Clinical Lecture Problem 12 - Renal problems Flashcards Preview

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Flashcards in Clinical Lecture Problem 12 - Renal problems Deck (38):

Describe Case 1 in detail on arrival?

29yo PI woman presents with 2-3 days history of dysuria (painful when she pees), feels run down, last 2-3 weeks feels thirsty and has been drinking more often. She has nocturia (peeing at night) and polyuria (lots or urine). On examination BP was 125/82, lost 10kg in the past 6 months. Has lab tests done and has candida albicans - yeast infection.


What are fasting blood sugars?

Normal = <5.6mmol/L.
Glucose intolerance = 5.6-6.9mmol/L.
Diabetes = >7mmol/L on two occasions.


What are post-prandial blood sugars?

Normal = <7.8mmol/L.
Glucose intolerance = 7.8-11mmol/L.
Diabetes = >11mmol/L.


Describe case 1 after 3 days post arrival?

Patient has been treated for yeast infection. She is now feeling nauseated and is drinking frequently. Pt is getting up every night to pee/urinate. Blood sugars are:
Baseline = 15mmol/L.
Peak = 38mmol/L.
HbA1C = 11.5% or 102mmol/L (normal = <42mmol/L or <6%).


Based on the patient's blood sugar what do you suggest she has?

Pt has diabetes - based on baseline blood sugar levels. Also patient is getting up every night to pee and is very thirsty. So her osmolarity has increased in her body, most likely due to the increased sugar in her blood.


Describe case 1 after patient is diagnosed with diabetes?

She is referred to ED the next day. On arrival she is nauseated, has vomited several times, BP 115/70, HR 140bpm she is clinically dehydrated and breathing rapidly and deeply. Patient was given 30ml/kg of NaCl before transfer to specialist hospital and a bolus dose of insulin (0.11U/kg). On arrival at base hospital she is passing lots of urine and her glucose is 18mmol/L and her mental status is impaired.


What are the patient's (case 1) blood results at ED?

Venous blood glucose = 29.5mmol/L (normal 3-6mmol/L).
Na+ = 132mmol/L (normal 135-146mmol/L).
pH = 7.2 (normal 7.36-7.44).
HCO3- = 12.1mmol/L (normal 22-28mmol/L).
PaCO2 = 32mmHg (normal 36-44mmHg).
K+ = 5.1mmol/L at time of admission but after treatment was 2.8mmol/L (3.5-5.3mmol/L).


Why is the patient (case 1) thirsty?

The patient is thirsty because she has diabetes - too much glucose in her blood. Because her blood is hypertonic, there is more water moving from the cells (ICF) into the blood (ECF) to make it isotonic. This increases the blood volume, which increases the amount of volume passing through the kidneys. This means that more water is filtered out - wee pee out more water (polyuria). Because our cells are now dehydrated (from the water moving to the ECF) it causes our thirst mechanism to start - in the hope that she starts to drink more water. This is known as osmotic diuresis.


How does the body compensate for reduced volume and water loss?

1. Thirst mechanism.
2. ADH release - ADH stimulates aquaporin 2 channels which reabsorb water in the collecting ducts.
3. Aldosterone release - causes reabsorption of Na+ and consequently water.


What is causing the patient (case 1) to hyperventilate?

The patient is breathing rapidly and deeply due to the metabolic acidosis occuring in her body. Patient has DKA, so she has low bicarbonate and excess H+ ions thus her pH will drop. Because her pH has dropped, her body will try and compensate this by increasing the rate of her breathing to decrease the amount of carbon dioxide. This sends the equilibrium towards the "loss" carbon dioxide which will decrease the amount of hydrogen ions, this is in hope to increase her pH levels. This is known as respiratory compensation and the breathing is known as "KUSSMAUL'S" respiration.


What is the reason behind the patient (case 1) having a slightly low serum Na+ (sodium)?

This is known as pseudohyponatraemia. It is because the high amount of glucose in her blood is causing more water to move from the cells (ICF) to the blood (ECF), this causes the apparent "dilution" of sodium.


