Causes of priapism

Hello lovely medical students!

Priapism is persistent, painful erection that develops without sexual simulation.

Here are a few causes of priapism:

Prazosin
(Mnemonic: PRazosin causes PRiapism)

Trazodone
(Mnemonic: Trazodone causes a boner - TrazoBone)

Perineal or genital trauma

Neurogenic lesions

Sickle cell disease and leukemia

Always check medications first, since it is often drug induced.

That's all!
-IkaN

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It's like the broadcast list on Whatsapp

https://t.me/medicowesome

Nephrotoxic antimicrobials

Hello! In this post, I'll be talking about nephrotoxic antimicrobials.

Let's start with Aminoglycosides!

Aminoglycoside toxicity manifests in the form of tubular necrosis.

Did you know AKI due to Aminoglycosides manifest 5-7 days after therapy even after the drug has been discontinued? :O

Aminoglycosides accumulate in the renal cortex and cause non oliguric AKI. Hypomagnesemia is a common finding.

Amphotericin B also causes tubular necrosis. It binds to tubular membrane cholesterol and introduces pores. Clinical findings include polyuria, hypomagnesemia, hypocalcemia and NAGMA.

Mnemonic for nephrotoxic drugs: Drugs with A!

Aminoglycosides
Amphotericin B 
Antivirals like acyclovir, tenofovir, cidofovir, foscarnet, pentamidine.
(Cause tubular toxicity)

Antibiotics like penicillin, cephalosporins, quinolones, sulfonamides, rifampin.
(Cause acute interstitial nephritis)

Remember, in acute interstitial nephritis, WBCs, WBC casts and urine eosinophils will be seen. However, in AKI, the urine sediment will show granular casts.

That's all!
The predominant feeling I have is that if gratitude (=
-IkaN

Pathophysiology of Absence Seizures

Currently, the best understood of the primary generalized seizures is the Absence Seizure(also called Petit Mal seizure).

So we will focus on it. In contrast to secondary generalized seizures, where synchronicity begins in a specific foci in the brain within an aggregate of neurons and then spreads to the entire brain; the primary generalized seizures arises from central brain regions like Thalamus and then spreads rapidly to both hemishpheres.

To understand the pathophysiology of absence seizures, we first have to be acquainted with the physiology of slow-wave(Stage 3) sleep; since they both have similar EEG reading patterns; i.e., the 3-per-second spike-and-wave activity.

In the awake state, the thalamocortical circuits are in "transmission" mode, whereby incoming sensory informations are faithfully transmitted to the cerebral cortex. Whereas in slow-wave sleep, these circuits are in"burst" mode, because of the bursting activity of a unqiue, dendritic T-type Calcium channel in the thalamus which alters the incoming sensory signals in such a way that the output signals to the cortex have an oscillatory firing rate; but no sensory information is transmitted to the cortex. Something similar happens in Absence Seizure.

In absence seizure, there is abnormal, abrupt activation of this T-type calcium channel in the awake state. This has been postulated to be due to hyperpolarizaion of relay cells in thalamus which in turn is due to increased GABAergic input from the reticular nuclei. 

Hence, drugs that block T-type calcium channels (Ethosuximide, Valproate, Lamotrigine, Clonazepam) are used in the treatment of these seizures while Barbiturates which augment the GABAergic activity in the reticulothalamic relay circuits exacerbate the condition. 

-VM

Pathophysiology of Secondary Generalized Seizures

To understand the pathophysiology of seizures in brief, lets take the following case.

“Two brothers, Ram and Shyam were playing chess. When all of  a sudden Ram noticed that his 40-year old brother seemed to be daydreaming  and seemed to be confused and having a petrified stare for about 20 seconds. Then suddenly his right hand began to bend into an awkward position and then to shake. The shaking grew worse, progressing gradually from the hand to the arm and then to the entire right side of the body. Then his body stiffened for about 15 seconds, followed by shaking movements of all four limbs that lasted another 30 seconds or so. Then he became limp and unconscious.”

1. Now here Rob first showed the symptoms of daydreaming, confusion and petrified stare, this is known as Aura. Since its a behavioural disturbance, we can guess that the foci of this seizure activity is in the temporal lobe(hippocampus, amygdala etc).

2. So there is abnormal synchronous electrical activity(ASET) somewhere in the temporal lobe which could have been due to any pathology like tumour, tuberculoma, stroke, viral encephalitis, neurocysticercosis etc.

3. It took the seizure activity 20 seconds to override the Surround inhibition  of the temporal lobe and then spread to the neighbouring areas.

4. Next there is contraction of muscles followed by shaking first in his right hand, then arm, then the complete right side. This means now the abnormal synchronous electrical activity(ASET) has spread to the left motor cortex and progressively involved the entire homunculus.

