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Question 1
Incorrect
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On her most recent blood tests, a 55 year-old female with a history of hypertension was discovered to be hypokalaemic. She is diagnosed with primary hyperaldosteronism.
Which of the following is a direct action of aldosterone?
Your Answer: Reabsorption of K + into the proximal convoluted tubule
Correct Answer: Secretion of H + into the distal convoluted tubule
Explanation:Aldosterone is a steroid hormone produced in the adrenal cortex’s zona glomerulosa. It is the most important mineralocorticoid hormone in the control of blood pressure. It does so primarily by promoting the synthesis of Na+/K+ATPases and the insertion of more Na+/K+ATPases into the basolateral membrane of the nephron’s distal tubules and collecting ducts, as well as stimulating apical sodium and potassium channel activity, resulting in increased sodium reabsorption and potassium secretion. This results in sodium conservation, potassium secretion, water retention, and a rise in blood volume and blood pressure.
Aldosterone is produced in response to the following stimuli:
Angiotensin II levels have risen.
Potassium levels have increased.
ACTH levels have risen.
Aldosterone’s principal actions are as follows:
Na+ reabsorption from the convoluted tubule’s distal end
Water resorption from the distal convoluted tubule (followed by Na+)
Cl is reabsorbed from the distal convoluted tubule.
K+ secretion into the convoluted distal tubule’s
H+ secretion into the convoluted distal tubule’s -
This question is part of the following fields:
- Physiology
- Renal Physiology
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Question 2
Incorrect
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The renin-angiotensin-aldosterone system (RAAS) controls blood pressure and fluid balance.
Which of the following sites produces the most angiotensinogen?
Your Answer:
Correct Answer: The liver
Explanation:Angiotensinogen is an alpha-2-globulin generated predominantly by the liver and released into the blood. Renin, which cleaves the peptide link between the leucine and valine residues on angiotensinogen, converts it to angiotensin I.
Angiotensinogen levels in the blood are raised by:
Corticosteroid levels have risen.
Thyroid hormone levels have risen.
Oestrogen levels have risen.
Angiotensin II levels have risen. -
This question is part of the following fields:
- Physiology
- Renal Physiology
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Question 3
Incorrect
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The hypothalamus produces antidiuretic hormone (ADH), also known as vasopressin, which is a peptide hormone. It is important for maintaining water and electrolyte balance, as well helping control arterial pressure.
To have an effect on blood arteries, ADH binds to which of the following receptors?
Your Answer:
Correct Answer: V 1 receptor
Explanation:ADH, or antidiuretic hormone, is a hormone that regulates water and electrolyte balance. It is released in response to a variety of events, the most important of which are higher plasma osmolality or lower blood pressure. ADH increases plasma volume and blood pressure via acting on the kidneys and peripheral vasculature.
It causes vasoconstriction by binding to peripheral V1 Receptors on vascular smooth muscle via the IP3 signal transduction and Rho-kinase pathways. The systemic vascular resistance and arterial pressure rise as a result. High levels of ADH appear to be required for this to have a major impact on arterial pressure, such as in hypovolaemic shock.
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This question is part of the following fields:
- Physiology
- Renal Physiology
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Question 4
Incorrect
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A 60-year-old patient with a history of hypertension and chronic kidney disease (CKD) walks into the clinic to discuss her most recent blood results indicating an accelerated progression of CKD.
Which of the following is the correct definition for accelerated progression of CKD?
Your Answer:
Correct Answer: A sustained decrease in GFR of 15 ml/minute/1.73 m 2 per year
Explanation:Chronic kidney disease (CKD) is a disorder in which kidney function gradually deteriorates over time. It’s fairly prevalent, and it typically remains unnoticed for years, with only advanced stages of the disease being recognized. There is evidence that medication can slow or stop the progression of CKD, as well as lessen or prevent consequences and the risk of cardiovascular disease (CVD).
CKD is defined as kidney damage (albuminuria) and/or impaired renal function (GFR 60 ml/minute per 1.73 m2) for three months or longer, regardless of clinical diagnosis.
A prolonged decline in GFR of 25% or more with a change in GFR category within 12 months, or a sustained drop in GFR of 15 ml/minute/1.73 m² per year, is considered accelerated CKD progression.
End-stage renal disease (ESRD) is defined as severe irreversible kidney impairment with a GFR of less than 15 ml/minute per 1.73 m² and a GFR of less than 15 ml/minute per 1.73 m². -
This question is part of the following fields:
- Physiology
- Renal Physiology
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Question 5
Incorrect
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Antidiuretic hormone (ADH) levels are found to be increased in a young lady with unexplained hyponatraemia.
Which of the following is a result of the release of ADH?Your Answer:
Correct Answer: Small volumes of concentrated urine
Explanation:ADH, or antidiuretic hormone, is a hormone that regulates water and electrolyte balance. It is released in response to a variety of events, the most important of which are higher plasma osmolality or lower blood pressure. ADH increases plasma volume and blood pressure via acting on the kidneys and peripheral vasculature.
