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ESA3 Harpreet :) > Urinary System > Flashcards

Urinary System Flashcards

1
Q

Describe the position of the kidneys (2)

A
  • Paired retroperitoneal organs

- Lie either side of the vertebral column between T12 and L3

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2
Q

Explain why the two kidneys are not perfectly horizontal with each other (2)

A
  • Right kidney is pushed upwards by position of the liver

- Left kidney is pushed downwards by position of the heart

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3
Q

Name 4 functions of the kidneys (4)

A
  • Regulation of key substances in ECF
  • Excretion of waste products e.g. Urea
  • Endocrine function (renin, prostaglandins, erythropoietin)
  • Metabolism e.g. active form of vitD, PTH etc.
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4
Q

Which portions of the nephron are in the kidney medulla?

A
  • Loop of Henle

- Collecting duct

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5
Q

Where is the site of ultrafiltration?

A

Glomerulus in the kidney cortex

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6
Q

What is filtered out of the blood at the glomerulus?

A
  • Water
  • Electrolytes
  • Small molecules e.g. Glucose, AA
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7
Q

Why is the oncotic pressure of the Bowman’s capsule lower than that of the capillary oncotic pressure?

A
  • Proteins are too large to be filtered out of the capillaries
  • The protein composition of the filtrate relative to that of the capillary is therefore very low
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8
Q

Where is the major site of reabsorption of filtrate?

A

Proximal convoluted tubule (PCT)

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9
Q

What determines GFR and how is this maintained?

A
  • Capillary filtration pressure in glomerulus

- Maintained by the difference in lumen sizes between the afferent and efferent arterioles

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10
Q

Explain how the osmolarity of the filtrate is maintained during selective reabsorption (2)

A
  • Ions (mainly Na+ and Cl-) are reabsorbed from the filtrate using specialised iron channels into the interstitium, therefore the osmolarity of the filtrate in the nephron decreases (filtrate is hypertonic)
  • Water follows ions and moves down an osmotic gradient out of the filtrate into the interstitium, therefore the osmolarity of the filtrate increases - solution remains ISOSMOTIC
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11
Q

Where is the majority of Na+ reabsorbed?

A

PCT (60-70%)

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12
Q

What is normally reabsorbed at the PCT?

A
  • 100% Glucose and AA
  • 60-70% Na+ and water
  • 80-90% K+ and HCO3-
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13
Q

Which pump is mainly responsible for setting up the Na+ gradient at the PCT and where is this located? (2)

A
  • Na+/K+ ATPase

- Located on the basolateral membrane

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14
Q

Explain how glucose is reabsorbed at the PCT (3)

A
  • Na+/K+ ATPase transported 3Na+ out of the tubule cell and into the interstitium therefore the [Na+]i decreases
  • This sets up a gradient and Na+ moves from the filtrate into the tubule cell from a high to low concentration
  • Na+/Glucose symporter utilises the passive transport of Na+ to actively transport Glucose into the cell via secondary active transport
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15
Q

How much fluid does the glomerulus filter in a day?

A

~180L

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16
Q

What is a renal corpuscle?

A

Structure formed from the glomerular tuft and the Bowman’s capsule

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17
Q

Embryologically, how is the Bowman’s capsule formed?

A

Ureteric bud extends from minor calyces and dilates at end, wrapping around the glomerular tuft and enclosing it in a double membrane (parietal and visceral)

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18
Q

What kind of epithelia lines the Bowman’s capsule?

A

Simple squamous

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19
Q

Which two membranes form the filtration barrier of the glomerulus?