5. Next this tonic-clonic activity involves the entire body. This means that ASET has spread to the contralateral hemishphere via corpus callosum and other commissures and that it has involved Thalamus, which is the gateway to the entire cerebral cortex. Now since it is bilateral, we can call it a Generalized seizure.

6. Lets learn the mechanism of Tonic-Clonic seizure(Grand Mal seizure) activity.

A: First there is sudden inhibition of all GABAergic activity leading to overriding       of the Surround Inhibition, causing contraction of both agonist and antagonist group of muscles, referred to as the Tonic phase.

B: Then the GABA-mediated inhibition is gradually restored and while increasing it starts      oscillating with the excitatory activity mediated by Glutamate via its NMDA and AMPA receptors. If this oscillation involves the motor cortex, there is shaking movements, referred to as Clonic phase.

C: Ultimately the GABA-mediated inhibition prevails, resulting in all the muscles               becoming flaccid and the patient becomes unconscious until normal brain function is restored.   

-VM

Radiolucent stones mnemonic and uric acid calculi

Good morning! =)

I was studying about radiolucent kidney stones and thought of sharing what I learnt with you all.

Mnemonic for radiolucent renal calculi: CATIX URL
Cysteine
Adenine (2,8-Dihydroxyadenine)
Triamterene
Indinavir
Uric acid
RadioLucent

Another mnemonic for medication stones: GUEST MIC
Guaifenesin stones (Radiolucent)
Ephedrine stones (Radiolucent)
Sulphonamides stones (Radiolucent)
Triamterene stones (Poorly radiopaque)
Magnesium trisilicate stones (Poorly radiopaque)
Indinavir stones (Radiolucent)
Cephalosporins stones (Radiolucent)

If you are asked to choose the radiolucent one between Orotic acid stones and cysteine stones, choose orotic acid. It is radiolucent, cystine is poorly radioopaque.

Magnesium ammonia phosphate (struvite) and Cystine calculi are less radiodense and are more difficult to visualize. Uric acid, orotic acid, xanthine, triamterene, dihydroxy­adenine, and indinavir calculi are radiolucent and might not be seen on a plain radiograph.
(Source.)

Predisposing factors for uric acid stones:
1. Low urinary pH
2. High uric acid excretion

Treatment for uric acid stones:
1. Alkalinization of urine
(Sodium bicarbonate, potassium citrate)
2. Increase fruits, veggies. Decrease animal flesh.
3. XOI - Allopurinol, Febuxostat

Alkalinization of urine mnemonic: ABC.
Alkalinization. Bicarbonate. Citrate.
(Sodium bicarbonate and potassium citrate are used for alkalinization of urine)

That's all!
-IkaN

Study group discussion: Cold agglutinin disease and extravascular hemolysis in liver

We were discussing a MCQ from pathologystudent.

Here's the question:

On a routine physical examination of an elderly male patient with no other medical problems, you note that his earlobes and fingertips are pale and slightly bluish. A CBC shows a hemoglobin of 10.6 g/dL (12 – 16) and an MCV of 88 (80 -100). Numerous red blood cell agglutinates are seen on the blood smear, made by smart technologists in your laboratory. Which of the following statements is true?

1. The antibody bound to the patient’s red blood cells in this disorder is probably IgG
2. Complement is probably bound to the patient’s red cells
3. The spleen is the main site of red cell destruction in this patient
4. 1 and 3
5. 1, 2, and 3

1 is not true. It's cold agglutinin disease. The main antibody is IgM here.

2 is correct since complement is involved.

The main site of destruction is liver macrophages (Kupffer cells). Therefore, 3 is incorrect.

Is there a specific reason for it?

Liver RECs have loads of C3 specific receptors. So most extravascular hemolysis that occurs in cold agglutinin disease is in the liver.

Another common mechanism of hemolysis in cold agglutinin disease is direct complement mediated intravascular hemolysis.

There's C3b on RBC and macrophage has CR3 (Complement receptor 3).

Liver macrophages lack the capacity of spleen to sequester cells. Hence, here the RBC destruction in liver occurs by phagocytosis predominantly.

Thanks, Divya, for explaining this.

Tourette syndrome mnemonic

Hello!

For those who don't know -

Tourette syndrome is a disorder involving multiple motor and vocal tics, for at least a year, before 18 years of age.
Mnemonic: T for Tourette, T for Tics!

Tourette syndrome is associated with ADHD and OCD.

Mnemonic: TAO!
Tourette - ADHD, OCD.

Treatment - Antipsychotics like tetrabenazine, risperidone, fluphenazine are preferred.
Clonidine and Clonazepam maybe useful.

That's all!