ADH causes extensive vasoconstriction by acting on peripheral V1 Receptors.ADH binds to B2 Receptors in the terminal distal convoluted tubule and collecting duct of the kidney, increasing transcription and aquaporin insertion in the cells that line the lumen. Aquaporins are water channels that allow water to pass through the tubule and into the interstitial fluid via osmosis, lowering urine losses.
The permeability of the distal collecting duct (the section within the inner medulla) to urea is likewise increased by ADH. More urea travels out of the tubule and into the peritubular fluid, contributing to the counter current multiplier, which improves the Loop of Henle’s concentrating power.Overall, there is enhanced urea and water reabsorption in the presence of ADH, resulting in modest amounts of concentrated urine. There is minimal urea and water reabsorption in the absence of ADH, resulting in huge amounts of dilute urine.
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This question is part of the following fields:
- Physiology
- Renal Physiology
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Question 6
Incorrect
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A 28-year-old female arrives after taking an unknown chemical in excess. She is tired and her speech is slurred. The following are her observations and results:
HR 118,
BP 92/58,
SaO2 96%
HR 118, 11/15
The following are the results of his arterial blood gas (ABG):
pH: 7.24
pO 2 : 9.4
kPa PCO2 : 3.3
kPa HCO 3 -: 22 mmol/l
Na + : 143 mmol/l
Cl – : 99 mmol/l
Lactate: 5 IU/l
Which of the following statements about this patient is TRUE?Your Answer:
Correct Answer: Her anion gap is elevated
Explanation:The interpretation of arterial blood gas (ABG) aids in the measurement of a patient’s pulmonary gas exchange and acid-base balance.
The normal values on an ABG vary a little depending on the analyser, but they are roughly as follows:
Variable
Range
pH
7.35 – 7.45
PaO2
10 – 14 kPa
PaCO2
4.5 – 6 kPa
HCO3-
22 – 26 mmol/l
Base excess
-2 – 2 mmol/lThe patient’s history indicates that she has taken an overdose in this case. Because her GCS is 11/15 and she can communicate with slurred speech, she is clearly managing her own airway, there is no current justification for intubation.
The following are the relevant ABG findings:
Hypoxia (mild)
pH has been lowered (acidaemia)
PCO2 levels are low.
bicarbonate in its natural state
Lactate levels have increasedThe anion gap represents the concentration of all the unmeasured anions in the plasma. It is the difference between the primary measured cations and the primary measured anions in the serum. It can be calculated using the following formula:
Anion gap = [Na+] – [Cl-] – [HCO3-]The reference range varies depending on the technique of measurement, but it is usually between 8 and 16 mmol/L.
The following formula can be used to compute her anion gap:
Anion gap = [143] – [99] – [22]
Anion gap = 22As a result, it is clear that she has a metabolic acidosis with an increased anion gap.
The following are some of the causes of type A and type B lactic acidosis:
Type A lactic acidosis
Type B lactic acidosis
Shock (including septic shock)
Left ventricular failure
Severe anaemia
Asphyxia
Cardiac arrest
CO poisoning
Respiratory failure
Severe asthma and COPD
Regional hypoperfusion
Renal failure
Liver failure
Sepsis (non-hypoxic sepsis)
Thiamine deficiency
Alcoholic ketoacidosis
Diabetic ketoacidosis
Cyanide poisoning
Methanol poisoning
Biguanide poisoning -
This question is part of the following fields:
- Physiology
- Renal Physiology
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Question 7
Incorrect
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The syndrome of inappropriate antidiuresis due to excessive antidiuretic hormone (ADH) secretion is diagnosed in a male patient with a history of recurrent hyponatraemia.
Which of the following produces ADH?Your Answer:
Correct Answer: Hypothalamus
Explanation:Antidiuretic hormone (ADH), commonly known as vasopressin, is a peptide hormone that controls how much water the body retains.
It is produced in the magnocellular and parvocellular neurosecretory cells of the paraventricular nucleus and supraoptic nucleus in the hypothalamus from a prohormone precursor. It is subsequently carried to the posterior pituitary via axons and stored in vesicles.
The secretion of ADH from the posterior pituitary is regulated by numerous mechanisms:
Increased plasma osmolality: Osmoreceptors in the hypothalamus detect an increase in osmolality and trigger ADH release.Stretch receptors in the atrial walls and big veins detect a decrease in atrial pressure as a result of this (cardiopulmonary baroreceptors). ADH release is generally inhibited by atrial receptor firing, but when the atrial receptors are stretched, the firing reduces and ADH release is promoted.
Hypotension causes baroreceptor firing to diminish, resulting in increased sympathetic activity and ADH release.