A
  • Capillary endothelium

- Visceral layer of the Bowman’s capsule

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20
Q

Explain how the composition of the filtration barrier aids in the filtration of the blood through the glomerulus (3)

A
  • Fenestrated capillary endothelium = very leaky!
  • Podocytes invest in capillary endothelium using foot processes and produce filtration slits between processes
  • Shared basement membrane minimises resistance to filtration
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21
Q

Describe the histological appearance of the PCT (3)

A
  • Simple cuboidal epithelia arranged in circles
  • Pronounced BRUSH BORDER on luminal/apical surface to increase surface area for reabsorption
  • Centrally positioned nuclei
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22
Q

What type of cells line the limbs of the loop of Henle and how can they be distinguished from other structures? (2)

A
  • Simple squamous epithelia line the thin descending limb (looks like small capillary but no RBC)
  • Simple cuboidal epithelia line the thick ascending limb (but no brush border like PCT)
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23
Q

How does the DCT differ histologically from the PCT? (3)

A
  • Larger lumen
  • Nuclei positioned towards the apical/luminal surface
  • NO BRUSH BORDER
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24
Q

Where does the DCT make contact with the glomerulus?

A

Juxtaglomerular apparatus

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25
Q

Name 3 types of cells which are located in the juxtaglomerular apparatus (3)

A
  • Macula densa (DCT)
  • Juxtaglomerular cells (afferent arteriole)
  • Extraglomerular mesangial cells
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26
Q

Describe the histological appearance of the collecting duct (3)

A
  • Simple cuboidal epithelia (continuation of DCT)
  • Similar appearance to thick ascending limb of loop of Henle however lumen is larger and more irregular
  • No brush border
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27
Q

Describe the histological appearance of the ureter (4)

A
  • Transitional (stratified) epithelia
  • Lamina propria
  • NO SUBMUCOSA
  • Muscularis externa (2 layers - circular and longitudinal, however 3rd layer appears in the lower 1/3)
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28
Q

Describe the composition of the bladder wall and how it is adapted to its function (3)

A
  • Transitional stratified epithelia with 3 layers of muscle
  • Allows distension of bladder for urine storage
  • Provides thick barrier to prevent leaking of urine and bacteria into rest of body
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29
Q

Which part of the embryo does the urogenital system develop from?

A

Intermediate mesoderm

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30
Q

Why is the development of the urogenital system described as “sequential”?

A
  • 3 systems develop sequentially from the intermediate mesoderm (pronephros, mesonephros and metanephros)
  • Disappearance of one system marks start of development of the next in a craniocaudal direction
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31
Q

Roughly at what time during development does the pronephros regress and mesonephros begin to develop?

A

End of the 4th week

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32
Q

What is the role of the pronephros in humans?

A
  • No significant role in humans

- HOWEVER the pronephric duct extends from the cervical region to the cloaca so drives the next developmental stage

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33
Q

What is the urogenital ridge?

A

Region of intermediate mesoderm which gives rise to both the embryonic kidney and gonad

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34
Q

What does the mesonephros consist of and what is its role?

A
  • Consists of the mesonephric tubule and mesonephric duct

- Functions as the interim/embryonic kidney before development of the true kidney (metanephros)

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35
Q

What are the two main roles of the mesonephric duct in the development of the urogenital system?

A
  • Sprouts the ureteric bud which induces development of the definite kidney
  • Contributes to the development of the male reproductive system
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36
Q

What does the ureteric bud contribute to? (4)

A
  • Ureters
  • Renal pelvis
  • Major and minor calyces
  • Collecting ducts
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37
Q

What part of the metanephros is the nephron formed from?

A

Metanephric blastema (mesenchyme)

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38
Q

Explain the role of the ureteric bud in the development of the collecting systems and excretory systems of the kidney (2)

A
  • Collecting system derived from the ureteric bud itself
  • Excretory system derived from the metanephric blastema under the influence of growth signals released from the ureteric bud
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39
Q

What is the main cause of renal agenesis?

A

Ureteric bud fails to interact with the intermediate mesoderm

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40
Q

Name two consequences of splitting of the ureteric bud (2)

A
  • Duplicate kidney

- Ectopic ureteral openings

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41
Q

What might be a potential consequence of atresia of a ureter?

