre
  • highly effeicnt small solute clearances
  • no lag time to commence (PD requires several weeks before catheter can be used and training needed)
259
Q

what are the (-) of haemodialysis

A
  • hospital based
  • scheduled treatment
  • vascular access problems
  • haemodynamic stress(blood moving from central to periphery)
  • bleeding risk
  • post dialysis : hypotension
  • complications: infections, access failure
260
Q

what are the (+) of peritoneal dialysis

A
  • home based
  • increased flexibility
  • preservation of residual renal function
  • less fluid restriction due to maintenance of residual urine output
  • no anti-coagulation
261
Q

what are the (-) of peritoneal dialysis

A
  • dedicated space required for storage of equipment and fluid
  • membrane failure - finale lifespan
  • hyperglycaemia/ glucose load- disrupts diabetic control
  • protein losses
  • complications: hernias, peritonitis, sclerosing peritonitis (inflamtion of both parietal and visceral layers)
262
Q

who is considered for a kidney transplant

A
  • patients on dialysis or approaching dialysis

- patients must be fit to undergo surgery

263
Q

describe the process fir a kidney transplant surgery

A
  • a curved incision in the lower abdomen
  • the kidneys vein is joined to the iliac vein which drains blood from the leg
  • kidneys artery is joined to the iliac artery which supplies the leg with blood
264
Q

what are the immediate post operative complications of a kidney transplant

A
  • infections : bacterial pathogens (wound, urinary tract, respiratory tract)
  • delayed kidney transplant functions: ischemia reperfusion injury
  • rejection
265
Q

there is administration of lifelong immunosuppressants in kidney transplant. what are the long term side effects of immunosupressents

A
  • skin cancer (avoid direct sunlight)
  • post transplanproliferative disorder (PTLD)
  • infections : opportunistic infections, bacterial infections (UTI, pneumonia), viral infections (influenzas, covid)
266
Q

what are the signs and symptoms of post transplant lymphoproliferative disorder

A
  • weight loss
  • fever
  • lymphadenopathy
267
Q

what is the main cause of death after a functioning kidney transplant

A

CVD

268
Q

What are ACE inhibitors?

A

Prevent the conversion of angiotensin 1 to angiotensin 2 in the RAAS

269
Q

How are the kidneys implicated in the RAAS?

A

Kidneys produce renin

which aids the conversion of angiotensiongen to angiotensin 1

270
Q

What is the role of beta blockers?

A

Have an effect on the sympathetic system therefore inhibiting renin release

271
Q

What does aldosterone stimulate?

A

Sodium uptake

Potassium excretion

272
Q

Describe granular cells

A

contain renin

enter the Bowman’s capsule through afferent tubule

273
Q

What stimulates renin secretion? (x4)

A
  • Pressure changes in the afferent arteriole
  • Sympathetic tone
  • Macula densa (chloride and osmotic concentration)
  • Local prostaglandin and NO release
274
Q

What is the role of ACEi?

A

Inhibits the vasoconstrictive effect of angiotensin II

275
Q

How do ACEi inhibit the vasoconstrictive effect of angiotensin II?

A
  • dilates efferent arteriole
  • reduces intra-glomerular pressure
  • increases sodium and water excetretion
276
Q

What are the indications for the use of ACEi?

A
  • hypertension
  • cardiac failure
  • CKD (reduces the intra-renal pressure)
277
Q

What are the side effects of ACEi?

A
  • hypertension
  • hyperkalaemia
  • cough
278
Q

Why may ACEi lead to hyperkalaemia?

A

They inhibit the effect of aldosterone

279
Q

What are common examples of ACEi?

A

Ramipril and Lisinopril

280
Q

What is an ARB?

A

Angiotensin Receptor Blocker

281
Q

What is the role of ARBs?

A

Inhibits vasoconstrictive effect of angiotensin II on the receptor

282
Q

How do ARBs inhibit the vasoconstrictive effect of angiotensin II on the receptor?

A
  • dilates efferent arteriole
  • reduces intra-glomerular pressure
  • increases sodium and water excretion
283
Q

What are the indications for ARBs?

A
  • hypertension
  • cardiac failure
  • CKD
284
Q

What are the side effects of ARBs?

A

Hypotension

Hyperkalaemia

285
Q

What are examples of ARBs?

A
  • valsartan

- irbesartan

286
Q

What is an examples of an osmotic diuretic?

A

Mannitol

glucose in diabetes

287
Q

Where do osmotic diuretics act?

A

The Bowman’s capsule

- they modify the contents of the filtrate

288
Q

What is an example of a carbonic anhydrase inhibitor?

A

Acetazolamide

289
Q

Where does acetazolamide act?

A

Before and after the loop of Henle

290
Q

What are examples of loop diuretics?

A

Furosemide

Bumetamide

291
Q

What do loop diuretics inhibit?

A

Uptake of:

  • sodium
  • potassium
  • chloride
  • water
292
Q

What are the indications of loop diuretics?

A
  • CKD
  • Hypertension
  • Cardiac failure
  • Nephrotic syndrome
293
Q

What are the side effects of loop diuretics?

A
  • hypovalaemia

- hypokalaemia

294
Q

What may hypovolaemia lead to?

A

AKI and cramps

295
Q

What is the role of thiazides?

A

Inhibit sodium uptake so remove sodium and water

296
Q

What are the indications for thiazide?

A
  • CKD
  • hypertension
  • cardiac failure
  • nephrotic sundrome
297
Q

What are the side effects of thiazides?

