Conn's syndrome - Hyperaldosteronism - MADE EASY - USMLE

Primary Hyperaldosteronism - Conn's Syndrome - MADE EASY

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Are there any other causes of Hyperaldosteronism?

Yes, other than Conn’s syndrome which is a primary cause of Hyperaldosteronism we also have “Secondary” causes of Hyperaldosteronism which present very similar to  Conn’s syndrome “primary hyperaldosteronism”.

The secondary causes of hyperaldoteronism are not due to tumors but rather, due to other manifestations that reduces the amount of blood that reaches the kidneys. Our kidney is a one of the main organs of our body which also has a huge part in maintaining the blood pressure. Kidneys maintain blood pressure through Juxtaglomerular apparatus (JGA) which includes:

1. Juxtaglomerular cells (JG cells) which are modified smooth muscle of Afferent arterioles,
2. Macula densa which are sodium sensors that are part of the distal convoluted tubules.

Juxtaglomerular cells secrete renin in response to decrease renal blood pressure, therefor activating the Renin Angiotensin Aldosterone System (RAAS) by secreting Renin. It is important to know that Renin also increases the sympathetic tone (β1) activity of the heart leading to increase cardiac output.

What are some of the causes of Secondary hyperaldosteronism?

• Renal artery stenosis: This causes the kidney to assume there is hypotension throughout the body since not enough blood is reaching the kidney due to vasoconstriction of the afferent arterioles. Therefore the kidney will assume there is low blood pressure and it starts secreting renin which activates the Renin Angiotensin Aldosterone System, leading to increase aldosterone production.

• Congestive heart failure: Since the heart is failing to pump out blood, no enough blood will reach different organs in our body, especially the kidneys. Therefore the kidney will again assume there is low blood pressure and it starts secreting renin which activates the Renin Angiotensin Aldosterone System, leading to increase aldosterone production.

• Liver Cirrhosis: causes decreased protein production especially albumin. Decreased amount of protein in the serum leads to decreased Colloid osmotic pressure, which will lead to intravascular volume depletion. This makes the kidney think that there is low blood pressure, and there fore it starts secreting renin which activates the Renin Angiotensin Aldosterone System, leading to increase aldosterone production.

• Nephrotic syndrome: Like liver cirrhosis, nephrotic syndrome leads to decreased serum protein concentration, but in the case of nephrotic syndromes it is due to loss of protein and not protein production. Decreased amount of protein in the serum leads to decreased Colloid osmotic pressure, which will lead to intravascular volume depletion. This makes the kidney think that there is low blood pressure, and there fore it starts secreting renin which activates the Renin Angiotensin Aldosterone System, leading to increase aldosterone production.

What are the laboratory values of Hyperaldosteronism?

The laboratory values for both Conn’s syndrome (primary hyperaldosteronism) and Secondary Hyperaldosteronism are exactly the same,

• Hypertension
• Hypernatremia
• Hypokalemia
• Metabolic alkalosis

How to differentiate between Conn’s syndrome (primary hyperaldosteronism) and Secondary Hyperaldosteronism?

• Best initial test –> Measure the ratio of plasma aldosterone to plasma renin. An elevated plasma renin excludes Conn’s syndrome (primary hyperaldosteronism).

• Most accurate test to confirm the presence of a unilateral adenoma –> is sample of the venous blood draining the adrenal. It will show a high aldosterone level.

• CT scan of the adrenals –> Should only be done after biochemical testing confirms:
  • Low potassium
  • High aldosterone despite a high-salt diet
  • Low plasma renin level

How to treat Hyperaldosteronism?

• Laparoscopy: for removal of a unilateral tumors.
• Spironolactone or Eplerenone: for treatment of Bilateral tumors or Secondary hyperaldosteronism.

Angelina Jolie undergoes double mastectomy

Angelina Jolie underwent preventive double mastectomy, she announced in a New York Times article on Tuesday. She decided to undergo this surgery after learning she is a carrier for BRCA1 gene mutation, which increases her risk for developing breast cancer and also ovarian cancer.

“My doctors estimated that I had an 87% risk of breast cancer and a 50% risk of ovarian cancer, although the risk is different in the case of each woman,” Jolie wrote. “Once I knew that this was my reality, I decided to be proactive and to minimize the risk as much as I could. I made a decision to have a preventive double mastectomy.”

