Endocrinology Flashcards
1
Q
What are the three ways hormones are distributed through?
A
Endocrine – blood-borne, acting at distant sites
Paracrine – acting on adjacent cells
Autocrine – feedback on same cell that secreted hormone
2
Q
Features of water-soluble hormones
A
Transport - unbound
Cell interaction - bind to surface receptor
Half-life - short
Clearance - fast
3
Q
Features of fat-soluble hormones
A
Transport - protein bound
Cell interaction - diffuse into cells
Half-life - long
Clearance - slow
4
Q
What are the 4 classes of hormones?
A
- Peptides
- Amines
- Iodothyronines
- Cholesterol derivatives and steroids
5
Q
What are the different mechanisms used to control hormone secretion?
A
Basal secretion – continuously or pulsatile
Superadded rhythms e.g day-night cycle – ACTH, prolactin, GH and TSH
Release inhibiting factors – dopamine inhibiting prolactin, sum of positive and negative effects (GHRH and somatostatin on GH)
Releasing factors
6
Q
What hormones does the posterior pituitary synthesise?
A
NONE! Oxytocin and vasopressin (ADH) is stored in the posterior pituitary but is synthesised in the hypothalamus.
7
Q
What would stimulate vasopressin release?
A
Vasopressin is an antidiuretic hormone. It is stimulated to absorb water from the kidney.
*Hypertonic concentration
*Loss of blood volume
*Stress
8
Q
What does vasopressin do?
A
*Vasoconstricts blood vessels
*Increased release of aldosterone which leads to increased absorption of water
*Stimulates the release of ACH which in turn stimulates the release of cortisol
9
Q
Where is oxytocin released?
A
Posterior pituitary gland
10
Q
Function of oxytocin?
A
- Uterine contraction during labour.
- Milk ejection
11
Q
What hormones are produced in the anterior pituitary gland and what are they stimulated by?
A
TSH - stimulated by TRH from hypothalamus
ACTH - stimulated by CRH from hypothalamus
FSH and LH - stimulated by GnRH from hypothalamus
GH - stimulated by GHRH from hypothalamus
PRL - inhibited by dopamine from hypothalamus
12
Q
What are the three ways that someone with pituitary dysfunction would present?
A
*Tumour mass effects
*Hormone excess
*Hormone deficiency
13
Q
What investigations should be conducted in patients with pituitary dysfunction?
A
- Make a clinical diagnosis
- Hormonal tests
- If hormonal tests abnormal or tumour mass effects perform MRI pituitary
14
Q
When is oxytocin released?
A
It is stimulated by cervical dilation
15
Q
Where does growth hormone act?
A
In the liver
16
Q
What hormone does GH stimulate?
A
Insulin-like growth factors (IGFs)
17
Q
Functions of thyroid hormone
A
*Accelerates food metabolism
*Increases protein synthesis
*Stimulation of carbohydrate metabolism
*Enhances fat metabolism
*Increase in ventilation rate
*Increase in cardiac output and heart rate
*Brain development during foetal life and postnatal development
*Growth rate accelerated
18
Q
Main function of cortisol?
A
Major metabolic and stress hormone
19
Q
Describe the structure of the adrenal gland.
A
Adrenal gland is divided into the medulla and cortex.
The cortex is made up of three layers:
GFR
*Zona glomerulosa
*Zona fasciculata
*Zona reticularis
20
Q
Where in the adrenal cortex are mineralocorticoids produced and give an example of one.
A
Zona glomerulosa.| - Aldosterone.
21
Q
Where in the adrenal cortex are glucocorticoids produced and give an example of one.
A
Zona fasciculata.| - Cortisol androgens
22
Q
Where in the adrenal cortex are androgens produced and give an example of one.
A
Zona reticularis.| - androstenedione and DHEA
23
Q
What is released by the adrenal medulla?
A
Epinephrine and norepinephrine
24
Q
What happens in the zona glomerulosa
A
Renin-angiotensin system
*Low Na, sympathetic
*Renin acts on zona glomerulosa producing aldosterone
*Increases absorption of Na+ and increased K+ excretion
*Blood volume increases and/or BP
25
What happens during stress?
Stress
*CRH released
*ACTH released
*Drives adrenal gland to release glucocorticoids (ie cortisol)
*Helps body overcome stress
26
What does FSH and LH stimulate?
