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Semester Three > REN L10-L20 > Flashcards

REN L10-L20 Flashcards

1
Q

What osmolality are all bodily fluids except the interstitial space of the renal medulla? (L10 Osmoregulation)

A

285mOsm/kg

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2
Q

Osmolality is detected by which part of the brain? L10

A

Anterioventral third ventricle (AV3V) region

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3
Q

Where do AV3V neurones project to? L10

A

Supraoptic and paraventricular parts of the hypothalamus

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4
Q

What is released from the hypothalamus in response to an increase in osmolality? L10

A

ADH

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5
Q

What is co-released with ADH as its co-peptide? L10

A

Neurophysin

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6
Q

What receptors does ADH act upon and where are they? L10

A

V2 receptors on the basolateral membrane of the cortical collecting duct

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7
Q

Activation of V2 receptors causes what? L10

A

AQP2 receptor exocytosis

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8
Q

What effect does oxytocin have at V2 receptors? L10

A

It is an agonist

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9
Q

If maximum ADH was released what volume of urine would be produced per day and at what osmolality? L10

A

300ml at 1400mOsm

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10
Q

If no ADH was released what volume of urine would be produced per day and at what osmolality? L10

A

2.5L at 60mOsm

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11
Q

What are symptoms of the hyperosmolar hyperglycaemic state seen in diabetes mellitus? L10

A

Altered mental status, seizures and other neurological signs

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12
Q

Give example of ADH analogue given in diabetes insipidus. L10

A

Desmopressin

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13
Q

Where are juxtaglomerular cells, and what do they release? (L11 Volume regulation)

A

In the wall of afferent arterioles in the kidney

They release renin

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14
Q

What type of cell are juxtaglomerular cells? L11

A

Smooth muscle cells

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15
Q

What is the thickening of the early distal tubule in the kidney? L11

A

Macula densa

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16
Q

What is the function of the macula densa? L11

A

They sense changes in NaCl

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17
Q

What happens in the macula densa senses a fall in NaCl? L11

A

Causes vasodilation of afferent arterioles, increasing GFR

Stimulates renin release from the JG cells

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18
Q

What is the aim of the RAA system? L11

A

To increase effective circulating volume

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19
Q

Where is angiotensinogen produced? L11

A

Liver

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20
Q

What converts angiotensinogen into angiotensin I? L11

A

Renin

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21
Q

What does angiotensin-converting enzyme do and where is it mainly found? L11

A

Converts angiotensin I to angiotensin II

In the lungs

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22
Q

What are four effects of angiotensin II? L11

A

Efferent arteriole vasoconstriction
Increases Na+ reabsorption in proximal tubule
Aldosterone release
ADH release

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23
Q

Where is aldosterone released from? L11

A

Adrenal cortex

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24
Q

What receptor does angiotensin II act upon? L11

A

AT1 receptors

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25
Q

How is renin release stimulated in haemorrhage? L11

A

Low cardiac output and low circulating volume leads to a lower BP; the sympathetic nervous system increases its activity and renin is released. Also the afferent arteriole senses the BP drop by decreased wall tension and hence releases renin.

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26
Q

What are the three actions of activating sympathetic innervation of the afferent arteriole? L11

A

Vasoconstriction upstream of JG cells causes a further fall in pressure sensed by the cells

Direct stimulation of renin release by direct innervation

Afferent arteriole vasoconstriction drops glomerular hydrostatic pressure hence lowering GFR

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27
Q

Name some stimuli for ADH release. L11

A

Activation of baro-reflex
Angiotensin II action
Nicotine
Increased osmolality

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28
Q

What effect on sodium can ADH have? L11

A

Hyponatraemia; water is retained to maintain circulating volume but this does not retain Na+

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29
Q

Name stimuli that suppress ADH release. L11

A

Alcohol
Decreased osmolality
Increased circulating volume

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30
Q

Define effective circulating volume. L11

A

The component of blood that is perfusing the tissues (may be different from total blood volume e.g. in heart failure)

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31
Q

What are three ways that a decreased effective circulating volume can stimulate renin release? L11

A

Sympathetic activation: from baro-reflex activation

Decreased wall tension in aff. arteriole: lowered renal perfusion pressure

Macula Densa mechanism: less NaCl delivered to distal tubule

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32
Q

What is normal arterial pH? (L12 Acid-base regulation)

A

7.4

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33
Q

What is normal venous pH? L12

A

7.35

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34
Q

What is normal arterial PCO2? L12

A

40mmHg or 5.3kPa

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35
Q

What is normal venous PCO2? L12

A

46mmHg or 6kPa

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36
Q

When does excess H+ production occur? L12

A

ATP hydrolysis
Ketone production
Anaerobic respiration
Acid ingestion

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37
Q

How is excess H+ removed? L12

A

Reacts with bicarbonate producing CO2 which can be exhaled. The kidney reabsorbs bicarbonate to replace the losses elsewhere.