An increase in angiotensin II stimulates angiotensin II receptors in the hypothalamus, causing ADH production to increase.The main sites of action for ADH are:
The kidney is made up of two parts. ADH’s main job is to keep the extracellular fluid volume under control. It increases permeability to water by acting on the renal collecting ducts via V2 Receptors (via a camp-dependent mechanism). This leads to a decrease in urine production, an increase in blood volume, and an increase in arterial pressure as a result.Vascular system: Vasoconstriction is a secondary function of ADH. ADH causes vasoconstriction via binding to V1 Receptors on vascular smooth muscle (via the IP3 signal transduction pathway). An increase in arterial pressure occurs as a result of this.
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This question is part of the following fields:
- Physiology
- Renal Physiology
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Question 8
Incorrect
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Which of the following best describes the order in which blood passes through the nephron?
Your Answer:
Correct Answer: Afferent arteriole→Glomerular capillary→Efferent arteriole→Peritubular capillary→Vasa recta
Explanation:The nephron’s blood flow is as follows:
Afferent arteriole – Glomerular capillary – Efferent arteriole – Peritubular capillary – Vasa recta – Afferent arteriole – Glomerular capillary – Efferent arteriole – Peritubular capillary – Vasa rectaThe kidney is the only vascular network in the body with two capillary beds. With arterioles supplying and draining the glomerular capillaries, higher hydrostatic pressures at the glomerulus are maintained, allowing for better filtration. A second capillary network at the tubules enables for secretion and absorption in the tubules, as well as concentrating urine.
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This question is part of the following fields:
- Physiology
- Renal Physiology
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Question 9
Incorrect
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An ambulance transports a 40-year-old man to the hospital. He ingested a significant amount of aspirin.
In the early stages of an aspirin overdose, which form of acid-base problem should you anticipate?
Your Answer:
Correct Answer: Respiratory alkalosis
Explanation:When you take too much aspirin, you have a mix of respiratory alkalosis and metabolic acidosis. Respiratory centre stimulation produces hyperventilation and respiratory alkalosis in the early phases. The direct acid actions of aspirin tend to create a higher anion gap metabolic acidosis in the latter phases.
Below summarizes some of the most common reasons of acid-base abnormalities:Respiratory alkalosis:
– Hyperventilation (e.g. anxiety, pain, fever)
– Pulmonary embolism
– Pneumothorax
– CNS disorders (e.g. CVA, SAH, encephalitis)
– High altitude
– Pregnancy
– Early stages of aspirin overdoseRespiratory acidosis:
– COPD
– Life-threatening asthma
– Pulmonary oedema
– Respiratory depression (e.g. opiates, benzodiazepines)
– Neuromuscular disease (e.g. Guillain-Barré syndrome, muscular dystrophy
– Incorrect ventilator settings (hypoventilation)
– ObesityMetabolic alkalosis:
– Vomiting
– Cardiac arrest
– Multi-organ failure
– Cystic fibrosis
– Potassium depletion (e.g. diuretic usage)
– Cushing’s syndrome
– Conn’s syndromeMetabolic acidosis (with raised anion gap):
– Lactic acidosis (e.g. hypoxaemia, shock, sepsis, infarction)
– Ketoacidosis (e.g. diabetes, starvation, alcohol excess)
– Renal failure
– Poisoning (e.g. late stages of aspirin overdose, methanol, ethylene glycol)Metabolic acidosis (with normal anion gap):
– Renal tubular acidosis
– Diarrhoea
– Ammonium chloride ingestion
– Adrenal insufficiency -
This question is part of the following fields:
- Physiology
- Renal Physiology
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Question 10
Incorrect
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Antidiuretic hormone (ADH) levels are found to be increased in a young lady with unexplained hyponatraemia.
In a healthy patient under normal circumstances, in which of the following conditions would ADH not be released?
Your Answer:
Correct Answer: Increased alcohol intake
Explanation:Antidiuretic hormone (ADH) is produced in the hypothalamus’s supraoptic nucleus and then released into the blood via axonal projections from the hypothalamus to the posterior pituitary.
It is carried down axonal extensions from the hypothalamus (the neurohypophysial capillaries) to the posterior pituitary, where it is kept until it is released, after being synthesized in the hypothalamus.
The secretion of ADH from the posterior pituitary is regulated by numerous mechanisms:
Increased plasma osmolality: Osmoreceptors in the hypothalamus detect an increase in osmolality and trigger ADH release.Hypovolaemia causes a drop in atrial pressure, which stretch receptors in the atrial walls and big veins detect (cardiopulmonary baroreceptors). ADH release is generally inhibited by atrial receptor firing, but when the atrial receptors are stretched, the firing reduces and ADH release is promoted.
Hypotension causes baroreceptor firing to diminish, resulting in increased sympathetic activity and ADH release.
An increase in angiotensin II stimulates angiotensin II receptors in the hypothalamus, causing ADH production to increase.Nicotine, Sleep, Fright, and Exercise are some of the other elements that might cause ADH to be released.
Alcohol (which partly explains the diuretic impact of alcohol) and elevated levels of ANP/BNP limit ADH release. -
This question is part of the following fields:
- Physiology
- Renal Physiology
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