A

Multicystic kidney disease

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42
Q

What separates the cloacal membrane into the urogenital sinus and the hindgut?

A

Urorectal septum

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43
Q

What connects the urachus to the umbilicus?

A

Medial umbilical ligament

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44
Q

Describe the division of the urogenital sinus (2)

A
  • Upper portion forms future bladder

- Lower portion split into pelvic and phallic regions which form the male and female urethra

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45
Q

Which two structures make openings in the urogenital sinus which contribute to the formation of the male reproductive tract?

A
  • Ureteric bud

- Mesonephric duct

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46
Q

What is the fate of the mesonephric duct in males and females? (2)

A
  • Males: contributes to the formation of the prostate and prostatic urethra
  • Female: regresses as the urogenital sinus expands
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47
Q

What does the pelvic portion of the urogenital sinus contribute to in the female?

A

Female urethra

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48
Q

What are the 4 parts of the male urethra? (4)

A
  • Pre-prostatic
  • Prostatic
  • Membranous
  • Spongy
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49
Q

Which part of the male urethra does the phallic portion of the urogenital sinus contribute to?

A

Spongy portion

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50
Q

What is hypospadias and how is it caused? (2)

A
  • Urethra opens up onto the ventral surface of the penis instead of the glans penis
  • Defect in the fusion of urethral folds
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51
Q

What is normal renal blood flow?

A

1.1L/min

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52
Q

What percentage of blood is plasma?

A
  • ~55%

- ~45% is haemocrit (RBC and plasma proteins)

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53
Q

How do you calculate the renal plasma flow (RPF)?

A
  • Renal blood flow x %plasma in blood

- 1.1L/min x 0.55 = 0.605L/min (605mL/min of plasma)

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54
Q

Describe the composition of a renal lobe

A

Consists of a renal pyramid and the renal cortex above it, containing a nephron, arcuate artery and many interlobular arteries

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55
Q

The afferent arteriole is a branch of which artery?

A

Interlobular artery

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56
Q

Name the two types of nephron and state their %distribution in the kidneys (2)

A
  • Cortical (90%)

- Juxtomedullary (10%)

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57
Q

Describe the location of a juxtamedullary nephron

A

Inner cortex of the kidney, in close proximity to the medulla

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58
Q

Roughly how much blood is filtered by the glomerulus at any one time?

A

20%

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59
Q

Describe how the arteriolar structure helps to maintain a high hydrostatic pressure in the glomerulus

A
  • Afferent arteriole is wider than efferent arteriole so the rate of blood flow into glomerulus is greater than the rate of blood flow out
  • This increases the hydrostatic pressure of the blood in the capillaries which is the main force used to drive fluid out into the filtrate
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60
Q

What is the function of the basement membrane?

A
  • Forms a glycoprotein mesh which is negatively charged

- Repels proteins from being filtered out of the glomerulus but allows the passage of cations and small molecules

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61
Q

Describe the filtration barrier surrounding the glomerulus (3)

A
  • Fenestrated capillary endothelium allow passage of solutes and plasma but not RBC or large proteins
  • Glycoprotein basement membrane allows passage of plasma but repels proteins due to negative charge
  • Podocyte foot processes wrap around capillaries and interdigitate to form a mesh against large molecules passing through
62
Q

What is the consequence of losing the negative charge of the basement membrane?

