Causes of primary hypothyroidism mnemonic

Hi!

Common causes of primary hypothyroidism:
( mnemonic: DR. HIT )

Glucagon-like peptide-1 (GLP-1) receptor agonists

Hello everyone!

Let's talk about glucagon-like peptide-1 (GLP-1) receptor agonists today!

What are APS?

APS or Autoimmune Polyendocrine Syndromes are exactly what the name suggests.
They’re autoimmune in origin and they attack more than one endocrine system.

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Let’s not forget autoimmunity begets autoimmunity.

APS are commonly seen with hypogonadism, vitiligo, alopecia, pernicious anaemia and coeliac disease, among others.

That’d be all. Happy studying!

- Ashish Singh.

History, physiology and medical aspects of fasting

Hello everyone,

My senior resident at JFK Medical Center did a presentation on fasting. I thought of sharing it with you (especially since it is Ramazan/Ramadan).

Hook effect of prolactin in large pituitary adenomas

Hello everyone,

Here's something I learnt today when a case of large pituitary adenoma causing visual field loss was presented today.

But let's talk about my favorite subject first - Immunology!

The intensity of an antigen-antibody interaction depends primarily on the relative proportion of the antigen and the antibody. A relative excess of either will impair adequate immune complex formation. This is called the “high-dose hook effect” or the “prozone phenomenon.”

This is important consideration whe measuring prolactin. Extremely high levels of prolactin can interfere with the assay and produce falsely low readings.

This high-dose hook effect occurs because there is not enough antibody to bind to both ends of all antigenic peptides, in this case, prolactin.

Most prolactin is complexed to a single antibody. Only few remaining prolactin peptides are “sandwiched” and therefore detectable.

This results in a falsely low prolactin value.

Hence, as the antigen concentrations increase, there is a proportional increase in assay titers up to a certain level. Antigen concentrations above this threshold level would “hook” down the assay values resulting in very low measurements.

In order to avoid the high-dose hook effect, the serum prolactin should be estimated in appropriate dilution in all patients with large pituitary tumors.

-IkaN (tired Internal Medicine Resident)

Source:
The 'hook effect' on serum prolactin estimation in a patient with macroprolactinoma. https://www.ncbi.nlm.nih.gov/m/pubmed/11303248/

Work up of thyroid nodule

Hello,

Here is the shorter version of this post: Investigating thyroid nodule for Step 2 CK (link: https://www.medicowesome.com/2016/06/step-2-ck-investigating-thyroid-nodule.html)

So - if you find a thyroid nodule on physical examination - what do you do next?

Diabetic Retinopathy

Here is Upasanas video on Diabetic Retinopathy.

I edited the slides so you can see better :)

Slides are available for download here:

Pathophysiology: Diabetic Ketoacidosis

Hello guys, here’s a whiteboard summary of how DKA happens.

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- DKA is a medical emergency. It’s a complication of type 1 diabetes.
- DKA has a triad of hyperglycemia, ketosis [metabolic acidosis] and dehydration.
- Main ketone bodies are beta-hydroxybutyrate and acetoacetate. Acetone is only a minor ketoacid.
- Lactic acidosis also contributes to metabolic acidosis.
- More glucose in blood leads to more glucose filtered into urine causing osmotic diuresis.


- Ashish Singh 

Types of Sphenoid Sinues.

Hello Guy's!

Here's a sneak peek into the world of Neurosurgery!

In cases of Pituitary Adenomas, the general surgical approach is a TransNasal TransSphenoidal Approach for the excision of the lesion.

To know the type of sphenoid sinus is an important step in the pre-operative planning for the surgery. It also helps in estimating the site where we are most likely to encounter the tumor and the pituitary gland.

Hamburger classified 3 types of pneumatization based on its relationship to the sella turcica.

1)Conchal (rudimentary or absent sphenoid sinus)

2)Presellar (a posterior sphenoid sinus wall that is separated from sella by thick bone).

3)Sellar (a posterior sphenoid sinus wall that is adjacent to sella).

That's all for now... Time to Scrub.

Let's learn Together!

~Medha Vyas.

Cogan's Syndrome

●Cogan's syndrome (CS) is a chronic inflammatory disorder that most commonly affects young adults. Clinical hallmarks are interstitial keratitis (IK) and vestibuloauditory dysfunction, and associations between CS and systemic vasculitis, as well as aortitis, also exist. There are a range of pathologic findings, most of which reflect immune-mediated injury of the affected tissues; however, despite an association with systemic vasculitis, eye and inner ear specimens of those with CS do not reveal any evidence of vasculitis. The underlying mechanisms responsible for the eye and inner ear disease in CS are unknown.