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38
Q

Name the enzyme that catalyses HCO3- + H+&raquo_space;> H20 + CO2. L12

A

Carbonic anhydrase

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39
Q

Where is 90% of bicarbonate reabsorbed? L12

A

Proximal tubule

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40
Q

How does the bicarbonate cross the basolateral membrane? L12

A

Na+/HCO3- co-transporter

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41
Q

What happens if there is still excess H+ in the filtrate? L12

A

Buffered with hydrogen phosphate

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42
Q

What is the name of the cells that secrete H+ ions in the distal tubule and why are they needed? L12

A

Intercalated cells; have to secrete the H+ as it is against a much larger conc.grad.

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43
Q

How is ammonium produced in the proximal tubule? L12

A

Deamination of glutamine

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44
Q

What happens to the pH along the nephron? L12

A

Becomes progressively acidic, can be as low as 4.5 in the collecting duct (urine usually acidic)

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45
Q

What is a typical cause of respiratory acidosis? L12

A

Hypoventilation

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46
Q

How does the ____ compensate respiratory acidosis? L12

A

Kidney; it increases bicarbonate production to return pH to normal

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47
Q

What is a typical cause of metabolic acidosis? L12

A

Renal failure, keto-acidosis, lactic acidosis

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48
Q

How does the ____ compensate metabolic acidosis? L12

A

Lungs; increase ventilation rate

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49
Q

What is a typical cause of respiratory alkalosis? L12

A

Hyperventilation

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50
Q

How does the ____ compensate respiratory alkalosis? L12

A

Kidney; it decreases bicarbonate production to return pH to normal

51
Q

What is a typical cause of metabolic alkalosis? L12

A

Vomiting

52
Q

How does the ____ compensate metabolic alkalosis? L12

A

Lungs; decrease ventilation rate

53
Q

Factors affecting serum creatinine. (L13 CKD)

A

Age, gender, ethnicity, body mass

54
Q

What is used to calculate eGFR? L13

A

Creatinine, age, gender, ethnicity

55
Q

What is the eGFR for end-stage (stage 5) kidney disease? L13

A

<15ml/min

56
Q

What is normal eGFR? L13

A

> 90ml/min

57
Q

Name some causes of CKD. L13

A

Infectious diseases e.g. TB, HIV
Systemic diseases e.g. DM, hypertension
Genetic diseases e.g. polycystic kidneys
Obstruction e.g. tumour, stones, fibrosis

58
Q

Describe the pathology of CKD. L13

A

Thickening of the basement membrane
Mesangial expansion
Glomerulosclerosis

59
Q

State and explain the reasons for why there are CKD complications. L13

A

Anaemia; decreased EPO production

Hypertension; volume expansion, Na+ retention, RAS activation

Bone disease; disturbed calcium-phosphate homeostasis

Secondary hyperparathyroidism; from increased PTH

Abnormal drug handling; failure to excrete

60
Q

What can be the effects of failure to excrete water load? L13

A

Dilutional hyponatraemia
Oedema
Hypertension

61
Q

Treatment for fluid overload? L13

A

Diuretics
Salt and fluid restriction
(Dialysis + transplant)

62
Q

What effect does CKD have on sodium levels? L13

A

Hypernatraemia

63
Q

What effect does CKD have on potassium levels? L13

A

Hyperkalaemia when eGFR <10ml/min

64
Q

Treatment for hypernatraemia and hyperkalaemia? L13

A

Salt and K+ restriction

Dialysis + transplant

65
Q

Treatment to prevent bone disease as a result of CKD? L13

A

1alpha-hydroxylated vit D replacement
Phosphate binders
Parathyroidectomy

66
Q

Treatment for anaemia as a result of CKD? L13

A

Recombinant EPO

67
Q

Treatment for high BP in CKD? L13

A

RAS blockage
ACE inhibitors
Diuretics

68
Q

What is a risk from failure to excrete insulin? L13

A

Hypoglycaemia

69
Q

What is a risk from failure to excrete antibiotics? L13

A

Encephalopathy

70
Q

What is a risk from failure to excrete digoxin? L13

A

Cardiac arrhythmias

71
Q

Signs of renal failure? (many of them) (L14 Renal failure)