A
  • Proteinuria

- Large proteins are not repelled so can be filtered through - this may also cause damage to the filtration barrier

63
Q

Describe why the clearance ratio for anions is less than the ratio for cations

A

Anions are negatively charged so are repelled by the glycoprotein basement membrane, therefore less are filtered out of the blood (~less clearance by kidneys)

64
Q

Explain the forces involved in the filtration of plasma to form ultrafiltrate (3)

A
  • Hydrostatic force of the glomerular capillaries drives fluid out into the tubule
  • Hydrostatic force of the Bowman’s capsule opposes hydrostatic force of glomerulus
  • Oncotic pressure difference in Bowman’s capsule opposes hydrostatic force of glomerulus
65
Q

Explain why there is an oncotic pressure difference between the glomerulus and the Bowman’s capsule

A
  • As plasma is filtered out of the blood and proteins remain, the oncotic pressure of the glomerular capillaries increases
  • The ultrafiltrate is relatively protein-free compared to the blood therefore there is an oncotic pressure gradient driving fluid back into the capillary from the tubule, however this is counteracted by the hydrostatic capillary pressure so the net movement of plasma is out of the capillary and into the tubule
66
Q

Explain how capillary filtration pressure is maintained despite changes in MABP (3)

A
  • Myogenic auto-regulation of SM cells in the afferent arteriole controls the amount of blood entering the glomerulus
  • Increases in blood pressure will stimulate vasoconstriction of SM cells in afferent arteriole which increases resistance to flow
  • Flow decreases therefore pressure decreases so capillary pressure is maintained
67
Q

Explain the role of the macula densa cells of the DCT in regulating GFR (3)

A
  • Increase in MABP causes increase in GFR which causes increase in Na+ and Cl- filtration
  • Increase in [NaCl] is sensed by macula densa in the DCT which stimulates release of Adenosine which dilates the efferent arteriole therefore decreasing glomerular hydrostatic pressure and GFR
68
Q

Describe the tubular-glomerular feedback mechanism in response to a low [NaCl] in the DCT (2)

A
  • Low [NaCl] sensed by macula densa suggests decreased GFR
  • Release of prostaglandins from macula densa cells causes vasodilation of the afferent arteriole ~ increased blood flow into glomerulus so hydrostatic pressure increases, therefore GFR increases
69
Q

Where does the majority of reabsorption of solutes take place?

A

PCT

70
Q

Explain how a Na+ gradient is produced in the cells of the PCT (2)

A
  • Na+/K+ ATPase on the basolateral membrane actively transports 3Na+ out of the cell into the interstitium
  • This decreases the [Na+]i therefore Na+ from the tubule fluid diffuses passively into the cell down a concentration gradient
  • This gradient is utilised by other channels via secondary active transport
71
Q

Which 2 sodium channels are present on the apical surface of the PCT?

A
  • Na+/H+ antiporter

- Na+/Glucose symporter

72
Q

Describe the mechanism of glucose uptake in the PCT (2)

A
  • SGLUT channel on the apical surface utilises Na+ gradient (set up by Na+/K+ ATPase) to actively transport glucose across into the cell against its conc gradient
  • Glucose is then transported across the basolateral membrane by facilitated diffusion
73
Q

What is the consequence of exceeding the transport maximum, Tm? (2)

A
  • POLYURIA
  • If the plasma conc of glucose exceeds Tm then the rest is excreted in the urine (glycosuria)
  • Water follows to maintain an isosmotic gradient in the tubule therefore more water is excreted resulting in polyuria
74
Q

What is the difference between transcellular and paracellular transport?

A
  • Transcellular is transport of substances through the cell, from the apical to basolateral membrane
  • Paracellular is transport of substances across epithelium by passing through the intercellular spaces between cells
75
Q

Name 3 substances which can be secreted into the tubule lumen (3)

A
  • K+
  • H+
  • HCO3-
76
Q

Name 2 substances which can be used to estimate GFR and explain how (2)

A
  • Inulin or Creatinine
  • RC = UV/P where RC= renal clearance, U= urine conc (mg/mL), V= volume of urine per min (mL/min), P= plasma conc
  • Use to estimate GFR
77
Q

Which equation would you use to calculate eGFR and why? (2)

A
  • Cockcroft-Gault formula

- Takes into account mass and age to predict creatinine clearance

78
Q

What are the 4 stages of drug pharmacokinetics?

