Morphology of Rapidly progressive glomerulonephritis

The morphology of crescentic glomerulonephritis seen in rapidly progressive glomerulonephritis (RPGN) is quite easy, so here i am just sharing the difference between differences in the types of RPGN only:

Points of difference		Immune complex mediated	Anti GBM antibody mediated	Pauci immune type
Endocapillary proliferation		ü	û	û
Mesangial proliferation		ü
Immunofluorescence	Linear staining	û	ü	û
	Granular staining	ü	û	û
Dense immune complex deposits		ü	û	û

I hope it will help you in remembering the morphology 

In Sha Allah

see you soon with something new again IA

Thank you 😊

Mnemonic | Morphology of IgA nephropathy

 Morphology of IgA nephropathy will be derived from its pathogenesis and the disease name.

so the mnemonic is presented here:

Pathogenesis = indicates about role of immunoglobulins and mesangial cells

now about these 2 things take the name of the disease:

IgA = A = All 

= all main antibodies in infections (IgA, IgG, IgM) 

= all mainly possible mesangial morphologies ranging from mesangial widening, diffuse mesangial proliferation endocapillary proliferation, segmental sclerosis, , to crescentic glomerulonephritis  

(remember it by keeping in mind the structure of glomerulus in which from center to periphery comes mycangium, capillaries and then epithelium of glomerulus)

I hope it works for you all again 👽

In Sha Allah!

Thank you 💓

Mnemonic | Uncinate Herniation / Transtentorial Herniation

The word that comes first in my mind when i see uncinate written in the book is UNCLE

I don't know why but this is what it is!

so my UnKle is PHD

U = uncinate herniation

K = Kernohan's Notch 

P = posterior cerebral artery compression

H = hemiparesis (ipsilateral)

D  = Duret hemorrhage (midbrain and pons)

• and from posterior cerebral artery point and hemiparesis, another thing can be linked which is CN# 3 paralysis

because posterior cerebral artery supply mainly occipital lobe so some problem with eye may occur which is actually related to oculomotor nerve compression (just a linker not the actual pathophysiology)

I hope it works for you all again!

In Sha Allah!

Thank you 💓

Mnemonic | Morphology of Membranoproliferative Glomerulonephritis

Here again I am back with another mnemonic to remember the morphology of Membranoproliferative Glomerulonephritis 

Pathology is fun 😭😂

I hope the feelings are obvious to everyone now lol 😁

this mnemonic will be mainly derived from the name of the disease:

Membrano proliferative Glomerulonephritis:

• if I abbreviate this disease to MG (membranoproliferative glomerulonephritis), than i can make you remebr that MG is a car manufacturing company so its cars would make a tram track appearance on roads when they are driven

and then comes the breakdown of the disease name:

• Membrano = meaning something wrong is with basement membrane of glomerular capillaries

tram track appearance 

• Proliferative  = meaning something is proliferating 

so endothelium, mesangium is proliferating (ME from membrano)

• Glomerulonephritis = inflammation indicates infiltration of leukocytes as it is a nephritic syndrome mainly

specific types of Membranoproliferative glomerulonephritis have these all above said features but certain differences which are mentioned in this table below:

Differences	Membranoproliferative glomerulonephritis type 1	Membranoproliferative glomerulonephritis type 2 (C3 glomerulopathy)	Dense deposit disease
C3 deposits	↑   Deposited in irregular pattern (subendothelial ONLY)	↑↑   Waxy deposits (mesangial, subendothelial and tubular BM)	↑↑↑   Ribbon like highly dense deposits (mesangial, subendothelial and tubular BM)
Classic complement system components	Present	Absent	Absent

I hope this was fun also for you like always!

I hope it works you again

In Sha Allah!

Thank you 💓

feel free to ask any study related question in the comment section👽

Mnemonic | Morphology of Membranous Nephropathy |

Morphologies are always very difficult, atleast for me and my colleagues 😥

so I have made a mnemonic for the membranous nephropathy morphology:

I will try to keep it simple and make the name of the disease a major hint for the morphology:

4 things will get evident from the name of the disease:

1.  Word membranous indicates towards basement membrane of capillaries of glomerulus, and what can happen to it in inflammation or disease?

mostly thickening of basement membrane of capillaries

2.  M stands for Mehrab (the place where Muslim religious leader of stands to lead the prayer) - picture is shown below

   

took this image from alamy website (and these pictures are downloadable from there without any consent)

so the leader stands in it and it appears like dome if seen from outside = dome and spike pattern 

3.   next comes the dome again,  as I described the dome appearance from outside of this mehrab so if I imagine that dome being the outside of capillaries which will blink in mind the point of 

sub epithelial deposits 

(as epithelium is on the outside of capillaries in glomerulus)

   

4.  remaining morphology is same as in other nephrotic syndromes (effacement of podocytes, etc.)