A 
Volume overload
Hypertension
Hypoalbuminaemia 
Oedema 
Hyponatraemia
Hyperkalaemia 
Metabolic acidosis
Decreased renal clearance of drugs
Hyperphosphataemia
Hypocalcaemia (potentially hypercalcaemia) 
Anaemia
72
Q

Why do you get volume overload in renal failure? L14

A

GFR falls, so water and salt accumulate

73
Q

Treatment for volume overload? L14

A

Furosemide
ACE inhibitors
AT1 blocker

74
Q

Why do you get hypertension in renal failure? L14

A

RAA system activation

Volume expansion

75
Q

Why do you get hypoalbuminaemia in renal failure? L14

A

Leaky glomerulus means albumin and other proteins can be lost in the urine

76
Q

Why do you get oedema in renal failure? L14

A

Fall in circulating oncotic pressure, means more fluid leaves vessels to go into the interstitial space, causing oedema

77
Q

Why do you get hyponatraemia in renal failure? L14

A

A decrease in effective circulating volume means ADH is released, but this does not retain Na+ so sodium is lost in the urine. Osmolality is sacrificed to maintain volume

78
Q

Why do you get hyperkalaemia in renal failure? L14

A

Drop in GFR means a decrease in K+ clearance. Initially this is regulated by aldosterone, but as kidney function declines, this is no longer sufficient

79
Q

Treatment for hyperkalaemia? L14

A

Acute: insulin or glucose
Chronic: diuretics, potassium restricted diet

80
Q

Treatment for hyponatraemia? L14

A

V2 receptor antagonists

81
Q

Why do you get metabolic acidosis in renal failure? L14

A

Loss of ability to secrete H+ and produce new HCO3- leads to H+ ion increase and decrease in pH

82
Q

Examples of drugs that have side effects from decreased renal clearance? L14

A

Opiates
Metformin
Digoxin
Furosemide

83
Q

Why do you get hyperphosphataemia in renal failure? L14

A

Decreased GFR means decreased phosphate clearance

84
Q

Why do you get hypocalcaemia in renal failure? L14

A

Decrease in active vit.D leads to increase in PTH, so more calcium is resorbed from bone, can lead to osteomalacia and hyperparathyroidism

85
Q

Why do you get anaemia in renal failure? L14

A

Decreased EPO

86
Q

Signs of uraemia? L14

A 
Uraemic frost on skin
Encephalopathy
Seizures
Pruritis
Nausea
Sexual dysfunction
87
Q

Who is at risk for acute kidney injury? (L15 Acute renal injury)

A 
Elderly
DM pts
Hypertensive pts
Heart disease pts
CKD pts
88
Q

Pre-renal causes of acute kidney injury? L15

A

Hypotension
Hypovalaemia
Renal artery occlusion

89
Q

Treatment for pre-renal cause of acute kidney injury? L15

A

Treat underlying cause

Fluid volume replacement

90
Q

Post-renal causes of acute kidney injury? L15

A

Obstruction of urinary system e.g. tumour, stones, fibrosis, benign prostate

91
Q

Renal causes of acute kidney injury? L15

A

Intrinsic disease of kidney or systemic disease affecting kidney

92
Q

Treatment of inflammatory renal disease? L15

A

Steroids

Cyclophosphamide

93
Q

Causes of death from AKI? L15

A 
Underlying disease
Infection
Hyperkalaemia
Acidosis 
Pulmonary oedema
94
Q

What separates a patient’s blood and dialysis fluid during dialysis? L16

A

Semi-permeable membrane

95
Q

Two types of dialysis? L16

A

Peritoneal

Haemolysis

96
Q

Possible complications from dialysis? L16

A 
Infection
Does not last for every pt
LVH due to hypertension and fluid overload
Anaemia
Bone disease
97
Q