In 2007 Angelia Jolie’s mother Marcheline Bertrand, at age 56 died of ovarian cancer. Jolie is 37 years old.

In the Times op-ed, titled “My Medical Choice,” Jolie said she finished three of medical procedures at the Pink Lotus Breast Cancer in California on April 27 that included the mastectomies and reconstruction.

A mastectomy is an operation that removes all or part of the breast.

Jolie wrote that her experience involved a 3 step process. The actress had a procedure on February 2nd, that increases the chance that the nipple can be saved. She then had a major surgery where the breast tissue was removed and temporary fillers were put in the place, which was done two weeks later. After nine weeks from her second surgery she underwent “reconstruction of the breast with an implant.”

“There have been many advances in this procedure in the last few years,” she said, “and the results can be beautiful.”

Jolie also wrote that, “I wanted to write this to tell other women that the decision to have a mastectomy was not easy. But it is one I am very happy that I made,” Jolie wrote. “my chances of developing breast cancer have dropped from 87% to under 5%.”

BRCA stands for breast cancer susceptibility genes, which are a class of genes known as tumor suppressors which will normally suppress the growth of tumor, but if mutated they will lose that ability and the tumor will grow.

Mutations of the BRCA1 and BRCA2 (most common in male) genes have been linked to hereditary breast and ovarian cancer. A blood test can determine if a woman is “highly susceptible” to the cancer.

Jolie acknowledged that surgery might not be the right choice for every woman.
“For any woman reading this, I hope it helps you to know you have options,” Jolie wrote. “I want to encourage every woman, especially if you have a family history of breast or ovarian cancer, to seek out the information and medical experts who can help you through this aspect of your life, and to make your own informed choices.”

The decision for Jolie ultimately came down to her kids. “I can tell my children that they don’t need to fear they will lose me to breast cancer,” she said.

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Heparin Induced thrombocytopenia - MADE SIMPLE

This tutorial has been provided by: Medical Institution

Heparin Induced Thrombocytopenia.

Heparin is an anticoagulant agent which inhibits Thrombin and it does this by activating "antithrombin III", which inhibits conversion of fibrinogen to Fibrin. 

Heparin is also an immediate anticoagulant with a short half life, therefor we can use it in conditions such as:

• Pulmonary embolism
• Stroke
• Deep vein thrombosis (DVT)
• Safe to use in Pregnancy (because heparin does not cross the placenta).

Heparin side effects:

• Bleeding
• Osteoporosis (Give enoxaparin to patients who are already suffering from osteoporosis)
• Heparin induced thrombocytopenia (HIT)

Mechanism of Action:

If someone receiving heparin develops a new or a worsening thrombosis or if their platelet count falls we can assume Heparin induced thrombocytopenia.

Sometimes heparin acts as a hapten by biding to Platelet factor 4 (PF4) which will causes the immune system to start producing antibodies (mostly IgG class) which will cause a complex with heparin+PF4. 

This complex formation will result in platelet activation which causes formation of blood cloths leading to decrease platelet counts and eventually thrombocytopenia.

So if we have pt who suffers from HIT, he or she will be in a hypercoagulable state and at the same time they will have thrombocytopenia.

Treatment for HIT:

• Take them off of Heparin
• Lepirodin
• Bivalirudin
• Argatroban

Schilling Test - MADE SIMPLE

Schilling test: Is a Medical investigation tool used for patients with B12 Deficiency to determine the underlying cause.

1. Stage 1: Give ORAL vitamin B12 “Radiolabeled B12” + Intramuscular Vitamin B12 “Unlabeled B12” and we wait 24 Hours and measure patients Urine for "Radiolababeled Vitamin B12"

The reason for Intramuscular injection of B12 is to saturate all B12 receptors in the liver with NORMAL B12 (unlabeled b12) so we PREVENT binding of oral vitamin B12 “Radiolabeled B12”. Therefore if Radiolabeled vitamin B12 is absorbed from the GI tract, it will get excreted into the urine. After 24 hours the patients urine is collected for assessment.