I know it has got long but to remember morphologies and then forgetting is worst than understanding this mnemonic and keeping the memory long enough atleast till final exam. lol 😂

I hope it works again for you like my other mnemonics

In Sha Allah!

Thank you 💓

Mnemonic for Morphology of Focal Segmental Glomerulonephritis

 Morphology of Focal segmental glomerulonephritis is derived mostly from its name and its pathophysiology.

so here it is:😍

1st word = Focal = only some glomeruli are involved (mainly juxtamedullary)

but it can extent later to whole of cortex as well

2nd word = segmental = only a portion of glomerulus is involved

but later may extend to whole of glomerulus which may extend into interstitium and ultimately tubular atrophy can occur

3rd word = glomerulosclerosis = scarring/fibrosis of glomerulus

scarring hints scarring obviously (fibrosis I mean)

and scarring links to capillary lumen obliteration of glomerulus 

(imagine a situation when glomerulus will be sclerosed, it will get contracted and so capillary lumen will also start collapsing) - now link obliteration of capillary lumen with increased mesangial matrix

for this see the diagram of glomerulus and understand that mesangial growth can also compress upon the capillary lumen and cause lumen obliteration

Pathophysiology:

link the morphology with pathophysiology if you are reading pathophysiology of FSGS from Robbins pathology then it has said that some people think that FSGS is a derivative of minimal change disease and the hall mark of minimal change disease is 

EFFACEMENT OF PODOCYTES - SO this morphology is also here

and this effacement means leakage of plasma contents seen in minimal change disease that is proteins and lipids so here we see 

HYALINOSIS AND LIPID LADEN MACROPHAGES

I HOPE IT WORKS WELL.👀

In Sha Allah!

Mnemonic for causitive agents of Acute Postinfectious glomerulonephritis

How to remember that which organisms can be the cause of postinfectious glomerulonephritis?

Sometimes it gets very problematic, not because that is important to know, but because sometimes you just want to remember everything  from ROBINS PATHOLOGY. lol

so here it is:

BACTERIAL CAUSES:

Post infectious glomerulonephritis is also called post streptococcal glomerulonephritis and it is a quite obvious things. From this we have:

                                                                    PostSTreptococcal

the name itself indicates Streptococcus

P indicates Pneumococcus and ST for Staphylococcus 

VIRAL CAUSES:

From the name of post streptococcal glomerulonephritis, the first thing that comes to mind is some relation with children because when we studied these topics in our immunology chapters than glomerulonephritis and post infectious endocarditis were written next to each other. so children picture is now clear in our little brains, now what children do most of the time? CRY! lol And how:

MM AHu ahu....................................................aaaaaaaaaaaaaaaaaaaaaaaaaaaaa lol and mother says CHHHHH tos top him from crying (or may even slap - a vicous cycle may begin or terminate. you can relate yourself. lol - sorry for your nostalgia!)

M = mumps

M = measles

A = aaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaa (thats nothing. lol)

H = HBV HCV

CHHH = chickenpox

and that's it! 

I hope it works for you 

In Sha Allah !

Thank you 💓

Acute rheumatic fever and RHD - diagnostic criteria

Hello

Diagnosis of ARF and RHD based on modified Jones' criteria - let's review:

Rheumatic chorea - variable clinical presentation timelines

 Hello

Variations in clinical presentation of rheumatic/ sydenham's chorea -

Job's syndrome

Job's syndrome is also known as hyper- IgE syndrome.

It has autosomal dominant inheritance ( STAT3 gene).

Here is the mnemonic to remember its key features :

A - Abscesses of face and lungs by staphylococcus aureus ( pneumatocele)

B - Bone fragility

C - Coarse facies

D - Dermatological features like eczema.

E - Eosinophilia, increased Ig E.

Trick to remember important points: 

"Steve Jobs is a dominant person, interested in business STATs"

That's all!

Dr. Madhuri.

Fact of the day - hypercalcemia in sarcoidosis

 Hi!

Hypercalcemia and hypervitaminosis-D is seen in patients with sarcoidosis and other granulomatous inflammatory conditions. This is because the granulomatous macrophages have high 1-alpha hydroxylase activity --> high levels of 1,25-OH2 vitamin D (calcitriol), produced in addition to this enzyme's normal activity in the kidneys.