Hypothalamus -> GnRH -> AP -> FSH/LH -> ovaries/testes.
FSH acts on granulosa cells to produce oestrogen and sertoli cells to stimulate spermatogenesis.
LH acts on theca cells to produce androgens or leydig cells to produce testosterone.
27
BMI thresholds
<18.5 underweight
18.5 - 24.9 normal
25.0 - 29.9 overweight
30.0 - 39.9 obese
>40 morbidly obese
28
What is obesity a risk factor of?
1. Type II diabetes
2. Hypertension
3. Coronary artery disease
4. Stroke
5. Osteoarthritis
6. Obstructive sleep apnoea
7. Carcinoma
- Breast
- Endometrium
- Prostate
- Colon
29
How would you calculate BMI?
wt (kg)/ht (m^2)
30
Give a reason to why working night shifts could increase obesity?
Disruption of the Circadian rhythm, this could increase insulin resistance leading to obesity.
31
What are the two factors that can affect weight regulation?
- Genetics
- Environment
32
What are the three main organs that influence appetite regulation?
- GI tract
- Brain
- Adipose tissue
33
Why are the two factors that drive us to eat?
Internal physiological drive to eat
- feeling that prompts thought of food and motivates food consumption
External psychological drive to eat
- sometimes even in the absence of hunger (ie buffet)
34
What are the 4 main stages in the satiety cascade?
1. Sensory
2. Cognitive
3. Post ingestive
4. Post absorptive.
35
Which brain structure is responsible for appetite regulation?
Hypothalamus
Lateral hypothalamus - hunger centre
Ventromedial hypothalamic nucleus - satiety center
36
Which hormones suppress appetite?
- Leptin
- Insulin
- PYY
- CCK
- POMC
- CART
- GLP 1
- Serotonin
37
Which hormones increase appetite?
- Ghrelin
- NPY
- MCH
- AgRP
- Orexin
- Endocannabinoid
38
Where is leptin released from?
White adipose tissue
39
What is the mechanism of action of leptin on the hypothalamus?
*Leptin inhibits NPY and AgRP
*Leptin stimulates POMC and CART
*Appetite decreases
40
What might happen if someone was deficient in leptin?
They might become obese.
41
Where does CCK act on?
Stretches receptors on the pyloric sphincter
- Delays gastric emptying
- Gall bladder contraction
- Insulin release
42
Where is ghrelin expressed?
In the stomach
43
How does ghrelin stimulate appetite?
Ghrelin stimulates NPY and AGRP = increases appetite.
44
Which hormone decreases following gastric bypass surgery?
Ghrelin
45
What hormone might it be possible to use in the treatment of anorexia?
Ghrelin
46
What can POMC be broken down into? What roles do they play?
Three main hormones:
- ACTH
- MSH
- endorphin
47
What can POMC deficiency lead to?
- Pale skin
- Adrenal insufficiency
- Hyperphagia and obesity
48
What does high levels of agouti-related peptide (AgRP) cause?
Causes excess eating, increases appetite
49
What is the role of Malonyl CoA in satiety?
In a fasted state, action of different hormones will lead to activation of AMPK
Increased AMPK will reduce acetyl CoA Carboxylase and decrease malonyl CoA and increase appetite.
In a fed state, the opposite occurs.
50
In non diabetic humans how does metabolism occur during the fasting state?
*All glucose comes from liver (and a bit from kidney)
- Breakdown of glycogen
- Gluconeogenesis (utilises 3 carbon precursors to synthesise glucose including lactate, alanine and glycerol)
*Glucose is delivered to insulin independent tissues, brain and red blood cells
*Insulin levels are low
*Muscle uses FFA for fuel
*Some processes are very sensitive to insulin, even low insulin levels prevent unrestrained breakdown of fat
51
In non diabetic humans how does metabolism occur after feeding ?
*Rising glucose (5-10 min after eating) stimulates insulin secretion and suppresses glucagon
*40% of ingested glucose goes to liver and 60% to periphery, mostly muscle
*Ingested glucose helps to replenish glycogen stores both in liver and muscle
*High insulin and glucose levels suppress lipolysis and levels of non-esterified fatty acids (NEFA or FFA) fall
52
Define diabetes mellitus
A disorder of carbohydrate metabolism characterised by hyperglycaemia.