• A NORMAL result shows High Radiolabeled Vitamin B12 in the urine over the first 24 hours and this gives your gives your diagnosis as "Dietary Deficiency of B12".
• If there is Low levels of Radiolabeled in the urine, then we go to the next stage (stage 2).

NOTE: We will give Intramuscular B12 only ONCE in the beginning since it takes years for B12 to be depleted from the body, therefore B12 receptors are going to be fully saturated after the first injection and there is no need for more B12 injection for the remaining steps of this test.

2. Stage 2--> Vitamin B12 + Intrinsic Factor

The reason we give Intrinsic Factor to our patient is to investigate to see if our patient has Intrinsic Factor deficiency. 

• If the patient's urine collection comes out normal (high Radiolabeled B12), we will then conclude that there is Intrinsic factor Deficiency (e.g. Pernicious Anemia which is an Autoimmune Gastritis)
• If the urine still has LOW radiolabeled B12, we will move onto stage 3.

3. Stage 3 --> Vitamin B12 + Antibiotics.

• If now the Urine collection is Normal (High Radiolabeled B12) then we conclude that patients B12 deficiency was due to Bacterial Overgrowth Syndrome which causes malabsorption. The Terminal ilium is very narrow due to the fact that it contains many lymphoid tissues known as (Peyer’s patches) which are responsible for secretion of IgA antibodies which defend the G.I. against bacterial invasion.
• If the urine still has LOW radiolabeled B12, we will move onto stage 3.

4.Stage4 --> Vitamin B12 + Pancreatic Enzymes (protease)

• If the Urine Collection is now NORMAL (HIGH Radiolabeled B12) then we conclude that the patient B12 Deficiency was due to Pancreatic Insufficiency (e.g. Chronic Pancreatitis). Because Pancreas contains many enzymes that aid digestion. One of these enzymes is called "protease" which is responsible for breaking off this group of protein called "R-proteins that is bound to Vitamin B12. The job of protease is to get rid of the "R-protein" so B12 can become a free and  bind to Intrinsic Factor which will help vitamin B12 absorption in the terminal ilium. Without protease, B12 will remind connected to R-protein and therefor will not be able to bind Intrinsic factor, and it will not get absorbed through the terminal ilium resulting in its malabsorption.

Vitamin B12 Deficiency Symptoms:

• Megaloblastic anemia ( look for Hypersegmented neutrophils)
• Neurological manifestations (e.g. Paresthesia, which is burning and tingling sensation in the extremities) 
• Homocystinuria which causes kyphosis, lens subluxation and atherosclerosis.

Renin Angiotensin Aldosterone System - MADE SIMPLE

This tutorial has been provided by: Medical Institution

Renin Angiotensin Aldosterone System

Here is a quick and simple review of Renin Angiotensin Aldosterone System (RAAS).

Renin Angiotensin Aldosterone System, is one of the ways that our body uses to maintain Blood Pressure. It is important to understand that this a chronic way in controlling blood pressure. The reason being there are Enzymes and Hormones required in this system which take some time to get synthesized.

The "ACUTE" way of compensating Low Blood Pressure, is through ANS system which releases Neurotransmitters such as Norepinephrine (NE). In turn NE acts on "α1" receptors located on Blood vessels and causes vasoconstrictions which results in Increase Blood pressure. It also Activates "Beta1" receptors on the heart and as the results Cardiac Output increases which supplies more blood to the tissues.

Aldosterone is a hormone that is produced by Adrenal glads (zona glomerulosa) which acts on the Distal tubules and collecting ducts of the nephrons resulting in Sodium reabsorption into the circulation and Potassium and Hydrogen Ions secretion into the tubules to be excreted out with urine.

What is important here is that, water always follows Sodium, therefor when Aldosterone causes Sodium reabsorption it will also lead to Water reabsorption as well which will eventually lead to increase in Blood Pressure.

Please watch and if you have any questions you can always ask me in the comment section and i will be more than happy to provide you a good explanation.

Therefor this system becomes very important in treating hypertensive patients due to many pharmacological drugs we now have available to us today which will inhibit key enzymes in the Renin Angiotensin Aldosterone System (RAAS), that will ultimately result in inhibition of Aldosterone synthesis. This will lead to inhibit of Sodium and Water reabsorption which will ultimately result in fluid loss and decrease in blood pressure.

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