A
  • Absorption
  • Distribution
  • Metabolism
  • Excretion
79
Q

Define ‘clearance’ of a drug

A

Rate of removal/elimination of the drug by the liver and kidneys through metabolism and excretion

80
Q

Give one use of knowing the half life of a drug

A

Can describe the way a drug is removed from the body thus can be used to inform dosing regimes

81
Q

How do you calculate the half life of a drug?

A

0.693 X Vd / Clearance

82
Q

What would you expect the clearance rate of a lipophilic drug to be and why?

A
  • Low

- Lipophilic drugs can diffuse freely across the lipid bilateral so are more easily reabsorbed

83
Q

Name 4 molecular factors that can affect the movement of free drug between tissue and fluid compartments

A
  • Lipophilicity (more easily reabsorbed)
  • Hydrophilicity (more easily excreted)
  • Degree of binding to plasma proteins (less filtered)
  • Degree of binding to tissue proteins (e.g. muscle)
84
Q

What is the main consequence of drugs binding to tissue compartments?

A

Reduces free plasma concentration of drug

85
Q

What is the ‘apparent volume of distribution’? (2)

A
  • Theoretical Vd by modelling all fluid and tissue compartments as one big ‘apparent fluid compartment’
  • Measure the real plasma concentration of the drug
86
Q

Which type of drug will have a large volume of distribution, lipophilic or hydrophilic? What effect will this have on the half life? (2)

A

Lipophilic - can dissolve in adipose tissue, so less available in plasma to be excreted, therefore will have a longer half life

87
Q

Explain how liver metabolism of a drug makes it more excretable by the kidneys

A
  • Phase I and phase II enzymes add polar groups to drug to increase its ionic charge
  • More hydrophilic so is more easily excreted by the kidneys into the urine (charge makes it difficult to reabsorbed as it cannot pass freely across tubule cells)
88
Q

What will happen to weak acid anions in an acidic urine (low pH)?

A
  • More likely to be PROTONATED so will become electroneutral

- Increases lipophilicity so more easily reabsorbed and less likely to be excreted

89
Q

What will happen to weak acid anions in an alkaline urine (high pH)?

A
  • Less likely to be protonated as less H+ available so will remain charged
  • Decreases lipophilicity so more easily excreted and less likely to be reabsorbed
90
Q

What will happen to weak bases in an alkaline urine (high pH)?

A
  • More likely to be DEPROTONATED so will become electroneutral
  • Increases lipophilicity so more easily reabsorbed and less likely to be excreted
91
Q

What will happen to weak bases in an acidic urine (low pH)?

A
  • Less likely to be deprotonated as more H+ available so will remain charged
  • Decreases lipophilicity so more easily excreted and less likely to be reabsorbed
92
Q

Name 3 organic cations (drugs) which are readily secreted in the PCT of the kidneys

A
  • Penicillin
  • Ranitidine
  • Metformin
93
Q

Explain how OCTs can be targeted therapeutically to increase the half life of some drugs e.g. Penicillin

A
  • OCTs can be competitively inhibited to block the secretion of certain drugs
  • This allows the drug to remain in the plasma for longer, thereby increasing its half life
94
Q

Describe how CHD may affect renal clearance

A

Reduced cardiac output leads to reduced renal vascular supply and therefore reduces GFR so will decrease renal clearance

95
Q

Describe how liver disease can affect renal clearance (2)

A
  • Decreased drug metabolism by phase I and II enzymes will reduce renal clearance
  • Decreased production of plasma proteins will cause increase in free plasma conc of drug therefore will increase renal clearance
96
Q

How would you calculate the clearance rate of a given solute?

A

Urine conc X rate of urinary flow / plasma conc

97
Q

What 2 concentrations must to know to calculate the physiological clearance of a marker?

A
  • Plasma concentration of marker

- Urine concentration of marker

98
Q

Which 2 substances are commonly used as physiological markers for measuring renal clearance?

