Virus Replication

There are 6 distinguish stages of viral replication;

1. Attachment
-affinity between the virus and the host cell's plasma membrane permits this stage.

2. Penetration
-virus particles are brought inside the cell, either by endocytosis or directly pass through the cell's plasma membrane.

3. Uncoating
-removal of capsid, to expose the viral nucleic acid.

4. Biosynthesis
-synthesis of viral nucleic acid, capsid, and enzymes.

5. Maturation
-two phases, phase I is assembly which the polypeptide chains assembled into capsomeres to form procapsid
-phase II is the intake of nucleic acid into the procapsid, forming a complete virion.

6. Release
-occurs by 3 mechanisms.
-cell lysis (host cell is killed by virus-induced)
-budding (no cell killing, usually by enveloped viruses)
-cell degeneration (after cell death, the virus released. non-virus-induced)

Skin and its Inflammatory pathologies.

Skin is the largest external organ of the body.

It consists of 3 layers;
1) Epidermis
2) Hypodermis
3) Dermis

Epidermis can be further classified into 5 sublayers;
i) Stratum corneum (outermost part, dead cells)
ii) Stratum lucidum
iii) Stratum granulosum
iv) Stratum spinosum
v) Stratum germinativum (innermost layer, all the above layers originate from this layer)

Any injury which does not involve stratum germinativum, will lead to complete healing without scarring.

Otherwise, any injury involving stratum germinativum will lead to scarring formation.

The scar will be less visible if the injury is perpendicular to the sophisticated linings of the skin, called Langer's lines.

These layers are made up of keratinocytes.

Apart from the structural part of the skin, the other functional cells are;
i) Melanocytes (produces melanin, which gives colour to the skin)
ii) Langerhans cells (antigen-transporter from skin, act as phagocytes)
iii) Merkel cells (touch-receptor cells)

melanocytes are stimulated by Melanocyte-stimulating hormone (MSH) from the anterior pituitary. in humans, it is less abundant compared to animals. That is why animals can change their colour of the skin abruptly, but not for humans, unless if you lie on a sunny beach for a whole-day long!

moreover, these MSH does not influence the melanocytes like ACTH does. thus in humans, melanocytes are known to be stimulated more by ACTH, not MSH.

Langerhans cells play an important part in immunity of the skin. And it plays a major role in initiating allergic reactions of the skin.

Merkel cells detect touch. if you do not have any, than you cannot feel anything that touches your skin!

Inflammatory pathologies of the Skin.

Acute Inflammatory Dermatoses
i) Urticaria
ii) Eczema
iii) Erythema Multiforme

Chronic Inflammatory Dermatoses
i) Psoriasis
ii)Lichen Planus
iii) Lichen Simplex Chronicus



Urticaria

Urticaria (hives) is a common disorder mediated by localized mast cell degranulation resulting in dermal microvascular hyperpermeability. Gives rise to wheals.

Character:
-Erythematous (kulit merah)
-Edematous (kulit berair)
-Pruritic (gatal2)

Pathogenesis:
-type I hypersensitivity reaction as a result of IgE sensitization (allergic reaction)
-results of mast cell degranulation
-in turn, releases chemical inflammatory mediators

the allergens (benda yg buat alergi) are mainly;
-pollens
-foods
-drugs
-insect venom

clinical features
-common in 20-40 years of age
-usually heals in a day

treatment (tak payah pun takpe, tapi kalau teruk sangat....)
-antihistamines
-steroids


Eczema

Eczema is a clinical term that embraces a number of conditions with different underlying etiologies.

characterised by;
- red (merah)
- papulovesicular (bintik2 berair)
- oozing (keluar nanah)
- crusted lesions (luka berkerak)

Pathogenesis
-allergens bind to Langerhans cell
-Langerhans cell goes to draining lymph nodes
-presents to naive T cells
-on re-exposure, CD4 cells release cytokines
-inflammatory cells gather to the site
-mediate epidermal damage

clinical features
-pruritic (gatal2)
-edematous (berbonjol. dan berair)
-oozing plaques (bernanah)
-vesicles and bullae
persistence of this leads to;
-scaly skin (kulit macam ada layer baru, sebab hyperkeratosis)
-epidermal thickening (acanthosis)

treatment
-avoid the underlying cause of the source of allergens (jauhi benda yg buat alergi)


Erythema Multiforme

Uncommon, hypersensitivity response to certain infections and drugs.

Characterised by;
-multiform lesions (bengkak bervariasi tempat dan bentuk)

Pathogenesis
-cytotoxic T-cells damages the basal layer of skin, from the stimulation of the infection or drugs

clinical features
-associated with infections
-associated with antibiotics (penicillin, sulfonamides, salicytes, hydantoins, antimalarials)
-associated with NSAIDs (aspirin, diclofenac, ibuprofen)

treatment
-insyaAllah hilang lepas infection subsides
-jangan overdose ubat
-doa byk2 la ye :)

ok, nak pergi ke kelas, chronic inflammatory dermatoses saya sambung bila ada kelapangan, insyaAllah!

Fungus.

Fungus is a plant that does not have any flower or leaves.

