Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Semester 3 > Urinary Session 6 > Flashcards

Urinary Session 6 Flashcards

1
Q

What ensures tight regulation of the narrow range of hydrogen ion concentration needed to control pH?

A

Kidney via variable recovery of HCO3- and active secretion of H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Is alkalaemia or acidaemia more severe?

A

Alkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens in alkalaemia?

A

Calcium crystallises causing hypocalcaemia and thus increased neuronal excitability –> parasthesia and tetany

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What causes respiratory alkalaemia?

A

Hyperventilation –> hypocapnia –> increased pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens in acidaemia?

A

Increases plasma potassium concentration affecting RMP –> arrythmias
Denatures proteins –> deranged muscle contractility, glycolysis and hepatic function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What causes respiratory acidaemia?

A

Hypoventilation –> hypercapnia –> decreased pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How are changes in pH detected by the body?

A

Peripheral chemoreceptors detect pCO2 and pH causing rapid but small effect
Central chemoreceptors detect pCO2 changes and take longer to come into effect but are responsible for 80% of effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the normal range of blood pH?

A

7.35-7.45

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the main site of HCO3- production?

A

Erythrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What controls HCO3- concentration?

A

Kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do the kidneys keep pH stable?

A

Compensate for changes in HCO3- concentration to keep [HCO3-]/[CO2] constant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the kidney reaction to respiratory alkalaemia?

A

Decrease [HCO3-]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is kidney control of [HCO3-] in respiratory alkalosis/acidosis correction as opposed to control?

A

Primary cause has not been altered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens when a decrease in pH is detected by peripheral chemoreceptors?

A

Stimulates respiratory neurones in medulla –> increases ventilation to decrease pCO2 –> shifts eqm to correct pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes decreased [HCO3-] in metabolic acidosis?

A

Acid from tissues reacting with and thus removing HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why does increasing ventilation compensate for metabolic acidosis?

A

Removes additional carbon dioxide which is formed due to reaction of acid from tissues and HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does repeated vomiting lead to an increase in pH?

A

Loss of H+ –> increased H+ production for replacement –> increased HCO3- as a by product

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What detects the decrease in pH seen in metabolic alkalosis?

A

Peripheral chemoreceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What can metabolic alkalaemia only be partially compensated for by decreasing ventilation?

A

Risk of hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What corrects metabolic driven changes in pH?

A

Kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How can the kidneys decrease [HCO3-]?

A

Easily by not recovering all that is filtered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What must the kidney do in order to increase [HCO3-]?

A

Recover all filtered HCO3- and make new HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does the kidney make new HCO3-?

A

Due to high metabolic rate produce lots of CO2 which reacts with water to form HCO3- which moves into the plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How can amino acids be used to make HCO3-?

A

a.a. –> HCO3- + NH4 + alpha-ketoglutarate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where does formation of HCO3- from amino acids take place?

A

PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Where does 80% of HCO3- reabsorption occur?

A

PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does the sodium gradient set up by Na-K-ATPase allow for reabsorption of HCO3-?

A

Drives H+ out via NHE-3 which reacts in the lumen with HCO3- to form CO2 –> CO2 moves into cell and reacts with water to reform HCO3- which moves into the ECF via Na-HCO3 co transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What needs to happen in order for cells producing CO2 to continue HCO3- production?

A

H+ needs to be secreted and buffered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How is H+ removed from the DCT?

A

Actively by H+ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How is urine pH buffered so that it remains >4.5 to prevent damage to cells lining the urinary tract?

A

H+ in lumen reacts with HPO4+ and excreted NH3+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Ammonia diffuses freely but ammonium does not, why?

A

Ammonium has a positive charge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What change in pH can tubular cells detect?

A

Intracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What happens in the tubular cells if ECF [HCO3-] decreases?

A

More HCO3- moves out of the cells into the ECF –> more H+ in cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What happens in the tubular cells if ECF [HCO3-] increases?

A

Tubular cell pH increases –> increased H+ secretion and deceased HCO3- recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe the action of NHE in volume depletion.