That's all

- Jaskunwar Singh

Ehler-Danlos Syndrome (EDS) - High yield only

Hi! So let's learn EDS together. I've tabled a list of high-yield points of all the types of EDS. It requires little bit of revision but once you get a pictorial familiarity you should be able to recall them all. 

Have fun!

So, how to remember?

Step 1. Divide the table into 2 halves. Sl no. 1,2,3 have in common a lot of features:

• They are all Autosomal Dominant. 
• They have common Clinical features - skin HYPERelasticity, joint HYPERmobility and HYPER (easy) bruising. 
• Go serially, Classical has the first 2, Type I and II and HYPERmobile is III and lastly Vascular is type IV 
• Vascular type has additionally - arterial & uterine rupture.

Step 2. Now the second section Sl no. 4,5,6

• EDS types with enzyme defects are Autosomal Recessive. So, 4 and 6 are AR. 
• Kyphoscoliotic EDS is Type VI (K rearranged is a V and I)
• For the last 2, mnemonic is ABCD😛 Arthrochalasia VII a, b and VII c is Dermatosparaxis.
• KyphoSCOLIOTIC EDS - defective lysyl hydroxylase (=> abnormal cross linking of collagen or KOLLAGEN => think of bones 🦴 => congenital SCOLIOSIS)
• ARTHROchalasia is COL IA (1st letter is A) and hence presents with severe JOINT hyper mobility.
• DERMATospARaxis is AR and a defective Procollagen-N-peptidase and presents with CUTIS laxa. (Cuties are Pros ;)

Step 2. For the Gene types, come down in descending order: 5 4 3 2 1 0 

Step 3. Remember Type V - DOEST NOT EXIST. 

Step 4. Revise again 😉

That's it! Stay safe 🌸

- Anagha :)

Creatinine clearance in elderly - basic notes

 Hi!

Elderly people have a decrease in creatinine clearance (CrCl), which means an increase in serum Cr. It is observed that annual rate of this decrease in CrCl is approximately 1 ml/min. after the age of 50 years.

Therefore, it is important to calculate the dose and dosing intervals of nephrotoxic drugs (eg., aminoglycosides) in these patients in order to prevent the precipitation of ARF.

In general,

CrCl <100 ml/min is abnormal.

However, CrCl <10 ml/min signifies the onset and worsening of acute renal failure.

Note -

• GFR is directly proportional to CrCl.

• GFR decreases by age, but not always accompanied by rise in Cr.

• Cockcroft-Gault formula is commonly referred to for calculating CrCl.

CrCl = (Ucr × V)/Pcr (~GFR)

• Double the Cr = Half the GFR.

Note that those patients with signs of worsening diabetes and resulting glomerulopathies, an increase in both GFR and CrCl is seen, which thus causes hyper filtration injury. 

That's all

- Jaskunwar Singh

Lyme's disease - a review

 Hi!

Lyme's disease/ Lyme borreliosis

A patient with a typical history of frequent visits to the woods with bull's eye rash, neurologic features, cardiac abnormalities, and musculoskeletal features.

Menkes disease and Wilson's disease - DDx

 Hi!

Okay so maybe they are the two of the options for a patient's clinical scenario question and you have a blurred memory for which is which in context to copper metabolism?

Let's clear the basic facts here...

Ampicillin-rash in infectious mononucleosis

 Hi!

Penicillins such as amoxicillin and ampicillin are currently not recommended in patients with infectious mononucleosis with bacterial secondaries (streptococcal tonsillo-pharyngitis). Why?

Genomic imprinting and Trinucleotide repeat -EXTRA EDGE

Hello Awesomites! 

1.Genomic imprinting IOC = methylation specific MLPA 

2.Trinucleotide repeat disorder = IOC is Trinucleotide primed PCR 

3.Fragile X Syndrome is XLR (mendelian inheritance) but once inherited during gametogenesis what happens is non - mendelian inheritance.

Confusing but thats the beauty. 

Can you tell me about Huntington disease what does mendelian and non mendelian inheritance mean? 

4.Angelman  that undergo whatever you learn (like maternal deletion and unipaternal disomy) involve chromosome 15 but gene is UBE3 ubiquitin protein. 

And praderwilli whatever you learn happens at chromosome 15 but gene is Sn RPN (small nuclear ribonucleoprotein polypeptide N)

 Hope it broadens your horizon.