The study of fungus is called mycology.

Mykos = Mushrooms.

Mushrooms are a type of fungus.

Differences with bacteria;
- rigid cell wall, comprises of chitin, mannan.
- cytoplasmic membrane contains sterol.

Classification of fungi (plural for fungus)

Taxonomical.
a)Zygomycetes
b)Ascomycetes
c)Basidiomycetes
d)Deuteromycetes

Morphological.
a)Yeasts
b)Yeasts-like fungi
c)Moulds
d)Dimorphic

Common features (for the ease of classification)

Unicellular, multiple by budding,
it is a YEAST
e.g. Cryptococcus

Pseudohyphae
it is a YEAST-LIKE
e.g. Candida

Hyphae in groups, tangled
it is a MOULDS
e.g. Penicillium

can live inside or outside the body, causing systemic mycosis
it is a DIMORPHIC
e.g. Blastomyces

Bacteria Gram-staining.

What is Gram staining?
A type of differential staining, commonly used to differentiate bacterial species into two large groups (Gram-positive and Gram-negative) based on the physical properties of their cell walls.

Gram-positive bacteria have a thick mesh-like cell wall made of peptidoglycan (50-90% of cell wall), which stains purple while Gram-negative bacteria have a thinner layer (10% of cell wall), which stains pink.

Aerobic bacteria.

Gram-positive cocci
- Staphylococci
- Streptococci
- Pneumococci

Gram-positive bacilli
- Corynebacterium
- Bacillus
- Clostridium
- Actinomycetes (filamentous)
- Mycobacterium (stains poorly)

Gram-positive coccobacilli
- Listeria
- Erysipelothrix

Gram-negative cocci
- Neisseria
- Moraxella

Gram-negative bacilli
- all aerobic bacteria which have not been mentioned.

Gram-negative coccobacilli
- Bordetella
- Brucella

Anaerobic Bacteria.

Gram-positive cocci
- Peptococcus
- Peptostreptococcus

Gram-positive bacilli
- Eubacterium
- Lactobacillus
- Bifidobacterium
- Propionibacterium
- Actinomyces
- Mobiluncus

Gram-negative cocci
- Veillonella

Gram-negative bacilli
- Bacteroides
- Prevotella
- Porphyromonas
- Fusobacterium
- Leptotrichia


tips : there are about 30 bacteria species which are Gram-negative bacilli. so in viva voce, if you unsure about the Gram staining of an aerobic bacilli, just say Gram-negative bacilli! insyaAllah, it worth a guess :)

Diuretic Drugs.

What is diuretics?
Diuretics are drugs that promote the excretion of Sodium (Na+) and water in urine.

It is commonly used in patients with;
a) Hypertension (by reducing blood volume)
b) Edema (by concentrating the blood, thus increases plasma oncotic pressure)

They can be classified by their efficacy;
a) High efficacy (Inhibitors of Na+ K+ 2Cl- co-transport)
-Sulphamoyl derivatives: Furosemide, Bumetanide, Torasemide
b) Medium efficacy (Inhibitors of Na+ Cl- symport)
- Benzothiazidines : Hydrochlorothiazide, Benzthiazide, Hydroflumethiazide, Clopamide
- Thiazide-like : Chlorthalidone, Metolazone, Xipamide, Indapamide
c) Weak or adjunctive diuretics
- Carbonic anhydrase inhibitor : Acetazolamide
- Potassium sparing
~Aldosterone antagonist : Spironolactone
~Inhibitors of renal epithelial Na+ channels : Amiloride, Triamterene
- Osmotic diuretics : Mannitol, Isosorbide, Glycerol

Uses of high ceiling diuretics;
1) Edema
- most preferred drug in congestive cardiac failure
2) Acute pulmonary edema
- Furosemide i.v. gives prompt relief
3) Cerebral edema
- Furosemide with osmotic diuretics have high efficacy
4) Hypertension
- given with the presents of renal insufficiency and congestive cardiac failure
5) Blood transfusion
- to prevent vascular overload
6) Hypercalcemia
- Furosemide promotes calcium excretion through the kidney

Uses of thiazides;
1) Edema
- good in maintenance therapy
2) Hypertension
- preferably better than Furosemide
3) Diabetes insipidus
- Reduces urine volume (unlike Furosemide)
4) Hypercalciuria
- Reduces calcium excretion (unlike Furosemide)

Adverse effects
1) Hypokalemia : excess potassium loss via urine
2) Acute saline depletion : Overdosage (esp. Furosemide) may cause dehydration and fall in blood pressure
3) Dilutional hyponatremia
4) GIT and CNS disturbances : Nausea, vomiting, diarrhoea
5) Hearing loss : rarely, but increases risk in renal insufficiency

Introduction.

This blog is mainly serves as a purpose of entering my medical notes.

This blog was inspired by my respected friend, Bro Na'im USM.

It may contain some errors. Do inform me by commenting on the particular post. Any corrections will be done immediately.

May this blog be beneficial to myself and all my readers, InsyaAllah.

Thank you.

Imanul Hassan bin Abdul Shukor
4th Semester MBBS
JJM Medical College, Davangere.