A

hypovolaemia

hyponatraemia

298
Q

What is the function of amiloride?

A

Inhibits sodium reabsorption in exchange for potassium

- removes sodium and water

299
Q

What are the indications of amiloride?

A

prevents hypokalaemia

300
Q

Why is amiloride descries as a weak diuretic?

A

It removes sodium and water

301
Q

What are the side effects of amiloride?

A

hyperkalaemia

302
Q

….. activate vitamin D

A

The kidneys

303
Q

What form of vitamin D is given to those with CKD?

A

Vitamin D analogues that only require hydroxylation by the liver to the active form

304
Q

What is an example of a vitamin D analogue?

A

Alpha calcidol

305
Q

What are the side effects of vitamin D analogues?

A
  • hypercalcaemia

- hyperphosphataemia

306
Q

What do vitamin D analogues lead to in the gut?

A

Increased uptake of calcium and phosphate

307
Q

Eryhtropoietin stimulates ….

A

erythropoiesis

308
Q

Erythropoietin is produced by

A

cells in the intesitium of the kidney

309
Q

Erythropoietin secretion is stimulated by

A

hypoxia

310
Q

At what eGFR is erythropoietin required?

A

eGFR<15

311
Q

How is erythropoietin administered?

A

subcutaneous injection

312
Q

What are the side effects of erythropoietin?

A
  • hypertension

- pure red cell aplasia

313
Q

What are the consequences of reduced renal perfusion?

A
  • reduced transglomerular pressure

- reduces GFR

314
Q

What is the response of the kidney to reduced renal perfusion?

A

intra-renal activation of RAAS

  • efferent arteriole vasoconstriction
  • increases transglomerular pressure
  • restores GFR
315
Q

What is the effect of prostaglandins on the kidney?

A
  • vasodilate the afferent arteriole

- maintain transglomerular pressure

316
Q

What is the effect of NSAIDs on the kidney?

A 
- inhibit prostoglanins
leads to
- vasoconstriction of afferent arteriole
- decrease transglomerular pressure
- decreased GFR
317
Q

What maintains transglomerular pressure and GFR?

A
  • prostoglandins of the afferent arteriole

- angiotensin II on the efferent arteriole

318
Q

Why do ACEi and ARBs lead to decreased transglomerular pressure and reduced GFR?

A

They inhibit efferent arteriolar vasoconstriction

319
Q

All penicillins except Flucoxacillin are removed by the …

A

kidneys

320
Q

Opiod analgesics are removed by …

A

the kidneys

321
Q

Opiates with minimal renal excretion are

A
  • fetanyl
  • oxycodone
  • hydromorphone
322
Q

What is digoxin used for?

A

Antiarrythmic drug

- eg atrial fibrilation

323
Q

Accumulation of digoxin in the kidneys leads to…

A
  • bradycardia
  • visual disturbances
  • mental confusion
  • aggrevation of hyperkalaemia
324
Q

Metformin is removed by

A

the kidneys

325
Q

Accumulation of metformin in the kidneys leads to

A

hypoglucaemia

lactic acidosis

326
Q

Metformin use should be avoided if

A

GFR < 30ml/min

327
Q

What herbal preparations may effect the kidneys?

A

aristocholic acid eg in cat’s claw

328
Q

What characterises nephrotic syndrome?

A

proteinuria
- therefore hypoalbuminaemia and oedema
hypercholestolaemia

329
Q

What protein is predominantly lost in proteinurea?

A

Albumin

330
Q

What are the signs and symptoms of nephrotic syndrome?

A
  • severe swelling, particularly around the ankles
  • foamy urine due to proteinuria
  • weight gain due to fluid retention
  • fatigue
  • loss of appetite
331
Q

What is the glomerular filtration barrier?

A

3 layered structure

facilitates flow of plasma, water and small molecules while restricting the flow of large plasma proteins

332
Q

The 3 layers of the glomerular filtration barrier (GFB) are …

A
  • endothelium
  • glomerular basement membrane
  • podocyte
333
Q

What is the glomerular basement membrane?

A

the extracellular matrix component of the selectively permeable glomerular filtration barrier (GFB) that separates the vasculature from the urinary space

334
Q

The GFB is synthesised by

A

glomerular endothelial cells and the podocytes (epithelial cells) that sit on the opposite side of the GBM within the urinary space

335
Q

The GFB has a … charge

A

net negative charge

336
Q

Why is the negative charge of the GFB significant?

A

It acts as a filtration barrier to plasma albumin which is negatively charged

337
Q

Why is the GFB compromised in nephrotic syndrome?

A

there is injury to the epithelial foot process
- podocyte fusion and collapse
- reorganisation of the actin cytoskeleton
means that albumin can pass through

338
Q

What medical conditions are causes of nephrotic syndrome?

A
  • diabetes
  • minimal change disease (children)
  • membranous nephropathy
  • focal segmental glomerulosclerosis
  • systemic lupus erythematosis
  • amyloid
339
Q

What infections cause nephrotic syndrome?

A

HIV
Hep B
Hep C
Malaria

340
Q

What medications cause nephrotic syndrome?

A

NSAIDs

341
Q

What genetic variant can the disparity in prevalence of diabetes be attributed to?

A

APOL1

342
Q

How is nephrotic syndrome treated?

A

specific therapy depending on the cause

  • diabetes = management
  • minimal change disease/membranous nephropathy/fsgs = steroids
  • amyloid= chemotherapy

year 1 flash cards (23 decks)

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