Lecture 7 & 8 - Renal & Electrolyte Flashcards

1
Q

what percentage of total body water is intracellular?

A

67%

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2
Q

what percentage of total body water is extracellular?

A

33%

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3
Q

what percentage of extracellular water is intravascular fluid?

A

80%

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4
Q

what percentage of extracellular water is interstitial fluid?

A

20%

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5
Q

what are some clinical manifestations of dehydration?

A

Affects appearance and function of cells, particularly skin and mucous membranes

concentrated urine
dry skin and mucous membrane
increased thirst
increased body temp
weight loss
dark sunken eyes
impaired consciousness

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6
Q

What effect does dehydration have on the body?

A

A fluid deficit mostly impacts the intracellular compartment,
Severe dehydration can lead to hypovolaemia (low blood volume)
Prolonged hypovolaemia can decrease tissue perfusion and organ failure

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7
Q

how is dehydration diagnosed?

A

physical examination of eyes, urine output, BP (hypotensive), HR, tissue turgor, temp, weight

Bloods - urea and electrolytes

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8
Q

how is dehydration managed?

A

fluid replacement either oral, IV or SC

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9
Q

how does an isotonic solution distribute throughout the body?

A

solution matches plasma concentration so distributes throughout intravascular, interstitial and intracellular spaces (i.e. restore fluid volume)

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10
Q

how does an hypotonic solution distribute throughout the body?

A

lower tonicity than plasma so moves fluid from intravascular space to interstitial and intracellular spaces

(from vessels into cells and space around cells)

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11
Q

how does an hypertonic solution distribute throughout the body?

A

higher tonicity than plasma so fluid moves from interstitial and intracellular spaces into intravascular space (i.e. increase intravascular fluid volume)

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12
Q

what is the risk of not correctly managing dehydration?

A

risk of imbalance and fluid overload which can lead to intra abdominal hypertension or compartment syndrome

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13
Q

what are the 4 main causes of oedema?

A
  1. Increase in capillary permeability
  2. increase in blood hydrostatic pressure
  3. alteration of blood osmotic pressure
  4. lymphatic fluid from tissue is obstructed
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14
Q

What can cause an increase in capillary permeability?

A

occurs in response to chemical mediators released in response to damage/injury

Intravascular fluid movement into interstitial space

i.e. burns mean a loss of plasma proteins which create low osmotic pressure which promotes movement of fluid to tissues

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15
Q

what are common causes of dehydration?

A

Ds and Vs
diuretic meds
diabetes issues
excessive sweat
burns

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16
Q

what are common risk factors for oedema?

A

pregnancy (pre-eclampsia)
CHF
Kidney disease
obstructive liver disease
lymphatic obstruction
deep vein thrombosis
chronic venous insufficiency
medications such as vasodilators, NSAIDs

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17
Q

What are some clinical manifestations of oedema?

A
  • Dependent edema - Specific to parts of the body that that are influenced by gravity (legs, feet, or arms)
  • pitting and non pitting oedema
  • weight gain
  • puffiness
  • swelling
  • hypoxemia
  • hypercapnia (high CO2 in tissue)
  • BP alterations
  • tissue perfusion
  • headache
  • convulsions
  • LOC changes
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18
Q

what are conditions that increase blood hydrostatic pressure?

A

hypertesnion
venous obstruction
excessive fluid intake
diseases characterised by fluid/sodium retention

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19
Q

what is a cause of venous obstruction?

A

Thrombosis or embolism

pressure increases because blood flow is restricted past obstruction

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19
Q

what is the functional role of sodium in the body?

A

AP generation
conduction in muscle and nervous tissue

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20
Q

what is the functional role of potassium in the body?

A

AP generation
conduction in muscle and nervous tissue
body fluid and acid base balance

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21
Q

what is the functional role of calcium in the body?

A

strong bones
role in coagulation
neurotransmitter release
muscle contraction
endo and exocytosis

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22
Q

what is the functional role of phosphate in the body?

A

component of blood buffer system
structure of bones and teeth
cell membrane component
energy storage and release
DNA and RNA nucleotide structure

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23
Q

what is the functional role of magnesium in the body?

A

bone structure
co-factor in enzyme reactions
neuromuscular function
nerve impulse generation
normal myocardial function

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24
Q

what is the cause of hypokalaemia?

A

skeletal and smooth muscle become hyperpolarised making them more responsive to stimuli = weakness and flaccidity

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25
Q

what are the clinical manifestations of hypokalaemia?

A

gut distension
decreased bowel sounds
paralytic ilues
hypotension
cardiac dysrhythmias
mental confusion

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26
Q

how is hypokalemia managed?

A

Oral/IV sumpplemenation via pump
K sparing medication
ECG monitoring

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27
Q

what is the cause of hyperkalaemia?

A

skeletal muscles more excited as resonium A binds with K+ preventing its absorption

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28
Q

what are the clinical manifestations of hyperkalaemia?

A

change in cardiac conduction
intestinal cramps
diarrhoea
restlessness
bradycardia

29
Q

how is hyperkalaemia managed?

A

non K+ sparing diuretics - to increase excretion
calcium chloride - reduce membrane potential for dysrythmias
Glucose/insulin - reduce serum K+

30
Q

what are the S&S of hypocalcemia?