A
  • Inulin

- Creatinine

99
Q

Describe 2 properties of a physiological marker

A
  • Must not be synthesised or stored in the kidneys

- Must be filtered but not reabsorbed or secreted

100
Q

Give an example of a physiological marker which can be used to measure RPF

A

ParaAmino Hippuric acid (PAH)

101
Q

Why is creatinine generally used over inulin as a physiological marker?

A

Although inulin is often more precise, it needs to be injected and is relatively expensive, so creatinine is a good endogenous alternative (produced by the body naturally through breakdown of creatine(phosphate))

102
Q

How can measuring creatinine sometimes lead to an overestimate of GFR?

A
  • Creatinine is also secreted from the blood in the PCT (10-20%)
  • Urine conc of creatinine will increase leading to an overestimate of the GFR
103
Q

Why can you not just add water to increase the plasma volume (ECV)?

A

This would change the plasma osmolarity - need to move osmoles (Na+) and water will follow to maintain an isosmotic solution

104
Q

How much of the filtered Na+ is reabsorbed in the PCT?

A

~60-70%

105
Q

What would happen to Na+ following an increase in renal BP?

A
  • Na+ reabsorption would DECREASE (reduced expression of Na/H channels and Na+/K+ ATPase in PCT)
  • Therefore decreased water reabsorption in PCT and increased excretion of water and Na+ (naturesis and diuresis)
  • Causes a decrease in ECF volume therefore reduces BP
106
Q

What would happen to Na+ following a decrease in GFR? (2)

A

Increase in Na+ (and therefore water) reabsorption to increase ECV and BP; activation of RAAS assists this

107
Q

What can a CT scan of the kidneys be used to identify? (4)

A
  • Stones
  • Infection
  • Tumour
  • Trauma
108
Q

What is a intravenous urogram and what is it used for? (2)

A
  • Plain radiograph with contrast (X ray)

- Good for viewing collecting system e.g. pelvis and ureters

109
Q

Give 3 advantages of using ultrasound (3)

A
  • Can asses flow
  • Non-ionising
  • Cheap
110
Q

What methods of radiology could be used to diagnose renal stones/canniculi? (2)

A
  • Plain radiograph/X ray +/- contrast

- CT scan +/- contrast

111
Q

What is the normal concentration of K+ in the ECF?

A

3-5mmol/L

112
Q

What percentage of total body K+ is intracellular/extracellular?

A

98% ICF and 2% ECF

113
Q

Why is it important to maintain EC[K+]? (2)

A
  • Effect on resting membrane potential

- Hyperkalaemia or hypokalaemia can have an effect on the RMP of cardiac myocytes, causing cardiac arrhythmias

114
Q

How does the K+ concentration contribute to the RMP? (2)

A
  • RMP is set up by the selective permeability of the membrane to K+
  • K+ moves out of cells passively down a conc gradient and moves into cells by the action of Na/K ATPase
  • Therefore RMP lies close to the equilibrium potential for K+
115
Q

Describe how EC[K+] affects the threshold for action potentials (2)

A
  • High ECF K+ raises the threshold for the resting membrane potential (becomes more positive)
  • Low ECF K+ lowers the threshold for the resting membrane potential (becomes more negative)
116
Q

Explain how ECF K+ balance is maintained (2)

A
  • Immediate control - adjusting K+ internal balance

- Longer term control - adjusting K+ renal excretion

117
Q

Which specific cells have a high intracellular concentration of K+? (4)

A
  • Skeletal muscle cells
  • Hepatocytes
  • Red blood cells
  • Bone
118
Q

How long does it take for K+ excretion from the kidneys?

A

6-12hrs after absorption from the gut

119
Q

Which channels are involved in maintaining an internal balance of K+?