●The predominant ocular feature of CS is IK, which typically causes eye redness, pain, photophobia, and blurred vision. Slit-lamp examination commonly demonstrates a patchy, deep, granular corneal infiltrate. IK is not essential for the diagnosis; ocular inflammation may involve other parts of the eye and may lead to iridocyclitis, conjunctivitis, episcleritis, anterior or posterior scleritis, or retinal vasculitis.

●The inner ear manifestations of CS are Ménière-like attacks consisting of vertigo, ataxia, nausea, vomiting, tinnitus, and hearing loss. Vestibular dysfunction may also cause oscillopsia, and caloric testing often reveals absent vestibular function. Recurrent episodes of inner ear disease frequently result in profound sensorineural hearing loss. Noninflammatory down-fluctuations in hearing may be difficult to distinguish from those of inflammatory origin. If hearing loss is associated with eye inflammation or other features of active CS or does not resolve within three to five days, an inflammatory origin is more likely.

●When present, the systemic vasculitis associated with CS is a large- or medium- to small-sized vessel vasculitis or an aortitis. The pattern of vessel involvement may be overlapping. Other systemic manifestations of CS include fever, fatigue, weight loss, lymphadenopathy, hepatomegaly, hepatitis, splenomegaly, pulmonary nodules, pericarditis, abdominal pain, arthralgia, arthritis, myalgia, and urticaria. An association with inflammatory bowel disease has also been observed.

●Evaluation of the patient with possible CS requires ophthalmologic examination to establish the presence of IK, scleritis, or episcleritis and to exclude other diseases and ocular pathology; neurologic and otologic examination to establish the presence of vestibuloauditory abnormalities; and rheumatologic examination to seek evidence of systemic vasculitis. We diagnose CS based upon the presence of characteristic inflammatory eye disease and vestibuloauditory dysfunction. The eye and inner ear are nearly equally likely to be the cause of presenting symptoms, while less than 5 percent of patients initially present with systemic manifestations

Bhopalwala. H

Low Alkaline Phosphatase

Subnormal values — Extremely low serum alkaline phosphatase concentrations can be seen in patients with fulminant Wilson disease complicated by hemolysis .
Low values can also occur in patients with hypothyroidism, pernicious anemia, zinc deficiency, congenital hypophosphatemia, and certain types of progressive familial intrahepatic cholestasis in children.

Bhopalwala. H

Amiodarone and thyroid dysfunction

Amiodarone, a class III antiarrhythmic drug is associated with a number of side effects, including thyroid dysfunction (both hypo- and hyperthyroidism)

AMIODARONE INDUCED HYPERTHYROIDISM:
There are two types of amiodarone-induced thyrotoxicosis (AIT):

Type I: This type is typically seen in patients with preexisting multinodular goiter or latent Graves disease, the excess iodine from amIODarone results in enhanced thyroid hormone production.

Type II: In type II AIT there is destructive thyroiditis caused by the drug itself that results in excess release of T4 and T3(There is no hormone production). It typically occurs in patients without underlying thyroid disease.

AMIODARONE INDUCED HYPOTHYROIDISM:
1)Normally after exposure to an iodine load (eg, radiocontrast), iodine transport and thyroid hormone synthesis are transiently inhibited to prevent normal individuals from becoming hyperthyroid(the Wolff-Chaikoff effect). Normally patients escape this Wolff-Chaikoff effect and come back to normal within a few weeks, but patients with pre-existing subclinical thyroid disease fail to escape and develop hypothyroidism.

2)Amiodarone also inhibits 5'-deiodinase which is responsible for the peripheral conversion of T4 to T3. So there is a decrease in T3 production.

-Srikar Sama

Diabetic amyotrophy

Hello everyone!

Today, I will be talking about diabetic amyotrophy.

Diabetic amyotrophy has a lot of names!

It is also known as Bruns-Garland syndrome, diabetic myelopathy, proximal diabetic neuropathy, diabetic polyradiculopathy, diabetic motor neuropathy, diabetic radiculoplexopathy, diabetic lumbosacral plexopathy, and diabetic LRPN.

Diabetic amyotrophy typically occurs in patients with type 2 diabetes mellitus. The traditional features include the acute, asymmetric, focal onset of pain followed by weakness involving the proximal leg, with associated autonomic failure and weight loss. Progression occurs over months and is followed by partial recovery in most patients.