-IkaN

Step 2 CK: CLL notes and staging mnemonic

Hey!

Chronic lymphocytic leukemia is proliferation of normal B lymphocytes that function abnormally.

The WBC count in CLL is > 20,000/flL with 80-98% lymphocytes.

Smudge cells are seen in CLL.

Staging of CLL mnemonic

High  LSAT score :D

Stage 0: High WBC
Stage 1: Lymphadenopathy
Stage 2: Splenomegaly + Hepatomegaly
Stage 3: Anemia
Stage 4: Thrombocytopenia

For stage 0 and stage 1, no treatment is required.

Therapy is indicated for patients with advanced stage disease, high tumor burden, severe disease-related "B" symptoms, or repeated infections.

Hepatosplenomegaly, anemia and thrombocytopenia are preferably treated with fludarabine and rituximab (FR).

For refractory cases, cyclophosphamide can be used (FCR regimen)

Older individuals (> 65 years of age) can be treated with ibrutinib, a bruton’s tyrosine kinase (BTK) inhibitor (preferred) or chlorambucil plus anti-CD20 monoclonal antibodies.

Autoimmune hemolysis or thrombocytopenia is treated with prednisone (Autoimmune warm IgG antibodies)

CLL has a good prognosis compared to other leukemias. Most common cause of death is due to infection.

That's all!
-IkaN

Bulbar and pseudobulbar palsy mnemonic

Hello! This is a mini post on bulbar and pseudobulbar palsy.

Bulbar palsy is the paralysis of the muscles supplied by the cranial nerves coming out from the bulb also known as the medulla (Cranial nerves 9, 10, 12) and it is lower motor neuron palsy.

Pseudobulbar palsy is paralysis of the same cranial nerves but the upper motor neuron type. Mostly due to lesions in the brain.

Mnemonic: pseUdo has a U for UMN lesion.

That's all!
-IkaN

Cataplesy and cataplexy mnemonic

Awesomite: Hi! Urgent mnemonic help. So can you tell me how I can remember this -

A case with dyspnea and blurring of vision

A 63-year-old male presented with increasing fatigability and dyspnoea for 2 months, and headache and blurring of vision for past 15 days. Physical examination was significant for pallor, mild hepatomegaly and a palpable spleen (2 cm).
Labs showed:
Hemoglobin concentration of 4.0 g/dL
Total white cell count of 25000/cmm
Platelet count of 60000/cmm
Monoclonal gammopathy (M spike) was seen in gamma globulin region, which turned out to be IgM on immunofixation.
Fundus examination revealed venous dilatation, tortuosity and superficial retinal hemorrhages.

Diagnosis? Treatment?

Tetanus are Anaerobic! Can Oxygen infusion into the wound, heal tetanus?

Think about it for a moment! Then look for the answer.

Non-Hodgkins lymphoma treatment (CHOP regimen) mnemonic

Hey!

If you can't remember the drugs used in the CHOP regimen of Non-hodgkin's lymhoma, I have a mnemonic for you.

Hodgkins lymphoma treatment (ABVD regimen) mnemonic

Hey!

If you can't remember the drugs used in the ABVD regimen of Hodgkin's lymhoma, I have a mnemonic for you.

Study group discussion: ADP fibrinogen test

What is ADP (Adenosine diphosphate) fibrinogen test?

ADP, formed by Ib receptor, acts on IIb IIIa receptor through fibrinogen and causes aggregation.

In vWD and Bernard Soulier disease (Ib defect), if you add ADP, aggregation would take place and test will be normal as it acts on IIb IIIa receptor.

In glanzmann thrombasthenia, the IIb IIIa receptor is deficient. ADP can not act on the receptor, if added. That's why, the test becomes abnormal.

Therefore, the test is normal in vWD, Bernard soulier disease and abnormal in glanzmann thrombasthenia.

Explained by Abhishek Shukla

Homocysteine metabolism notes for USMLE

Hey!

Let's do a quick and dirty Q&A post :D

Homocysteine metabolism

PATCHED: When the tonsils shows a membrane

Hello everyone.

I'm back with a simple mnemonic to deal with a questionably common but very important issue: The Patch On The Tonsil.

Difference between neuroleptic malignant syndrome and serotonin syndrome

Neuroleptic malignant syndrome:
Evolves over one to three days.
Sluggish neuromuscular responses (Rigidity, bradyreflexia)
Typical course: Mental status changes appear first, followed by rigidity, then hyperthermia, and autonomic dysfunction (Tachycardia, high BP, tachypnea)

Step 2 CK: AML (Acute myelogenous leukemia) notes

Hello! So these are my notes on AML :)

Treatment of AML mnemonic

Hi.

The mnemonic for treatment of AML is ABCD!