A

Works to reabsorb sodium thus favouring H+ secretion and HCO3- recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How is H+ buffered in the proximal tubule?

A

Ammonium formed by HCO3- production dissociates into NH3+ and H+ –> NH3+ diffuses out of cell and reacts with H+ in the lumen to reform NH4+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the tubular cellular responses to acidosis?

A

Na+/H+ exchanger activity increases
Enhanced breakdown of glutamine and therefore enhances ammonium production
Enhanced H+ATPase activity in DCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the overall result of the tubular cellular responses to acidosis?

A

Increased capacity to export HCO3- from tubular cells to ECF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How is the anion gap calculated?

A

([Na+] + [H+]) - ([Cl-] + [HCO3-])

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What increases the anion gap?

A

Other anions from metabolic acids replace HCO3- E.g. Lactate in profound shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Do all forms of metabolic acidosis create and anion gap?

A

No, in renal problems HCO3- is replaced with Cl- therefore the gap is constant but [HCO3-] is decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What post assign disturbance does metabolic acidosis lead to?

A

Hyperkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How does metabolic acidosis lead to a potassium disturbance?

A

Increased H+ outside cells –> increased movement in –> K+ move out into ECF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What effect does metabolic acidosis have on the distal nephron?

A

Increases potassium reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What potassium disturbance does metabolic alkalosis lead to?

A

Hypokalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How does metabolic alkalosis lead to a potassium disturbance?

A

Decreased H+ outside cells causes movement out –> K+ moves into cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What effect does metabolic alkalosis have on the distal nephron?

A

Decreases K+ reabsorption

48
Q

How does hyperkalaemia effect HCO3- excretion?

A

Increased pH of tubular cells –> H+ move out into ECF –> HCO3 excretion favoured

49
Q

How does hypokalaemia lead to an acid-base disturbance?

A

Decreased intracellular pH of tubular cells –> H+ into cells –> favours H+ excretion and HCO3- recovery –> metabolic alkalosis

50
Q

Why are the anions usually at a lower level than the cations when calculating the anion gap in a normal pt?

A

Unaccounted for anions which are associated with metabolic acids

51
Q

Where is the majority of K+ found in the body?

A

ICF of skeletal muscle, liver, bone and red blood cells

52
Q

What is the effect of ECF [K+] on establishing resting membrane potential?

A

Increasing [K+]i and decreasing [K+]o means K+ moves out of cell taking +be charge with it, establishing RMP

53
Q

What maintains the difference between ICF and ECF [K+] under tight control?

A

Na-K-ATPase

54
Q

How does increasing and decreasing ECF [K+] affect the RMP of cells?

A

Decrease: increases K+ gradient –> more K+ leaves, hyperpolarising cell
Increase: reduces K+ gradient –> less K+ leaves so depolarises cell

55
Q

What type of mechanism controls meal-driven kidney K+ excretion?

A

-ve feedback

56
Q

What happens upon absorption of dietary K+ in the intestine and colon which leads to meal-driven kidney K+ excretion?

A

Substantial amount of K+ enters ECF –> plasma K+ increases –> excretion

57
Q

What happens to 4/5ths of absorbed dietary K+?

A

Sequestered in liver and muscle cells

58
Q

What happens upon activation of splanchnic sensors by absorption of dietary K+?

A

Feed forward regulation signals from vagus nerve to stimulate meal driven K+ excretion

59
Q

Why does intracellular buffering have an important role in meal-driven potassium excretion?

A

Kidneys cannot excrete K+ fast enough

60
Q

Give some examples of potassium rich foods.

A 
Beans
Raisins 
Fruit
Potatoes
Milk
61
Q

What is internal balance of potassium regulation?

A

Net of 2 processes which shifts K+between ECF and ICF for immediate effects for moment to moment control

62
Q

How does K+ move from the ECF into cells?

A

Via Na-K-ATPase

63
Q

How does K+ move from cells into ECF?

A

ROMK

64
Q

What factors increase potassium uptake by cells?

A

Hormones
Increase [K+] in ECF
Alkalosis

65
Q

Which hormones increase K+ uptake by cells?