53
How does diabetes mellitus cause morbidity and mortality?
Causes morbidity and mortality through
*Acute hyperglycaemia which if untreated leads to acute metabolic emergencies diabetic ketoacidosis (DKA) and hyperosmolar coma (Hyperosmolar Hyperglycaemic State )
*Chronic hyperglycaemia leading to tissue complications (macrovascular and microvascular)
*Side effects of treatment- hypoglycaemia
54
What types of complications are associated with diabetes?
*Diabetic retinopathy
*Diabetic nephropathy
*Stroke
*Cardiovascular disease
*Diabetic neuropathy
55
What are the different types of diabetes?
*Type 1
*Type 2
- Includes gestational and medication induced diabetes
*Maturity onset diabetes of youth (MODY), also called monogenic diabetes
*Pancreatic diabetes
*“Endocrine Diabetes” (Acromegaly/Cushings)
*Malnutrition related diabetes
56
Diagnostic criteria for diabetes
If symptomatic:
*Random plasma glucose > 11 mmol/l
*Fasting plasma glucose > 7 mmol/l
If asymptomatic:
* Glucose tolerance test (75g glucose) fasting > 7 or 2h value > 11 mmol/l (repeated on 2 occasions)
*HbA1c of > 48mmol/mol (6.5%)
57
Pathogenesis of Type 1 diabetes
* no insulin produced -> glucose not transported to cells -> hyperglycaemia
* Insulin allows the glut4 transporter to transport glucose into the cell
*Body therefore thinks the patient is not eating
*Liver increases gluconeogenesis to compensate
58
What cells does Type 1 diabetes mellitus affect?
Caused by destruction of beta cells of the islet of Langerhans in the pancreas
59
In Type 1 diabetes what does failure of insulin secretion lead to?
*Continued breakdown of liver glycogen
*Unrestrained lipolysis and skeletal muscle breakdown providing gluconeogenic precursors
*Inappropriate increase in hepatic glucose output and suppression of peripheral glucose uptake
60
In Type 1 diabetes what does rising glucose concentrations result in?
Rising glucose concentration results in increased urinary glucose losses as renal threshold (10mM) is exceeded
61
In Type 1 diabetes what can failure to treat with insulin lead to?
Failure to treat with insulin leads to
*Increase in circulating glucagon (loss of local increases in insulin within the islets leads to removal of inhibition of glucagon release), further increasing glucose
*perceived ‘stress’ leads to increased cortisol and adrenaline
*progressive catabolic state and increasing levels of ketones
62
Aetiology of Type 1 Diabetes
* Younger patients (mostly)
* Higher association in northern europeans
* Associated with other autoimmune conditions
* HLA-DR3-DQ2 and HLA-DR4-DQ8
63
Aetiology of Type 2 Diabetes
- Older age
- Ethnicity (south Asians and Afro-Caribbean)
- Associated with obesity, lack of exercise, calorie and alcohol excess
- No immune disturbance
- No HLA disturbance but there is a stronger genetic link
- Polygenic disorder
64
In Type 2 diabetes what does insulin resistance and progressive failure of insulin secretion lead to?
*Impaired insulin action leads to
- Reduced muscle and fat uptake after eating
- Failure to suppress lipolysis and high circulating FFAs
- Abnormally high glucose output after a meal
*Even low levels of insulin prevent muscle catabolism and ketogenesis so profound muscle breakdown and gluconeogenesis are restrained and ketone production is rarely excessive
65
How often is HbA1c conducted? Why?
Every 3 months, as erythrocytes live for 120 days
66
What is the cut off mmol/mol for diabetes?
48 (42 is prediabetes)
67
Types of Insulin
- Rapid: aspart, lisporo, novorapid, glulisine
- Short: regular insulin
- Intermediate: NPH (half a day)
- Long: detemir, lantus, glargine
68
T1DM features
*Autoimmune condition (β-cell damage) with genetic component
*Profound insulin deficiency
69
T2DM features
Insulin resistance
Impaired insulin secretion and progressive β-cell damage but initially continued insulin secretion
Excessive hepatic glucose output
Increased counter-regulatory hormones including glucagon
70
How would you treat Type 2 Diabetes Mellitus?