A
  • Na+/K+ ATPase

- K+ channels

120
Q

Give 3 factors which affect the rate of K+ shift INTO cells (3)

A
  • Hormones (insulin, aldosterone, catecholamines act via Na+/K+ ATPase)
  • Hyperkalaemia (high ECF [K+])
  • Alkalosis (K+ shift into cells and H+ shift out)
121
Q

Give 5 factors which promote K+ shift OUT of cells (5)

A
  • Exercise
  • Cell lysis
  • Increase in ECF osmolality
  • Hypokalaemia (low ECF [K+])
  • Acidosis (K+ shift out and H+ shift into cell)
122
Q

Explain how insulin increases K+ shift into cells

A

Increases activity of Na+/K+ ATPase, therefore increases K+ uptake by muscle and liver cells

123
Q

Name 3 hormones which stimulate the Na+/K+ ATPase channel and therefore K+ uptake by cells (3)

A
  • Insulin
  • Aldosterone
  • Catecholamines e.g. Adrenaline
124
Q

Explain the effect of exercise on K+ uptake by cells (3)

A
  • Net release of K+ following action potential of skeletal muscle cells during contraction (K+ efflux)
  • Release of K+ by damaged muscle cells
  • Release of catecholamines during exercise promotes K+ uptake by non contracting cells to prevent hyperkalaemia
125
Q

Explain how acidosis can lead to hyperkalaemia (2)

A
  • High ECF [H+] promotes uptake of H+ by cells and K+ shift out of cells in exchange
  • This increases the ECF [K+] which can lead to hyperkalaemia
126
Q

Explain how alkalosis can lead to hypokalaemia (2)

A
  • Low ECF [H+] promotes excretion of H+ from cells and K+ shift to cells in exchange
  • This decreases the ECF [K+] which can lead to hypokalaemia
127
Q

Explain how hyperkalaemia can also lead to acidosis

A

Shift of K+ into cells in an attempt to decrease the ECF concentration leads to reciprocal shift of H+ out of cells which decreases the pH of the ECF leading to acidosis

128
Q

Which region(s) of the nephron are involved in regulating K+ secretion?

A

Late DCT and cortical collecting duct

129
Q

What determines the rate of renal K+ reabsorption/secretion?

A

Plasma concentration of K+

130
Q

Describe which regions of the nephron are involved in K+ REABSORPTION (3)

A
  • PCT (67% reabsorbed)
  • Thick ascending limb (20% reabsorbed)
  • DCT/collecting duct (10-15% reabsorbed)
131
Q

Which cells of the DCT/cortical collecting duct are involved in K+ secretion?

A

Principal cells

132
Q

Which cells of the DCT/collecting duct are involved in K+ reabsorption?

A

Intercalated cells

133
Q

Describe the action of K+ secretion in the principal cells of the DCT/cortical collecting duct (2)

A
  • Na+/K+ ATPase sets up intracellular gradients of Na+ and K+ (high K+ sets up chemical gradient)
  • Low intracellular Na+ promotes Na+ uptake into cell from lumen via ENaC which sets up a negative lumen potential, promoting K+ secretion into the lumen via apical K+ channels down an electrochemical gradient
134
Q

Explain the role of aldosterone in K+ secretion at the DCT (3)

A
  • Increases number of ENaC and apical K+ channels on apical membrane of principal cells
  • Increases activity of Na+/K+ ATPase on basolateral membrane
  • Aldosterone secretion promoted by high ECF [K+] therefore it promotes secretion of K+
135
Q

Explain how acid-base status of the plasma affects K+ secretion from the kidneys (2)

A
  • Acidosis stimulates K+ shift out of cells, therefore inhibits Na+/K+ ATPase on the basolateral membrane, so reduces K+ secretion
  • Alkalosis stimulates K+ shift into cells, therefore activates N+/K+ ATPase on the basolateral membrane, so increases K+ secretion
136
Q

Describe 2 luminal factors which increase K+ secretion in the nephron (2)

A
  • Increased distal tubular flow rate washes away K+ in lumen so maintains a gradient between the cell and lumen for K+ to flow
  • Increased Na+ delivery to distal tubule results in more Na+ reabsorbed therefore more K+ secreted
137
Q

Which channel is involved in K+ absorption in the DCT and where is it located?