A

muscle twitching
intestinal cramps
seizures
laryngospasms
cardiac dysrhythmia
hyperreflexia

31
Q

what are the common causes of hypocalcemia?

A

inadequate absorption, excessive excretion or poor availabiity of Ca

32
Q

how is hypocalcemia diagnosed?

A

Chvostek sign
Trousseau sign
Bloods
ECG

33
Q

how is hypocalcemia treated?

A

Supplementation PO/IV
assess airway due to laryngospasm risk

34
Q

what are signs and symptoms of hypercalcemia?

A

muscle fatigue
weakness and flaccidity
nausea adn vomiting
hyporeflexia
altered LOC
Kidney stones
pathological fractures

35
Q

what are causes of hypercalcemia?

A

increased absorption
decreased excretion
shift in Ca from bones to blood

36
Q

how is hypocalcemia diagnosed?

A

bloods
ECG changes

37
Q

how is hypercalcemia treated?

A

bisphosphoantes/calcitonin - inhibition of bone reabsorption and increase in calcium excretion

38
Q

what are the S&S of hypophosphatemia?

A

parasthesia
hyporeflexia
altered LOC
bone pain

39
Q

what are causes of hypophosphatemia?

A

decreased GI absorption
shift from blood to cells
excessive excretion

40
Q

how is hypophosphatemia diagnosed?

A

blood tests

41
Q

how is hypophosphatemia treatment?

A

supplementation PO/IV

42
Q

what are S&S diagnosed?

A

associated with hypocalcaemia

43
Q

what are causes of hyperphosphatemia?

A

Increased dietary intake/GI absorption
shift from intracellular to extracellular compartments

44
Q

how is hyperphosphatemia diagnosed?

A

blood tests

45
Q

how is hyperphosphatemia treated?

A

mylanta PO to reduce phosphate absorption
correction of hypocalcemia

46
Q

what are S&S of hypomagnesemia?

A

muscle twitching
hyperreflexia

47
Q

what are the common causes of hypomagnesemia?

A

inadequate absorption
decreased availability of extracellular magnesium
excessive excretion

48
Q

How is hypomagnesemia diagnosed?

A

chvostek sign
trousseau sign
blood test

49
Q

what are the S&S of hypermagnesemia?

A

hyporeflexia
cardiac arrest
flushed skin

50
Q

what are the possible causes of hypermagnesemia?

A

increased absorption
decreased excretion

51
Q

what is the treatment for hypermagnesemia?

A

glucose/insulin infusion
IVF (dilution of intravascular magnesium levels)
diuretics

52
Q

what is pyelonephritis?

A

bacterial infection
inflammation of the kidney due to UTI that reaches renal pelvis

53
Q

what are the clinical manifestations of pyelonephritis?

A

Flank pain
fever
tenderness
nausea
dysuria
frequency

54
Q

how is pyelonephritis diagnosed?

A

urinalysis
medical imaging

55
Q

how is pyelonephritis treated?

A

ABs - trimethoprim
kidney transplant

56
Q

What is glomerulonephritis?

A

refers to several kidney diseases
characterised by inflammation of glomeruli or small blood vessels

57
Q

what are the clinical manifestations of glomerulonephritis?

A

face puffiness
less urination
haematuria
frequents micturition at night
abdominal pain
oedema

58
Q

what is the treatment for glomerulonephritis?

A

high BP meds
steroids
diuretics
reduce intake of salt and K+
dialysis
kidney transplant

59
Q

what is urinary reflux?

A

valve defect essentially causes splash back in ureters causing uteritis

60
Q

what is hypoalbuminemia?

A

thickening of glomerular capillary wall injured by diabetes resulting in loss of protein

61
Q

what is a common result of hypoalbuminemia?

A

oedema due to fluid shift from intravascular to interstitial compartment

fluid retention also due to reduced plasma volume and reduced glomerular blood flow

62
Q

what is hydronephrosis?

A

a condition where one or both kidneys become stretched and swollen as the result of a build-up of urine inside them

63
Q

how are renal obstructions caused?

A

pregnancy
kidney stones
tumours
blood clots
infection and inflammation
prostate gland enlargement
blockages in catheter

64
Q

what are renal calculi?

A

aka nephrolithiasis or urolithiasis or kidney stones
can damage urinary tract or cause hydronephrosis

65
Q

what are the clinical manifestations of renal calculi?

A

nausea and vomiting
flank pain
hematuria
dysuria
urinary frequency

66
Q

how are renal calculi diagnosed?

A

ultrasound
IVP
renal stone analysis
x-ray
calcium oxalate serum/uric acid serum

67
Q

what are risk factors for renal calculi?

A

infection
urinary stasis and retention
immobility
dehydration
increase in uric acid and urinary oxalate

68
Q

how are renal calculi managed?

A

extracorporeal shockwave lithotripsy
ureteroscope removal

69
Q

what are are the clinical manifestations of AKI?

A

decreased GFR
increased concentration of blood urea nitrogen and creatinine
low urine output
hyperkalaemia and sodium retention

70
Q

how does dialysis work?

A

diffuses harmful waste out of body
control BP
keep safe level of chemicals in body