1. First line is lifestyle modifications and regular HbA1c appointments
2. Second line if HbA1c still >48 offer METFORMIN
3. Add one of these drugs:
* SGLT-2 inhibitors (preferred)
* DPP-4 inhibitors
* Sulfonylurea
4. Triple drug therapy or start insulin
71
Modern insulin therapy in T1D
Separation of basal from bolus insulin to mimic physiology
Pre-meal rapid acting boluses adjusted according to pre-meal glucose and carbohydrate content of food to cover meals
Basal insulin should control blood glucose in between meals and particularly during the night
Basal insulin given as either twice daily insulin levemir (basal analogue or once daily degludec) adjusted to maintain fasting blood glucose between 4–7 mmol/L
72
Advantages and disadvantages of basal insulin in T2DM
Advantages:
Simple for the patient, adjusts insulin themselves, based on fasting glucose measurements
Carries on with oral therapy, combination therapy is common
Less risk of hypoglycaemia at night
Disadvantages:
Doesn’t cover meals
Best used with long-acting insulin analogues which are considered expensive.
73
Advantages and disadvantages of pre-mixed insulin
Advantages:
Both basal and prandial components in a single insulin preparation
Can cover insulin requirements through most of the day
Disadvantages
- Requires consistent meal and exercise pattern
- Cannot seperately titrate individual insulin components
- Increased risk of nocturnal and fasting hypoglycaemia
74
What is the main factor preventing patients achieving tight glucose targets during treatment?
Hypoglycaemia
75
Why does hypoglycaemia occur in patients undergoing insulin therapy?
Hypoglycaemia occurs due to the inability of insulin therapy to mimic the physiology of the beta cell
76
How do you classify hypoglycaemia
Level 1:
Alert value
Plasma glucose <3.9 mmol/l (70 mg/dl) and no symptoms
Level 2:
Serious biochemical
Plasma glucose <3.0 mmol/l
(55 mg/dl)
Level 3:
Patient has impaired cognitive function sufficient to require external help to recover
77
Non-severe versus severe symptomatic hypoglycaemia
Non-severe: Patient has symptoms but can self-treat and cognitive function is mildly impaired
Severe: Patient has impaired cognitive function sufficient to require external help to recover
78
What pathophysiological effects does hypoglycaemia have on different organs and systems?
Brain:
Cognitive dysfunction
Blackouts, seizures, comas
Psychological effects
79
Common hypoglycaemia symptoms
(include the autonomic, neuroglycopenic and non-specific symptoms)
1. Development of symptoms
Autonomic:
- Trembling, palpitations, sweating, anxiety, hunger
Neuroglycopenic:
- difficulty concentrating, confusion, weakness, drowsiness, vision changes, difficulty speaking
Non-specific:
- nausea, headache
2. Low blood glucose (<3.9 mmol/l)*
3. Response to treatment with carbohydrate
80
Causes of hypoglycaemia
*Use of drugs (prescribed, alcohol)
*Increasing age
*Increased physical activity
*Long duration of diabetes
*Tight glycaemic control with repeated episodes of non severe hypoglycaemia
*Sleeping
81
Screening for risk of severe hypoglycaemia
Screening should be based on established risk factors
*Low HbA1c; high pre-treatment HbA1c in T2DM
*Long duration of diabetes
*A history of previous hypoglycaemia
*Impaired awareness of hypoglycaemia (IAH)*
*Recent episodes of severe hypoglycaemia
*Daily insulin dosage >0.85 U/kg/day
*Physically active (e.g. athlete)
*Impaired renal and/or liver function
82
Strategies to prevent hypoglycaemia
*Patient education
*Consider enrolling patients with frequent hypoglycaemia in a blood glucose awareness training programme
83
How would you treat hypoglycaemia?
Recognize symptoms so they can be treated as soon as they occur
Confirm the need for treatment if possible (blood glucose <3.9 mmol/l is the alert value)
Treat with 15 g fast-acting carbohydrate to relieve symptoms
Retest in 15 minutes to ensure blood glucose >4.0 mmol/l and re-treat (see above) if needed
Eat a long-acting carbohydrate to prevent recurrence of symptoms
84
What are the actions of PTH?
Acts on the kidney to
*increase Ca2+ reabsorption
*decrease phosphate reabsorption.