A
  • H+/K+ ATPase (extrudes H+ in exchange for K+ influx)

- Apical membrane of intercalated cells in late DCT

138
Q

Describe how ACE inhibitors may lead to decreased renal exertion of K+ (2)

A
  • Inhibit formation of Angiotensin II which stimulates aldosterone secretion
  • Aldosterone increases K+ secretion therefore a lack of will lead to K+ retention and hyperkalaemia
139
Q

Describe 3 ways in which diabetic ketoacidosis can lead to hyperkalaemia (3)

A
  • Lack of insulin in type I diabetics will lead to decreased activity of Na+/K+ ATPase therefore decreased K+ into cells
  • Ketoacidosis causes K+ shift out of cells in exchange for H+
  • Increased plasma osmolarity due to high glucose concentration of plasma promotes K+ shift out of cells into ECF
140
Q

Give 2 examples of where cell lysis may lead to hyperkalaemia (2)

A
  • Tumour lysis syndrome

- Muscle crush injuries

141
Q

Give 5 possible physiological causes of hyperkalaemia (5)

A
  • Metabolic acidosis
  • Acute/chronic kidney injury
  • Cell lysis (trauma)
  • Diabetic ketoacidosis
  • Addison’s disease
142
Q

Give 2 possible drug classes which may lead to hyperkalaemia (2)

A
  • ACEI

- K+ sparing diuretics

143
Q

Explain the effects of hyperkalaemia on the heart

A
  • Depolarised cardiac tissue is more difficult to repolarise following action potential - more Na+ changes remain in inactive form
  • Heart tissue is less excitable - can lead to arrhythmia/heart block
144
Q

Describe the ECG changes that occur in hyperkalaemia

A
  1. High T wave
  2. Prolonged PR segment, ST segment depression
  3. Absent P wave, intraventricular block, wide QRS complexes
  4. Ventricular fibrillation
145
Q

Give 3 clinical features of hyperkalaemia (3)

A
  • Heart: arrhythmia/heart block due to altered excitability
  • GI: paralytic ileus due to neuromuscular dysfunction
  • Acidosis
146
Q

Explain how you would treat a patient with hyperkalaemia in an emergency (3)

A
  • IV calcium gluconate (reduce K+ effect on cardiac tissue)
  • IV insulin + dextrose and nebulise β agonists (increase K+ uptake via Na+/K+ ATPase)
  • Dialysis (remove excess K+)
147
Q

Explain how you would treat hyperkalaemia in the long term (3)

A
  • Reduce dietary potassium intake
  • Stop medications which may be causing it (ACEI, diuretics)
  • Oral K+ binding resins to reduce absorption from gut
148
Q

Give 3 possible causes of hypokalaemia due to excessive loss of K+ from the kidneys (3)

A
  • Diuretic drugs promoting Na+ absorption (leads to K+ secretion)
  • Cushing’s syndrome (high mineralocorticoid levels)
  • Osmotic diuresis (diabetes)
149
Q

Describe the clinical features of hypokalaemia (4)

A
  • Heart: altered excitability (more excitable as membrane is easily hyperpolarised)
  • GI: paralytic ileus due to neuromuscular dysfunction
  • Skeletal: muscle weakness due to neuromuscular dysfunction
  • Renal: Diabetes insipidus (unresponsive to ADH)
150
Q

Describe the ECG changes that occur in hypokalaemia

A
  1. Low T wave (flattened)
  2. High U wave
  3. Low ST segment
151
Q

Describe the treatment for hypokalaemia (2)

A
  • IV/oral K+ replacement

- If mineralocorticoid related: K+ sparing diuretics e.g. Spironolactone (inhibits action of aldosterone)

ESA3 Harpreet :) (5 decks)

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