What is effective osmolarity of plasma?

Effective Osmolarity = (2xNa+) + Glucose )
Normal = 275-295mmol/L.

For case 1 = (2x132) + 29.5 = 293.5mmol/L.


What has caused the patient (case 1) to 1) initially pass little urine and 2) after rehydration pass copious amounts of urine?

1. Due to osmotic diuresis the pt is peeing out a lot of urine (polyuria) so after a wee while, pt gets dehydrated and eventually has hardly any water out to pee. This is because she has a low blood pressure, so her RAAS (aldosterone and ADH) is activated to conserve what little water she has, so pt retains as much water as she can hence does not pee out as much.
2. Because pt is given a large amount of water, her blood volume has increased so her brain thinks she does not need to conserve as much water, so her RAAS system is inactivated. This means that she does not reabsorb as much water and her urine output increases. Thus the reason as to why she passed copious amounts of urine after rehydration therapy.

N.B. Think of when you are given IV fluids (NaCl) when you go to hospital and how you go to the toilet a lot.


What has caused the patient (case 1) to have a high serum (ECF) K+?

Patient has a normal K+ (5.1mmol/L) but after treatment it has significantly dropped (2.8mmol/L) and she is hypokalaemic. This is mecause the IV fluids and insulin treatment cause potassium to be shifted outside of the blood (ECF) and into the cells (ICF). This then decreases the serum potassium levels.


What has caused the patient's (case 1) serum glucose to drop dramatically after treatment?

1. Insulin will cause the glucose to be pushed into cells (from ECF to ICF).
2. By giving pt fluids you are diluting the ECF.
3. Pt is peeing the glucose out (diuresis) after fluid loading.


What has caused the patient (case 1) to have an impaired mental status after treatment?

Because this pt has been dehydrated for some time (3 weeks) and has been hyperosmotic as well, her brain has adapted to it and has become used to less water. When they gave the pt fluids to rehydrate her, the blood around her brain became less osmotic so water rushed out of the serum (ECF) and into the brain cells (ICF) where it was more osmotic. This caused the brain cells to enlarged, in other words cerebral oedema occurred. This is what would have impaired her mental status.


Describe case 2 in detail on arrival?

15yo girl with 5month history of nocturia, and needing to urinate frequently throughout the day. There is no high amount of glucose in her urine or her blood.
Na+ = 142mmol/L (normal 135-146mmol/L).
Urine osmolarity = 200mOsm/L (normal 15-1200mOsm/L).


What happens in case 2 after her arrival?

Pt is sent to hospital and has some tests done.
Early morning blood osmolarity = 305mOsm/L (raised - normal 280-295mOsm/L).
Urinary osmolarity = 250mOsm/L.


What is this patient (case 2) most likely to have?

Diabetes Insipidus.


What happens in diabetes insipidus?

Basically there is not enough ADH or ADH is not able to bind to the kidneys. This means that water is unable to be reabsorbed when osmolarity is high in the blood (to dilute it). This means that more water is passed out of the urine and it is clear/pale. It can either be central (brain is not producing enough ADH) or nephrogenic (the kidneys are not functioning properly so ADH cannot bind and work - adequate levels of ADH being made).


Explain this patient's (case 2) initial sodium (Na+)?

Her serum Na+ is normal, this is due to her osmolarity of her blood not changing. The amount of water she pees out is the amount of water she takes in (she's thirsty, she drinks more and she pees out more so sodium is normal).


Why is the patient (case 2) thirsty?

1. Thirst mechanism.
2. Diabetes insipidus.


What is the significance of increase in early morning blood osmolarity in this patient (case 2)?

The blood is hyperosmotic due to the girl peeing at night (nocturia). Normally we don't pee at night so our blood should not have a rise in osmolarity. Because she is also peeing at night, she is not taking any water in (not drinking any water to replace lost fluids) nor is she able to reabsorb water (DI). Thus both of these things increase osmolarity.


Why is this patient's (case 2) early morning urinary osmolarity 350mOsm/L?