The diagnosis of diabetic amyotrophy is mainly based upon the presence of suggestive clinical features in a patient with known or newly diagnosed diabetes mellitus. Appropriate laboratory investigations, particularly electrodiagnostic studies, and neuroimaging in select patients, are useful to exclude other peripheral and central nervous system etiologies as a cause of the neurologic symptoms and signs.

No treatments are proven to be effective for diabetic amyotrophy or for idiopathic LRPN.

PS: Distal symmetric sensorimotor polyneuropathy is the most common type of diabetic neuropathy - it is characterized by a progressive loss of distal sensation correlating with loss of sensory axons, followed, in severe cases, by motor weakness and motor axonal loss. Classic "stocking-glove" sensory loss is typical in this disorder.

Source: UpToDate

That's all!

-IkaN

Management of Diabetic Ketoacidosis

Hi guys! Let’s look at how we manage one of the the most dreaded medical emergencies; a complication of Diabetes Mellitus type 2.

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- Patients with DKA have a triad of hyperglycaemia, ketosis and metabolic acidosis and they are severely dehydrated due to osmotic diuresis.

- Those with altered sensorium or pH < 7.0 require intensive care. A comprehensive flow sheet of changes in vital signs, fluid intake/output and lab values must be maintained.

- Despite a bicarbonate deficit, most DKA patients often do not require bicarbonate replacement but may be given if arterial pH < 7.0

- Serum phosphate, magnesium and calcium may rarely need supplementation.

- Patient education is of utmost importance to prevent future recurrences.

Happy studying!

- Ashish Singh.

Euvolemic hyponatremia algorithm

Just happened to create this image so I thought of sharing with you guys :)

-IkaN

Cushing's Syndrome: A Quick Review

Definition: Clinical syndrome characterized by signs and symptoms of raised blood cortisol levels.

Etiologic classification:

• Pituitary Cushing's is Cushing's disease.

• ACTH dependence simply means if raised ACTH is the cause of raised cortisol.

• Feedback loop, more correctly negative feedback loop, implies if cortisol level influences ACTH level inversely. Ectopic Cushing's is caused my malignant cells that continuously proliferate and hence, continuously make ACTH, regardless of cortisol levels.

• Therapeutic administration of ACTH hormone for long periods can cause ACTH-dependent Cushing's. However, they are exceedingly rare (and hence, omitted from the whiteboard for simplicity).

(MCC= Most Common Cause ; B/L= Bilateral ; U/L=Unilateral)

Clinical Features:

CUSHINGOID

Central obesity, Cervical fat pads (with moon face and fish mouth = Cushingoid habitus), Collagen fiber weakness, Comedones (acne)
Ulcers (peptic)
Striae, Skin thinning & bruising
Hypertension, Hyperglycemia, Hirsutism
Immunosuppression, Infections
Necrosis (Avascular) of femoral head, Neuropsychiatric symptoms
Glucose intolerance, Growth retardation
Osteoporosis, Obesity
Impotence and menstrual abnormalities
Diabetes


Diagnosis:

High dose DXM or CRH don't bother ACTH or cortisol levels in Ectopic Cushing's as they're out of the feedback loop.

Other tests include:

• 24 hour urinalysis

• Midnight salivary cortisol

• 9 am cortisol

• Overnight low-dose DXM suppression test

• B/L inferior petrosal sinus sampling

• Electrolytes and routine CBC

(DXM=Dexamethasone)

Management:

• Iatrogenic: Withdraw steroids slowly.

• Pituitary: Trans-sphenoidal resection OR radical hypophysectomy, less commonly

• Adrenal: Surgical resection with post-op prednisolone OR medically treat with Metyrapone or Aminoglutethimide.

• Ectopic: Chemotherapy and Radiotherapy for small cell lung cancer OR surgical resection for carcinoids.

Let me know if anything needs clarification.

Happy studying!

-- Ashish Singh.

Autonomic neuropathy in diabetes mnemonic

Autonomic neuropathy in diabetes mnemonic

Hi everyone! This is one of the longest mnemonic in my sleeve.

I made this one up because it comprises a group of bizzare symptoms which we seldom relate to diabetes and take less notice of. These symptoms are indications of poor glycemic control.