-Dr.Upasana Y. 

Clinical pearl : TNF-alpha therapy

Hello

In case of granulomatous diseases, macrophages activated by Th1 cells lead to increased levels of TNF-alpha. Now, TNF-alpha induces and maintains granuloma formation. Basic, right?

So we give anti-TNF drugs (adalimumab, infliximab, etc.). However, they cause the granuloma to break down, thus leading to disseminated disease.

Bottom line - Always remember to check for the presence of latent TB before starting anti-TNF therapy.

That's all
- Jaskunwar Singh

COVID-19: Coronavirus and hemoglobin

Hello Awesomites!

Please refer to the diagrams for better understanding.

Why do we have abnormal hemoglobin-related biochemical indices in COVID-19 patients?
Reports demonstrate that the hemoglobin and neutrophil counts decrease in most patients with SARS-CoV-2 infection, and values of serum ferritin, erythrocyte sedimentation rate, C-reactive protein, albumin, and lactate dehydrogenase increase significantly.

What makes hemoglobin an attractive molecule for the coronavirus?
Porphyrins!

Porphyrins in the human body are mostly iron porphyrins i.e heme. And a lot of heme is not free, but bound to hemoglobin. Viruses require porphyrins to survive. Therefore, the novel coronavirus targets hemoglobin, attacks heme, and hunts porphyrins.

Structure of SARS-CoV-2

Image by Upasana Yadav

The possible mechanism is that orf1ab bound to the alpha chain and attacks the beta chain, causing conformational changes in the alpha and beta chains; ORF3 attacks the beta chain and exposes heme. ORF10 then quickly attaches to the beta chain and directly impacts the iron atoms on the heme of the beta chain. The heme is dissociated into porphyrin, and orf1ab finally captures porphyrin. Orf1ab plays a vital role throughout the attack. Attack of oxidized hemoglobin by viral proteins leads to less and less hemoglobin that can carry oxygen. The invasion of viral proteins on deoxidized hemoglobin will cause less and less hemoglobin that can carry carbon dioxide.

This study found that ORF8 and surface glycoprotein had a function to combine with porphyrin to form a complex, while orf1ab, ORF10, ORF3a coordinately attack the heme on the 1-beta chain of hemoglobin to dissociate the iron to form the porphyrin. This mechanism of the virus inhibited the normal metabolic pathway of heme, and made people show symptoms of the disease.

What causes the high infectivity of the novel coronavirus?
Medical workers have detected the novel coronavirus from urine, saliva, feces, and blood. The virus can also live in body fluids. In such media, porphyrin is a prevalent substance. At the beginning of life, virus molecules with porphyrins directly move into the original membrane structure by porphyrin permeability. This study showed that the E2 glycoprotein and Envelope protein of the novel coronavirus could bind well to porphyrins. Therefore, the coronavirus may also directly penetrate the human cell membrane through porphyrin. (Means If the virus can bind with porphyrins, it can enter these secretory cells without ACE2 receptors by using the membrane permeability)

What is the importance of knowing the above information?
The drugs based on this mechanism: Chloroquine and Favipiravir.

The primary function of the Envelope protein is to help the virus enter host cells. The primary role of Favipiravir is to prevent the virus from entering host cells and catching free porphyrins. Favipiravir's ability to improve respiratory distress is lower. Favipiravir can only prevent the binding of Envelope protein and porphyrin.

Chloroquine could prevent orf1ab, ORF3a, and ORF10 from attacking the heme to form the porphyrin and inhibit the binding of ORF8 and surface glycoproteins to porphyrins to a certain extent, effectively relieve the symptoms of respiratory distress.

The infectivity of the nCoV pneumonia was not completely prevented by the drugs, because the binding of E2 glycoprotein and porphyrin was not inhibited.

Note for Diabetic patients
Diabetic patients and older people have higher glycated hemoglobin. Glycated hemoglobin was reduced by the attack, which made patients' blood sugar unstable. Since the porphyrin complexes of the virus produced in the human body inhibited the heme anabolic pathway.
Written by Upasana Yadav
(Courtesy:-Thank you Ikan for all the help) 

References:
1. Wenzhong, liu; hualan, Li (2020): COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism. ChemRxiv. Preprint. https://doi.org/10.26434/chemrxiv.11938173.v5
Link to the article: https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173

Rickettsia mnemonic

Hi!

Do you want to learn about Rickettsia today?

Rickettsia mnemonic (Rickettsia typhi, flea vector)