This patient's early morning osmolarity is inappropriately normal. Her urine osmolarity in the morning should be higher than this (say 800), hers is "normal". This is because her kidneys aren't concentrating the urine due to the lack of ADH hence lack of aquaporin channels to reabsorb water at night. This is all due to DI.


Why did the patient's (case 2) urine osmolarity rise after being given desmopressin?

Desmopressin is synthetic ADH. When the pt was given ADH, aquaporins were inserted and her kidneys reabsorbed water and her urine was concentrated. This caused her blood osmolarity to decrease and her urine osmolarity to rise.


What does it mean when the patient's (case 2) osmolarity rose after ADH?

It meant that she had central DI. The pt was not making enough ADH due to a problem in her brain (hypothalamus or post.pituitary).


What does it mean if there is not a rise in the patient's urine osmolarity?

It means that the pt is producing adequate amounts of ADH, yet her kidneys are not able to respond to it. This means the pt would have nephrogenic DI.


Describe case 3 in detail on arrival?

45yo male has 3 year history of feeling unwell, for the past 6months has had: several episodes of fainting at odd times; intermittent vomiting, aches and pains. On examination:
-Thinned and tanned.
-BP 85/50 and HR 90bpm.
-Na+ = 128mmol/L (135-145mmol/L).
-K+ = 5.2mmol/L (3.5-5.0mmol/L).
-Baseline cortisol 50mmol/L and peak 280mmol/L (normal >550mmol/L).


What does the patient (case 3) most likely have?

Addison's disease. This is where there is insufficient cortisol. This could be due to not enough ACTH being made in the brain or the adrenals not responding to ACTH and making cortisol. Addison's is a primary adrenal insufficiency.


What has caused the patient (case 3) to have low serum sodium?

Because the patient has a primary adrenal insufficiency they aren't making enough aldosterone, so they can't reabsorb sodium. Because they aren't making enough cortisol as well, there is a decrease in negative feedback (cortisol acts on ADH - negative feedback) so more ADH is being produced. Because more ADH is being produced (due to lack of cortisol and decreased BP) more water is being absorbed and not sodium.


What does the body release ADH faster to? 1) Osmolarity OR 2) Water depletion?

1. Osmolarity.


What has caused the patient (case 3) to have high serum potassium?

Because there is a primary adrenal insufficiency the adrenals aren't making enough aldosterone, so K+ is not being secreted from the blood into the kidneys. Therefore there is an increase in potassium.


What happens with ADH in chronic conditions such as Addison's?

Normally what happens in acute conditions, when we have less blood (decrease in BP) through the kidneys the RAAS is activated and ADH is released. When there is a chronic condition of low blood pressure (i.e. Addison's) and less blood flowing through the kidneys, the body compensates and shifts the "normal" to a lower osmolarity, this means that ADH can be released at a lower threshold.


What has caused the patient (case 3) to have low BP?

Lack of aldosterone - no sodium and water reabsorbed - due to primary adrenal insufficiency. Lack of cortisol leads to decreased cardiac tone.


What has caused the patient (case 3) to have a low peaked cortisol?

When the pt was given ACTH their cortisol levels did not increase to "normal" levels. This indicates that the person has an adrenal problem. This means that the pt's adrenal glands were not responding to ACTH, thus not producing cortisol.


What does it mean if the patient's (case 3) peaked cortisol was normal (higher than what it is now) after being given exogenous ACTH?

This means that the pt was not producing enough ACTH, so there was a problem with his posterior pituitary or hypothalamus.


What has caused the patient (case 3) to be tanned?

The pt has a primary issue with his adrenal glands, so the hypothalamus still makes ACTH. Because the adrenal glands cannot convert ACTH into cortisol, ACTH is converted into melatonin, hence why the pt has a bronzed complexion (tanned).


How would you treat this patient (case 3)?

You would give them replacement therapy:
-mineralocorticoids (e.g. aldosterone).
-glucocorticoids (e.g. cortisol).

You would also need to determine the primary cause.