Where is a transplanted kidney often placed? L16

A

In iliac fossa, retroperitoneal

98
Q

Where do transplanted kidneys come from? L16

A

Cadaveric donors- BSD or CDD

Living donors- must be assessed more carefully

99
Q

What do you screen potential donors for when wanting to transplant a kidney? L16

A

Human Leukocyte Antigen (HLA)- screen patients for anti-HLA antibodies

100
Q

What happens in cell-mediated rejection of an organ transplant? L16

A

Cellular debris goes to secondary lymphoid tissues –> presented on APC to T cell –> releases IL-2 which continues the T cell cycle –> cytokines released –> macrophages and B cells activated

101
Q

What does every pt need to take if they have received a donor organ? L16

A

Immunosuppressants

102
Q

Give examples of immunosuppressants and how they work. L16

A

Steroids prevent IL-2 release
Basiliximab block IL-2 receptors
Ciclosporin inhibits calcineurin

103
Q

Side of effects of steroids? L16

A

Weight gain
Thin skin
Hypertension
Osteoporosis

104
Q

Side effects of ciclosporin? L16

A

Infection

Nephrotoxic

105
Q

Define shock. L17

A

Inadequate perfusion of vital organs

106
Q

Two types of shock? L17

A

Distributive/ high-output

Non-distributive/ low-output

107
Q

What happens in cardiogenic shock? L17

A 
Due to any 'pump' failure, commonly MI
Decreased ABP and ECV
INCREASED CVP
Reflex widespread vasoconstriction
Increased symp activity to kidney, lowering GFR, activating RAA system
108
Q

What happens in hypovolaemia? L17

A

Due to haemorrhage, burns, vomiting, diarrhoea, dehydration
Decreased ABP and ECV
DECREASED CVP
Increased symp activity to kidney, lowering GFR, activating RAA system

109
Q

Effects of haemorrhage on tissues? L17

A

Anaerobic respiration leads to lactic acidosis
Tissue damage causes K+ release
Cardiac hypoxia further decreases CO
Renal hypoxia leads to AKI

110
Q

What is the adaptive renal response to shock? L17

A

Decreased venous pressure leads to ADH release which leads to water retention and hyponatraemia. This stimulates aldosterone release and so then the RAA system then retains both sodium and water.

111
Q

What cell type is EPO synthesised from? L18

A

Peritubular fibroblasts

112
Q

Stimulus for EPO production? L18

A

Hypoxia (HIF-2)

Low iron

113
Q

How is vit.D metabolised? L18

A

vit.D –> 25-vit.D in the liver

25-vit.D –> 1,25-vit.D in the kidney

114
Q

Four layers of bladder wall from the innermost layer? L19

A

Urothelium
Lamina propria
Detrusor smooth muscle
Serosa

115
Q

What is the function of the type of junction between urothelium cells? L19

A

Tight junctions; decrease permeability

116
Q

Parasympathetic transmitter and receptor on detrusor muscle? L19

A

Ach on M3 receptors, cause contraction

117
Q

Sympathetic transmitter and receptor on detrusor muscle? L19

A

Noradrenaline on beta-3 receptors, causing relaxation

118
Q

Which nervous systems are active/inactive in continence? L19

A

Somatic ACTIVE
Symp ACTIVE
Parasymp INACTIVE
= sphincters contracted

119
Q

Which nervous systems are active/inactive in voiding? L19

A

Somatic INACTIVE
Symp INACTIVE
Parasymp ACTIVE
= sphincters relax, walls contract

120
Q

Treatment for overactive bladder? L19

A

Anti-muscarinics
Botulinum toxin
Beta-3 agonists

121
Q

Treatment for urinary outflow obstruction? L19

A

TURP
Alpha-receptor antagonists
5alpha-reductase inhibitors

122
Q

Four effects of aldosterone? L11

A

Increase activity of basolateral Na+/K+ pumps in DT and CD
Upregulates ENaCs
Increases K+ secretion
Increases H+ secretion in the intercalated cells of the CCDs

123
Q

What are the levels of ADH in central diabetes insipidus? L10

A

Low due to decreased production from the hypothalamus

124
Q

What are the levels of ADH in nephrogenic diabetes insipidus? L10

A

High due to no response of ADH in the kidneys

Semester Three (12 decks)

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