*1 α - hydroxylation of 25-OH vit D
Increases bone remodelling
Bone resorption > Bone formation
85
PTH response to decreased serum calcium
*Increase bone resorption
*Increase Ca2+ absorption
*Increase Ca2+ reabsorption
86
A person with low serum albumin might have low total serum calcium but not a low ionised calcium. What is the corrected calcium if:
serum calcium = 2.08 mmol/L
serum albumin = 30 g/L
corrected calcium = total serum calcium + 0.02 * (40 – serum albumin)
2.08 + 0.02 * (40 - 30)
= 2.28 mmol/L
87
Consequences of Hypocalcaemia
*Parasthesia
*Muscle spasm
o Hands and feet
o Larynx
o Premature labour
*Seizures
*Basal ganglia calcification
*Cataracts
*ECG abnormalities
o Long QT interva
88
What two signs can be used as a physical test for hypocalcaemia?
- Chvostek sign
Tap over the facial nerve
Look for spasm of facial muscle
- Trousseau sign
Inflate the blood pressure cuff
to 20 mm Hg above systolic
for 5 minutes
89
Cause of hypocalcemia?
Vitamin D deficiency
90
Causes of hypoparathyroidism?
* Syndromes
- Di George syndrome
* Genetic
* Surgical
* Radiation
* Autoimmune
* Infiltration
* Magnesium deficiency
91
What leads to pseudohypoparathyroidism?
Resistance to parathyroid hormone
- Usually Type 1 Albright hereditary osteodystrophy - caused by mutation with deficient Gα subunit
92
Pseudohypoparathyroidism symptoms
*Short stature
* Obesity
* Round facies
* Mild learning difficulties
* Subcutaneous ossification
* Short fourth metacarpals
* Other hormone resistance
93
Common reasons for misdiagnosis of hypercalcemia
* Tourniquet on for too long
* Sample old and haemolysed
94
Hypercalcaemia: Symptoms and Consequences
* Thirst, polyuria
* Nausea
* Constipation
* Confusion coma
* Renal stones
* ECG abnormalities - Short QT
95
Causes of hypercalcaemia
90% is due to
*Malignancy: bone met, myeloma, lymphoma
*Primary hyperparathyroidism
Other causes:
*Thiazides
* Thyrotoxocosis
* Sarcoidosis
* Familial hypocalciuric / benign hypercalcaemia
* Immobilisation
* Milk-alkali
* Adrenal insufficiency
* Phaeochromocytoma
96
Primary Hyperparathyroidism consequences
*Bones
o Osteitis fibrosa cystica
o Osteoporosis
* Kidney stones
* Psychic groans
o confusion
* Abdominal moans
o Constipation
o Acute pancreatitis
97
What is hyperparathyroidism usually caused by?
80% due to single benign adenoma
15-20% due to four gland hyperplasia
<0.5% malignant
98
What does excess cortisol lead to?
Cushing's syndrome
99
What does Cushing's syndrome lead to?
* Central obesity
* Proximal muscle wasting
* Hirsutism (females grow male facial hair)
* Easy bruising
100
What leads to excess cortisol being released - leading to Cushing's syndrome?
Most commonly caused by pituitary adenoma
101
Health consequences of Cushing's syndrome?
Metabolic - HTN, T2DM, Dyslipidaemia, osteoporosis
Mental - anxiety, depression, insomnia
102
How would you diagnose Cushing's syndrome? Describe briefly how it works
Dexamethasone suppression tests
Dexamethasone given -> negative feedback on hypothalamus -> reduced CRH -> reduced ACTH from pituitary -> low cortisol
No cortisol suppression -> suggests Cushing's syndrome
103
Common cause of Graves disease?
Most common - Graves disease
Also common - De Quervain's or acute thyroiditis
104
Complication of Graves disease
Thyroid storm
105
Common cause of hypothyroidism?
Hashimoto's
106
What deficiency is the most common cause of hypothyroidism in developing countries?
Iodine deficiency
107
What iatrogenic reasons may lead to hypothyroidism?
Treatments for hyperthyroidism such as lithium and amiodarone
108
Hypothyroidism symptoms?
* Dry skin and hair, brittle nails, lateral loss of eyebrows
* Fatigue and weakness
* Weight gain and fluid retention
* Cold sensitivity
* Constipation
* Heavy or irregular periods
109
Hyperthyroidism symptoms?
* Nervousness, anxiety, irritability
* Increased heart rate/ palpitations
* Weight loss and increased appetite
* Heat intolerance and sweating
* Oligomenorrhea
110
True or False:
Thyroxine is the active form of triiodothyronine?