A

Insulin
Aldosterone
Catecholamines

66
Q

How do insulin and aldosterone increase potassium uptake by cells?

A

Increased potassium levels in blood stimulate their release which then increases Na-K-ATPase activity

67
Q

How does physiological stress increase potassium uptake into cells?

A

Stimulate catecholamine release –> beta-2-adrenoreceptors –> stimulate Na-K-ATPase

68
Q

What factors cause increased potassium efflux from cells?

A 
Exercise
Cell lysis
Increase in ECF osmolality
Decreased ECF [K+]
Acidosis
69
Q

How does exercise increase potassium efflux from cells?

A

Potassium pump cannot keep up with increased demand so there is net post assist release during action potential recovery
Damage to myocytes causes potassium release

70
Q

When might cell lysis causing increased efflux of potassium by cells occur?

A

Rhabdomyolysis
Intravascular heamolysis
Chemotherapy

71
Q

How does an increase in ECF osmolality cause potassium efflux from cells?

A

Water moves out of cell thus increasing the ICF levels of potassium and creating a steeper gradient which the potassium moves down

72
Q

When is potassium efflux due to an increase is ECF osmolality seen?

A

Diabetic ketoacidosis

73
Q

How long does external balance of K+ regulation take to act?

A

6-12 hrs to excrete load

74
Q

What is external balance of K+ regulation responsible for?

A

Control of total body potassium over the longer term

75
Q

How do the kidneys adjust K+ excretion to match intake?

A

Controlling secretion

76
Q

Where is the majority of potassium reabsorbed?

A

PCT and thick ascending limb of Henle’s loop

77
Q

Where is potassium secreted?

A

DCT

Principal cells of cortical CD

78
Q

In renal handling of potassium, what remains constant regardless of K+ levels in the blood?

A

% reabsorption

79
Q

How are low-high K+ diets counteracted?

A

Variable K+ secretion by principal cells of DCT and cortical CD

80
Q

What luminal factors affect potassium secretion in the distal tubule and collecting duct?

A

High distal tubular flow rate to wash away luminal potassium and maintain gradient
High sodium delivery to DCT causes more sodium reabsorption and therefore increased potassium loss

81
Q

What tubular factors affect potassium secretion?

A

ECF [K+]
Aldosterone
Acid-base status

82
Q

How does ECF [K+] affect potassium secretion?

A

Directly stimulates Na-K-ATPase
Increase permeability of apical K+ channels
Stimulates aldosterone secretion

83
Q

How does aldosterone affect potassium secretion?

A

Increase transcription of Na-K-ATPase, K+ channels and ENaC therefore reabsorb more sodium and excrete more K+

84
Q

How does acid-base status affect K+ secretion?

A

Acidosis decreases potassium secretion as it inhibits Na-K-ATPase and decreased K+ channel permeability
Alkalosis increased potassium secretion by having an opposing action

85
Q

How is potassium absorbed by intercalated cells in DCT and cortical CD?

A

Active process mediated by H+-K+-ATPase in the apical membrane

86
Q

What effect does acidosis have on K+ absorption by intercalated cells in DCT and cortical CD?

A

Increases pumping of K+ into cells

87
Q

What can cause an external shift of potassium leading to hyperkalaemia?

A 
Increased intake and renal dysfunction 
Inappropriate IV dose
AKI/chronic kidney injury
K+ excretion blocking drugs
Decreased aldosterone state
88
Q

What can cause an internal shift of potassium and lead to hyperkalaemia?

A

Diabetic ketoacidosis
Cell lysis
Metabolic acidosis/exercise

89
Q

What effects of diabetic ketoacidosis cause an internal shift of potassium?

A

Lack of insulin
Plasma hyperosmolarity
Metabolic acidosis

90
Q

How does Addison’s disease lead to hyperkalaemia?

A

Causes low aldosterone state hence low plasma sodium and high plasma potassium levels

91
Q

What can cause an external shift of potassium leading to hypokalaemia?