The mnemonic is, 'AUTONOMIC NEUROPATHY' itself:

A - Abdominal fullness
U - Urinary incontinence
T - Tachycardia (Resting)
O - Oesophageal atony (Dysphagia)
N - Nocturnal sweats
O - Oedema (dependent)
M - Micturition delayed
I - Infection
C - Constipation

N - Nocturnal diarrhoea
E - Erectile dysfunction
U - Uncontrolled glycaemia
R - Retrograde ejaculation
O -
P - Pupillary signs (pupil size decreases, delayed or absent reflexes)
A - anhidrosis
T - Temperature (cold feet)
HY - Hypotension (postural)

This mnemonic was written by our Medical Student Guest Author, Nikhil

Steroid Hormone synthesis pathway (Clinical aspect)

Hello Awesomites :D

I was reviewing the corticosteroid synthesis pathway and its applied.
Let us begin. :))
Adrenal gland consist of two parts :-
1. MEDULLA
2.CORTEX
Adrenal dysfunction includes hyperfunction / hypofunction of medulla and cortex.
1. MEDULLA

A) HYPERFUNCTION - pheochromocytoma
                                        -Neuroblastoma
2.CORTEX

A)HYPERFUNCTION -Conn's disease
                                      -Cushing's syndrome (Primary tumors)
                                                                          (excess ACTH -pituitary hypersecretion,ECTOPIC)
B)HYPOFUNCTION -ACTH deficiency (Iatrogenic , pituitary insufficiency)

C)CONGENITAL ADRENAL HYPERPLASIA (from partial enzyme deficiencies due to mutation in genes)

Clinical features of CAH :-

1.DUE TO DECREASED ALDOSTERONE :-
-Sodium wasting (hyponatremia+dehydration+shock)
 (early presentation)
-increased potassium
-acidosis
2.DUE TO DECREASED CORTISOL:-
-Hypoglycemia
-increased ACTH
3.DUE TO INCREASED TESTOSTERONE :-
In female , virlization.
In male, No symptom, increased size and pigmentation of penis.

Q. What is the difference between 21-hydroxylase deficiency and 11beta hydroxylase deficiency ?
Ans. In 21-hydroxylase deficiency, hypotension occurs due to salt wasting.
Accumulation of 11-deoxycorticosterone as a result of 11 beta hydroxylase deficiency leads to "HYPERTENSION".

Q.Most common form of CAH is due to mutation or deletion of which gene?
Ans. CYP21A resulting in 21-HYDROXYLASE DEFICIENCY .

Q.Which Enzyme deficiency showing virlization in females?
Ans. -21 hydroxylase
        -3beta HSD
       -11 Beta hydroxylase.

Q. Two hypertensive form of CAH.
Ans. 11beta hydroxylase and 17hydroxylase deficiency.

Other points :
- Females with 17-hydroxylase deficiency appear phenotypically female at birth but do not develop breasts and mensturate in adolescent because of INADEQUATE ESTRADIOL PRODUCTION(17 hydroPregnenolone is also a precursor of estrogen). They may present with hypertension.
-CAH is a type of enzyme deficiency. So it can be partial or complete .There is a severity spectrum.
More severe form shows salt wasting.
Milder form shows "NON CLASSICAL TYPE of CAH".

Diagnosis:-

• 17hydropregnenolone with or without ACTH test
• CYP21A2 panel,sequencing,deletion
• Carrier screening test (Preconception test)
• Karyotyping ( In case of ambiguity of sex)
• Hormones and electrolytes

Treatment:-

• Counsel the parents.
• Protect from Adrenal insufficiency ( Give mineralocorticoid and glucocorticoid)
• Avoid salt wasting crisis during illness,stress,etc. ( Increase dose of glucocorticoid,Give IV fluids and sodium and dextrose)
• Surgery ,sex assignment.

(Note :- There are two more variants of CAH 1. Lipoid CAH 

2.POR deficiency ( P450 oxidoreductase enzyme deficiency) - also involved in both sterol and steroid synthesis pathway).

Study hard.

-Upasana Y. :)

SIADH vs Diabetes Insipidus, Osmolarity and Sodium levels in urine and serum in both (mnemonic)

Serum and urine findings in SIADH and  Diabetes Insipidus can really mess up our brains :S

A nice mnemonic to memorize SIADH is to recall the letters as  :
 "S"odium "I"s "A"lways "D"own "H"ere (by here: I mean serum) =>
so in SIADH:
=> low Na in serum
=> high Na in Urine & high Urine Osmolarity

Now ...just think of the opposite and you ll get Diabetes Insipidus
so in DI:
=> high Na in serum /high serum osmolarity
=> low Na in Urine

-Murad

Medicollabowesome: Does long-term coffee intake reduce type 2 diabetes mellitus risk?

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