False
Thyroxine - T4
Triiodothyronine - T3
T3 is the active form of T4
111
What is Graves' disease?
Thyroid stimulating hormone receptor antibodies stimulate the thyroid gland, leading to overproduction of thyroid T3/T4
112
Symptoms of Graves' disease
* Weight loss
* Increased heart rate
* Painless Goitre and Pathognomonic
* Exophthalmos
* Pretibial myxedema
* Thyroid acropachy
113
Graves' disease treatment?
Medical treatment is block (using Carbimazole and Propylthiouracil) and replace (using levothyroxine)
Carbimazole is contraindicated in pregnant women as it's teratogenic. Should use propylthiouracil.
* Reduction of thyroid gland surgically with thyroidectomy or radioiodine (Short/life, thyroid-specific)
114
What is De Quervain's thyroiditis caused by?
It is an inflammatory condition typically triggered by a viral infection - flu like symptoms are present. This causes the release of stored thyroid hormones (hyperthyroidism).
115
Hashimoto's cause?
Autoimmune disorder causing anti-thyroid antibodies to damage the thyroid. Decreasing production of T4/T3
Investigations show increased TSH with T3/T4. 90% will have TPO antibodies
116
Treatment of Hashimoto's
Levothyroxine
117
A 14 year old boy presents to your GP clinic with his mother. The patient is complaining of feeling tired and going to the toilet frequently. He mentioned that he always need to keep drinking because he's so thirsty all the time. His general appearance is quite slim. His PMhx is not significant but his mother mentioned that she suffers from hypothyroidism. What is the likely diagnosis?
a) Hashimoto's
b) Graves' disease
c) Type 1 diabetes meticullus
d) Type 2 diabetes meticullus
e) Diabetes insipidus
c) Type 1 diabetes meticullus
118
A 14 year old boy presents to the emergency department with his mother. He has been vomiting, looks drowsy and generally unwell. He is breathing very rapidly and you note that his breath smells fruity. On examination his skin has reduced turgor, his blood pressure is 90/50 and HR 135. What is the likely diagnosis?
Diabetic ketoacidosis
119
What is diabetic ketoacidosis?
It is metabolic acidosis caused by untreated type 1 diabetes (occasionally type 2) or undiagnosed diabetes
120
DKA diagnostic criteria
Glucose >11 mmol/l
pH < 7.3
Bicarbonate <15 mmol/l
Ketones >3 mmol/l
121
Pathophysiology of diabetic ketoacidosis?
Complete lack of insulin causes uncontrolled lipolysis. Breakdown of fats -> increased fatty acids -> converted to ketones -> metabolic acidosis
122
DKA management?
FIG PICK
F - fluids first
I - Insulin
G - glucose
P - potassium
I - infection
C - chart fluid balance
K - ketone monitoring
123
Main complication of DKA management?
Cerebral oedema - caused by rapid fluid replacement
124
You have given fluids to a patient with DKA what is the next step?
Insulin with dextrose
125
What serum ketones is needed to diagnose DKA?
>3 mmol
126
A 44 year old man presents to your GP clinic. He is complaining of always needing to urinate and increased thirst. He has a BMI of 30 and has noted that he is losing feeling in his toes. What is the likely diagnosis?
Type 2 diabetes mellitus
127
What is hyperosmolar hyperglycaemic state?
Medical emergency due to chronic T2DM. Severe hyperglycemia over time will cause
*severe osmotic diuresis
*severe dehydration
*electrolyte deficiency
128
Diagnosis of hyperosmolar hyperglycaemic state?
No specific criteria
*Hyperglycaemia > 30 mmol
*Serum Osmolarity > 320 mosmol/kg
*No ketonemia
129
Pathophysiology of diabetes insipidus?
Insufficient ADH secreted from posterior pituitary. Causes can be nephrogenic or neurogenic.
Nephrogenic - pathology of kidneys - unable to respond to ADH
Neurogenic - reduced ADH - excessive water loss
130
How would you diagnose diabetes insipidus
Water deprivation test and ADH suppression
131
Management of diabetes insipidus
Neurogenic
- desmopressin: increased water reabsorption
Nephrogenic
- Diuretics
132
What is the definitive treatment of Conn's syndrome?
Adrenalectomy