A

Excessive GI loss in diarrhoea/bulimia/vomiting
Excessive renal loss by diuretics
Osmotic diuresis
High aldosterone state

92
Q

What can cause an internal shift of potassium leading to hypokalaemia?

A

Metabolic alkalosis

93
Q

What is the clinical relevance of hyperkalaemia on the heart?

A

Depolarises cardiac tissue –> more fast sodium channels in inactive form –> heart less excitable –> arrythmias and heart block

94
Q

What is the clinical relevance of hyperkalaemia in the GI tract?

A

Neuromuscular dysfunction –> paralytic ileus

95
Q

How is paralytic ileus identified O/E?

A

Decreased bowel sounds

96
Q

What is the clinical relevance of hypokalaemia in the heart?

A

Hyperpolarises cardiac tissue –> more fast sodium channels in active form –> heart more excitable causing arrythmias

97
Q

What is the clinical relevance of hypokalaemia on the GI tract?

A

Paralytic ileus

98
Q

What is the clinical relevance of hypokalaemia in skeletal muscle?

A

Neuromuscular dysfunction –> muscle weakness

99
Q

What is the clinical relevance of hypokalaemia on the kidneys?

A

Unresponsive to ADH –> neohrogenic diabetes incipidus

100
Q

What are the progressive ECG changes seen in worsening hyperkalaemia?

A

High T wave –> increased PR, decreased ST, high T wave –> atrial standstill and IV block –> ventricular fibrillation

101
Q

What are the progressive ECG changes seen in worsening hypokalaemia?

A

Low T wave –> low T wave, high U wave –> low T wave, high U wave, decreased ST

102
Q

What is the emergency Tx for hyperkalaemia which should be carried out within 30 mins?

A

IV calcium gluconate
IV insulin and glucose
Nebulised beta-agonists (salbutamol)
Dialysis

103
Q

Why is calcium gluconate used to treat hyperkalaemia?

A

Restores RMP of cardiac myocytes

104
Q

Why is IV insulin used to treat hyperkalaemia?

A

Increases Na-K-ATPase activity

105
Q

What is the longer-term treatment for hyperkalaemia?

A

Treat cause: stop medication, treat DKA etc
Decrease potassium intake
Remove excess K+ with dialysis in AKI/CKI or oral binding resins to increase loss via GI tract

106
Q

How is hypokalaemia treated?

A

Treat cause
IV/oral potassium replacement
Potassium sparing diuretics in high mineralocorticoid activity

107
Q

Why are potassium sparing diuretics used to treat hypokalaemia if mineralocorticoid activity is high?

A

Block action of aldosterone on principal cells

108
Q

At what stage do the S/S of potassium balance disturbance present?

A

Late

109
Q

What is the physiological role of intracellular potassium on cell volume maintenance?

A

Net loss of K+ –> cell shrinkage

Net gain of K+ –> cell swelling

110
Q

What is the physiological role of intracellular K+ on intracellular pH regulation?

A

Net loss –> cell acidosis

Net gain –> cell alkalosis

111
Q

What is the physiological role of intracellular potassium on cell enzyme function?

A

Some enzymes are potassium dependent, e.g. ATPases, succinct dehydrogenase

112
Q

What is the physiological role of intracellular potassium on DNA/protein synthesis and growth?

A

Lack –> decreased protein synthesis –> stunted growth

113
Q

What are the effects of decreased plasma potassium causing deranged neuromuscular activity?

A

Muscle weakness and paralysis
Intestinal distension
Peripheral vasodilation
Respiratory failure

114
Q

What are the effects of increased plasma potassium affecting neuromuscular activity?

A

Increased muscle excitability –> muscle weakness –> paralysis

115
Q

What effect does low plasma potassium have in cardiac activity?

A

Slowed conduction of pacemaker –> arrythmias

116
Q

What effect does high plasma potassium have on cardiac activity?

A

Conduction disturbances

Ventricular arrhythmias and fibrillation

117
Q

What affect does intracellular potassium have on vascular resistance?

A

Low plasma potassium –> vasoconstriction

High plasma potassium –> vasodilation

Semester 3 (50 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions