Best Medical Videos

Development of Pituitary Gland : Embryology Video

2011-11-19T02:40:00.000-08:00

[starttext]The pituitary gland (hypophysis cerebri) is derived from 2 sources. The anterior lobe is an upgrowth of ectoderm from the roof of the stomodeum (primitive buccal cavity), while the posterior lobe is a down growth of neuroectoderm from the diencephalon.

In the middle of the 4th week, a diverticulum, Rathke's pouch, grows upwards from the roof of the stomodeum towards the developing brain.
As the upgrowth contacts a downgrowth from the brain, the infundibulum, Rathke's stalk (connection between Rathke's pouch and the Stomodeum) begin to degenerate.
By the 6th week the Rathke's stalk degenerates and Rathke's pouch loses its connection with the stomodeum.
The cells of Rathke's pouch proliferate to form the pars distalis, and extend up the anterior aspect of the infundibulum as the pars tuberalis. The posterior surface of Rathke's pouch does not proliferate but forms the poorly developed pars intermedia.
The infundibulum having grown down from the floor of the diencephalon, expands as the axons of cells in the diencephalon grow down into it.

Summary:
Rathke's pouch from stomodeum: Pars distalis, Pars tuberalis, Pars intermedia
Infundibulum from diencephalon: Pars nervosa, Stalk (infundibulum)

Congenital Anomalies of Pituitary Gland:

Craniopharyngioma: Failure of degeneration of Rathke's stalk
Pharyngeal pituitary: Failure of ascending of buccal pituitary
Agenesis of pituitary

[endtext]

http://www.youtube.com/watch?v=seOqXoyKiGIendofvid

ELISA test : Antibody Detection

2011-11-18T23:16:00.000-08:00

[starttext]The Enzyme Linked Immuno-sorbent Assay or ELISA is a commonly used format for serologic testing. ELISA serologies are usually done on multi-well microtiter plates so that dilution of serum are easily prepared and tested.

Procedure and Principle for Indirect Assay:

Wells of the plate are coated with the antigen of interest
Wells are filled with dilution of the patient's serum. If the antiboady (1st antibody) against the antigen are present in the serum, they will be immobilized due to binding to the antigen fixed to the bottom of the wells.
Wells are then washed to remove all the unbound antibodies (1st antibodies).
Then, a solution of animal antibody against the human antibody (2nd antibody) i.e. antihuman antibody or immunoglobulin covalently conugated (linked) with an enzyme.
Wells are washed again to remove the unbound enzyme linked antihuman antibody (2nd antibody).
Finally, a solution of colorigenic enzyme substrate is added.
The interaction of the substrate with the enzyme on the 2nd antibody (antihuman antibody) generates visible color.
Read results directly through the bottom of the microwell plate using an automated or semi-automated photometer (ELISA-reader).

Similarly, ELISA test can also be used to detect antigens in the specimen collected. The principle for antigen detection has been illustrated in the image below:

Some Common Uses of ELISA:

Screening test for HIV
Detecting potential food allergens
HCG pregnancy test

[endtext]

http://www.youtube.com/watch?v=RRbuz3VQ100endofvid

Lifecycle of Chlamydia : Animation Video

2011-10-09T04:46:00.000-07:00

[starttext]The 3 Chlamydia species are:

Chlamydia trachomatis
Chlamydia pneumoniae (Chlamydophila pneumoniae)
Chlamydia psittaci (Chlamydophila psittaci)

Chlamydia is especially fond of columnar epithelial cells that line mucous membranes. This correlates well with the types of infection that Chlamydia causes, including conjunctivitis, cervicitis, and pneumonia.

Lifecycle of Chalmydia

Duration: 48 to 72 hours

2 Morphologic forms:

A) Elementary Bodies (EB):

Extracellular form
Metabolically inert (does not divide)
Dense, round, small (300 nm), infectious particle
The outer membrane has extensive disulfide bond cross-linkages that confer stability for extracellular existence (resistant to harsh environmental conditions)

B) Reticulate Bodies (RB):

Intracellular form
Metabolically active (replicates by binary fission)
Non-infectious particles
Possess a fragile membrane lacking the extensive disulfide bonds characteristic of the EB

Steps in lifecycle:

The infectious particle is the elementary body (EB). The EB attaches to and enters columnar epithelial cells lining the mucous membranes via endocytosis.
Once within an endosome, the EB inhibits phagosome-lysosome fusion and is not destroyed. It transforms into a Reticulate body (RB).
Once enough RBs have formed by binary fission, some transform back into EB.
The resulting inclusions may contain 100 - 500 progeny
The life cycle is completed when the host cell liberates the elementary body (EB), which can now infect more cells.

[endtext]

http://www.youtube.com/watch?v=kpUzSbM4klgendofvid

Mechanism of Action of Steroid Hormones: Animation

2011-10-04T09:50:00.000-07:00

[starttext]Hormones are the chemicals produced within the body by some specialized cells and have specific effects on the activity of target organs through specific receptors. There are 2 types of hormones:

a) Lipid soluble:

Can pass through cell membrane
Act via intracellular and intranuclear receptors
Mechanism: Protein synthesis
eg. Steroid hormones and thyroid hormones

b) Water soluble:

Cannot pass through cell membrane
Act via membrane receptors
Mechanism: cAMP, cGMP, IP3, Calcium-calmodulin, Tyrosine kinase
eg. All other hormones except steroid and thyroid hormones

Before Moving on to the mechanism of action, we will list the major steroid and thyroid hormones.

Steroid hormones (Cholesterol derivatives):

Glucocorticoid (Cortisol)
Estrogen
Testosterone
Progesterone
Aldosterone
Vitamin D (Calcitriol)

Thyroid hormones (Amine derivatives):

Tri-iodothyronine (T3)
Thyroxine (T4)

Mechanism of Action of Steroid Hormones:

Simple Diffusion: The lipid soluble hormones diffuses through the cell membrane to enter the cell.
Hormone binds to the intracellular receptor composed of a "Hormone binding" domain, a "DNA binding" domain and a "amino terminal" which interacts with other transcription factors. Binding of the hormone leads to exposure of DNA binding zone.
Hormone-receptor complex enters nucleus and dimerizes.
Binding to HREs: Hormone-recpetor dimers bind to Hormone (Steroid) Receptor Elements (SREs or HREs) of DNA.
Transcription: DNA transcription leads to formation of mRNA.
Translation: mRNA undergoes translation to produce new proteins. e.g. Calbindin for Vitamin D
Physiologic action of hormones.

What is the difference in the mechanism of action of thyroid and steroid hormones?

After passing through the cell membrane, steroid hormones except calcitriol bind to the intracellular receptor in the cytosol before entering the nucleus while the thyroid hormones and calcitriol directly enter the nucleus to bind to the intranuclear receptor. Beside, this difference all other steps are similar for both the hormones.

Summary:

[endtext]

http://www.youtube.com/watch?v=oOj04WsU9koendofvid

Gastric Acid Secretion Physiology Animation: Video

2011-07-08T09:34:00.000-07:00

[starttext]Gastric glands

3 types:

Cardiac: small in number and secretes mucin
Fundic and Body: highest in number and secretes acid juice secretion
Pyloric: mucous type

A typical acid secreting gland is tubular and straight.
Each gland is divided into 3 parts: Neck, Body and Base.
Mucous membrane is maintained by dynamic equilibrium between production and desquamation of its cells.

Gastric gland cells and their secretion:

Chief cells of Peptic cells: Pepsinogens
Oxyntic or parietal cells: HCl and intrinsic factor
Amine precursor uptake and decarboxylation (APUD) cells: Gastrointestinal hormones
Mast cells: Histamine
Argentaffin cells: serotonin
'G' cells: Gastrin
'D' cells: Somatostatin
Neck and isthmus cells: Mucin

Phases of Gastric secretion:

Cephalic phase (20%)

occurs even before food enters the stomach
stimuli for unconidtioned reflex: presence of food in mouth, taste of food, act of chewing, act of swallowing
stimuli for conditioned reflex: sight, thought, smell of food
signals originate in cerebral cortex and in appetite centers of amygdala and hypothalamus
signal ---> dorsal motor nuclei of vagi ---> vagus nerve ---> stomach
starts with a latency of < 5 min and continues for 30 to 120 min
rate of secretion: 250 to 750 ml/hour
secretion of psychic or appetite juice: rich in acid and pepsin with high digestive power

Gastric phase (70%)

once food enters the stomach, it excites:

Long vagovagal reflex: from stomach to the brain and back to the stomach (afferent and efferent both being vagal fibers)
Short local enteric reflexes
Gastrin mechansim

starts with a latency of 15 minutes and continues as long as there is food in the stomach
composition of juice depends upon the composition of food
rate of secretion: 40 to 70 ml/hour

Intestinal phase (10%)

begins with the presence of food in the upper portion of small intestine
chemicals involved: bombesin and gastrin
starts with a latency of 2 to 3 hours and continues for 8 to 10 hours
rate of secretion: 40 to 60 ml/hour
inhibitory influences operate:

i) Neural inhibition-

increased fat content, tonicity, volume of chyme in small intestine
enterogastric reflex

ii) Chemical inhibition-

chalone: secretin, neurotensin, CCK-Pz, prostaglandins, VIP, GIP, etc.
enterogastrone

Interdigestive phase

when there is no food either in stomach or small intestine
basal secretion: resting acid secretion
mainly mucus, little pepsin and lamost no acid
emotional stimuli increase this secretion (highlt peptic and acidic) leading to peptic ulcers
mechanism similar to cephalic phase

Parietal or Oxyntic Cells:

situated mainly towards neck of glands
secrete hydrochloric acid (HCl) and intrinsic factor
cells have an extensive microcanlicular system which communicates with the lumen of the gland by a canaliculus
in resting stage of cell, part of the microcanalicular system is converted into the tubulovesicular structures (vesicles are fused with the microcanalicular system when cell is stimulated to secrete HCl)

HCl secretion:

The H+/K+-ATPase in the luminal membrane of parietal cells drives H+ ions into the glandular lumen in exchange for K+ (primary active transport), thereby raising the H+ conc. in the lumen. K+ taken up in the process circulates back to the lumen via luminal K+ channels. For every H+ ion secreted, one HCO3– ion leaves the blood side of the cell and is exchanged for a Cl– ion via an anion antiporter. (The HCO3 – ions are obtained from CO2+ OH–, a reaction catalyzed by carbonic anhydrase, CA). This results in the intracellular accumulation of Cl– ions, which diffuse out of the cell to the lumen via Cl– channels. Thus, one Cl– ion reaches the lumen for each H+ ion secreted.

Regulation of gastric acid secretion:

Factors that stimulate gastric acid secretion

ACh directly activates parietal cells in the fundus (M3 cholinoceptors).
GRP (gastrin-releasing peptide) released by neurons stimulates gastrin secretion from G cells in the antrum. Gastrin released in to the systemic circulation in turn activates the parietal cells via CCKB receptors (= gastrin receptors).
The glands in the fundus contain H (histamine) cells or ECL cells (enterochromaffin– like cells), which are activated by gastrin (CCKB receptors) as well as by ACh and adrenergic substances. The cells release histamine, which has a paracrine effect on neighboring parietal cells (H2 receptor). Local gastric and intestinal factors also influence gastric acid secretion because chyme in the antrum and duodenum stimulates the secretion of gastrin.

Factors that inhibit gastric acid secretion:

Low pH
Distension of duodenum
Fat and protein breakdown products in duodenum
Somatostatin
Secretin
Prostaglandin
Gastric Inhibitory Peptide (GIP)
Vasoactive Intestinal Peptide (VIP)

[endtext]

http://www.youtube.com/watch?v=S_74W6PsT7sendofvid

ZN staining technique for Acid Fast Bacilli: Demonstration Video

2011-06-11T04:29:00.000-07:00

[starttext]It is a differential staining that divides organisms (or their structures) into acid fast (AFB) and non-acid fast (non-AFB). Original method of acid fast staining involved staining with aniline-gential violet, followed by decolorisation using strong acid. It was later improved by Ziehl and Neelsen.

Requirements:

Glass slide with fixed smear
Bunsen flame or spirit lamp
Staining reagents

Reagents:

Primary stain: Concentrated carbol fuschin
Decoloriser: 20% H2SO4
Counterstain: Methylene blue or Malachite green

Principle:

Bacteria of the genera Mycobacterium and Nocardia have unusual cell walls that are waxy and nearly impermeable due to the presence of mycolic acid, and large amounts of fatty acids, waxes, and complex lipids. These organisms are highly resistant to disinfectants, desiccation and are difficult to stain with water-based stains such as the Gram stain.

Primary stain penetrates cell wall
Intense decolorization does not release primary stain from the cell wall of AFB
Color of AFB is based on primary stain
Counterstain provides contrasting background

Procedure:

Place the slide on the rack
Flood the slide and completely cover with carbol fuschin
Using the metal forceps, take a piece of cotton wool soaked in alcohol, pass it through the flame and heat the slide from below until the stain emits a vapor, but do not bring to boiling point
Repeat this operation twice, (within 10 minutes)
Add fuschin if necessary; the slide should be covered
Rinse with water, drain
Apply decolorizing solution 2 min
Rinse, drain
Apply Methylene blue counterstain, 30 seconds
Rinse, drain
Air dry or blot it dry
Observe under microscope

Result:

AFB: appears as bright red or pink rods against blue background
Non AFB: appears purple

Modifications:

20% H2SO4: Mycobacterium tuberculosis
5% H2SO4: Mycobacterium leprae
1% H2SO4: Actinomyces and Nocardia[endtext]

http://www.youtube.com/watch?v=YzTgHU-aCqoendofvid

How to Remember the branches of External Carotid Artery (ECA)?

2011-06-09T05:37:00.000-07:00

[starttext]Arch of Aorta gives off (ABCS):
A = Arch of Aorta
B = Brachiocephalic artery
C = Left common carotid artery
S = Left subclavian artery

Brachiocephalic artery gives right common carotid artery

The common carotid arteries branches into internal and external carotid arteries at the level of upper border of thyroid cartilage.

Mnemonics:

Some Attendings Like Freaking Out Potential Medical Students
Some Anatomists Like Forcinating, Others Prefer S & M
Some Angry Lady Figured Out PMS

Superior thyroid

Ascending Pharyngeal

Lingual

Facial

Occipital

Posterior auricular

Maxillary

Superficial temporal

Branches of External Carotid Artery:

Ventral branches:

Superior thyroid
Lingual
Facial

Medial branch:

Ascending Pharyngeal

Posterior branches:

Occipital
Posterior auricular

Terminal branches:

Maxillary
Superficial temporal

[endtext]

http://www.youtube.com/watch?v=AWHON3xKuscendofvid

Draw to Know it - Branches of Celiac Artery and Blood Supply of Stomach

2011-05-14T03:55:00.000-07:00

[starttext]Abdominal aorta extends from aortic opening of diaphragm at the level of lower border of T12 to lower part of body of L4.

Branches of Abdominal Aorta:

Ventral branches (unpaired): supply gut
1. Celiac trunk
2. Superior mesenteric artery
3. Inferior mesenteric artery

Lateral branches (paired): supply viscera derived from intermediate mesoderm
4. Inferior phrenic arteries
5. Middle suprarenal arteries
6. Renal arteries
7. Gonadal arteries

Dorsal branches: supply body wall
8. 4 pairs of lumbar arteries
9. Median sacral artery (unpaired)

Terminal branches: supply pelvis and lower limbs
10. A Pair of Common iliac arteries

Celiac Artery and Its Branches:
- supplies all derivatives of foregut lying in the abdomen
- arises from the ventral part of abdominal aorta at the level of T12-L1

Branches:

1. Splenic artery:
a. Pancreatic branches
b. 5 to 7 Short gastric branches
c. Left gastroepiploic artery

2. Left gastric artery: ends by anastomosing with right gastric artery
a. 2 to 3 esophageal branches
b. Numerous gastric branches

3. Common hepatic artery:
a. Gastroduodenal artery: Pancreaticoduodenal and Right gastroepiploic arteries
b. Right gastric artery
c. Supraduodenal artery
d. Left hepatic artery
e. Right hepatic artery: gives cystic artery to gall bladder

Blood Supply of Stomach:

Right and Left Gastroepiploic arteries
Right and Left Gastric atrteries
5 to 7 Short Gastric Arteries

[endtext]

http://www.youtube.com/watch?v=Wwo3EqQzEtkendofvid

Pathogenesis of Atherosclerosis : Video Animation

2011-05-10T18:42:00.000-07:00

[starttext]
Risk Factors for Atherosclerosis:

A. Major Factors:

Non-modifiable:
1. Increasing age
2. Male gender
3. Family history
4. Genetic abnormalities

Modifiable:
1. Hyperlipidemia (specially Familial hypercholesterolemia)
2. Hypertension
3. Diabetes
4. Smoking cigarettes
5. CRP (C-Reactive Protein)

B. Minor Factors:
1. Obesity
2. Physical inactivity
3. Stress (Type A personality)
4. Postmenopausal estrogen deficiency
5. High carbohydrate intake
6. Altered lipoprotein(a)
7. Transunsaturated fat intake
8. Chlamydia infection

Pathogenesis:

Atherosclerosis as defined by response to injury hypothesis is a chronic inflammatory response of the arterial wall initiated by injury to the endothelium.

1. Chronic endothelial injury mediated by various factors like hyperlipidemia, hypertension, smoking, toxins, immune reactions, hemodynamic factors, etc.

2. With chronic hyperlipidemia (low HDL and high LDL, abnormal lipoprotein), lipoproteins accumulate within the intima.

3. Endothelial dysfunction (increased permeability, leukocyte adhesion)

4. Endothelial cells express: VCAM-1 binds monocyte and T lymphocyte.
After monocytes adhere to the endothelium, they:
(a) migrate between Endothelial cells to localize in the intima
(b) transform into macrophages and engulf lipoproteins (largely oxidized LDL) to from foam cells

5. Macrophages produce
(a) IL-1 and TNF, which increase adhesion of leukocytes.
(b) Reactive oxygen species : cause oxidation of the LDL
(c) Growth factors that may contribute to Smooth muscle cell proliferation.

6. The activated leukocytes and intrinsic arterial cells can release fibrogenic mediators

7. Smooth muscle cell response:
Smooth Muscel Cells migrate from the media to the intima and proliferate and deposit ECM to form fibrofatty atheroma
Growth factors: PDGF, FGF, and TGF-α
Smooth Muscle Cells may also take up modified lipids, contributing to foam cell formation.

Complications:

1. Stenosis
2. Rupture
3. Ulceration
4. Erosion
5. Atheroemboli
6. Hemorrhage
7. Thrombosis
8. Aneurysm

[endtext]

http://www.youtube.com/watch?v=hVlZvr03XPcendofvid

Baroreceptor Reflex Animation Video

2011-05-06T09:55:00.000-07:00

[starttext]Also known as:
a. Baroreflex
b. Sinoaortic reflex
c. Pressure buffer mechanism

Components of Reflex:

Stimulus: Rise in arterial blood pressure

Baroreceptors (Pressosensors): Stretch receptors in -
a. Aortic arch
b. Carotid sinus
c. Left ventricle
d. Subclavian arteries,etc.

Afferent nerves:
a. Glossopharyngeal (CN IX) for Carotid sinus
b. Vagus (CN X) for other receptors

Medullary Centers:
Through Solitary Tractus nucleus (NTS) to-
a. Stimulation of Cardiac Inhibitory center (CIC)
b. Inhibition of vasomotor center (VMC)
c. Inhibition of respiratory center

Efferent:
VMC ---> Sympathetic
CIC ---> Parasymathetic

Response:
a) + Parasympathetic ---> Bradycardia ---> Decreased cardiac output ---> Decreased blood pressure

b) - Sympathetic:
i. Bradycardia ---> Decreased cardiac output
ii. Vasodilation ---> Decreased peripheral resistance ---> Decreased blood pressure

Stimulation of baroreceptors occurs linearly with increased blood pressure but when these are maximally stimulated, further rise in blood pressure cannot increase stimulation.

Resetting of Baroreceptor:
a. Persistent raised BP for > or = 2 days ---> receptors operate at new level ---> receptors not stimulated
b. Also observed with persistent low BP

Carotid Sinus Syndrome:
Hypersensitive baroreceptors ---> Slight pressure on neck ---> Severe inhibition of heart ---> Fall in Blood pressure
May faint on wearing a tight collar or a neck tie

[endtext]

http://www.youtube.com/watch?v=-_eucOGpzNYendofvid

Lipoprotein Metabolism : Animation video

2011-05-05T05:49:00.000-07:00

[starttext]
Composition of Lipoproteins:

Consists of non-polar core (Mainly Triglycerides and cholesteryl esters)
A single surface layer of amphipathic phospholipids and cholesterol
Protein moiety are known as Apoprotein or Apolipoprotein
Protein and lipid contents vary

Synthesis of Chylomicrons and VLDL:

Metabolism of Chylomicrons:

Synthesised in intestine
Transport TAG (Triacylglycerol) to tissues and deliver remaining cholesterol & cholesterol ester to the liver.

Metabolism of VLDL, LDL and IDL:

VLDL is synthesised in liver and converted to LDL which contain an increased proportion of cholesterol & cholesteryl ester (due to loss of TAG).
Transport TAG and cholesterol from liver to tissues.
Cholesterol in LDL referred to as “bad cholesterol” since LDLs are implicated in atherosclerosis

Metabolism of HDL (High Density Lipoprotein):

HDL carries “used” cholesterol (as CE) back to the liver. Also donate some CE to circulating VLDL for redistribution to tissues.
HDL taken up by liver and degraded. The cholesterol is excreted as bile salts or repackaged in VLDL for distribution to tissues.
Cholesterol synthesis in the liver is regulated by the cholesterol arriving through HDL (and dietary cholesterol returned by chylomicron remnants).
Cholesterol (CE) in HDL is referred to as “good cholesterol”.

[endtext]

http://www.youtube.com/watch?v=97uiV4RiSAYendofvid

Lecture Video: Cell Adaptation, Cell Injury and Cell Death

2011-05-03T10:33:00.000-07:00

[starttext]Lecture Video for the first chapter from Robbins from Medicalschoolpathology.com

Lecture Part 2

Lecture Part 3

Lecture Part 4

Lecture Part 5

Learn more about Cellular Adaptations
[endtext]

http://www.youtube.com/watch?v=m097UUkqU2Qendofvid

Tracheotomy Procedure : Animation

2011-05-03T10:21:00.000-07:00

[starttext]Tracheotomy and tracheostomy are surgical procedures on the neck to open a direct airway through an incision in the trachea (the windpipe). It is performed in emergency situations, in the operating room , or at bedside of critically ill patients. This procedure, technically called a cricothyroidotomy, should be undertaken only when a person with a throat obstruction is not able to breathe at all-no gasping sounds, no coughing-and only after you have attempted to perform the Heimlich maneuver three times without dislodging the obstruction.

Procedure

Find the person's Adam's apple (thyroid cartilage).
Move your finger about 1 inch down the neck until you feel another bulge. This is the cricoid cartilage. The indentation between the two is the cricothyroid membrane, where the incision will be made.
Take the razor blade or knife and make a 1/2 inch horizontal incision. The cut should be about half an inch deep. There should not be too much blood.
Pinch the incision open or place your finger inside the slit to open it.
Insert your tube in the incision, roughly one-half to one inch deep.
Breathe into the tube with two quick breaths. Pause 5 seconds, then give 1 breath every 5 seconds.
You will see the chest rise and the person should regain consciousness if you have performed the procedure correctly. The person should be able to breathe on their own, albeit with some difficulty, until help arrives.

The term tracheostomy is sometimes used interchangeably with tracheotomy. Strictly speaking, however, tracheostomy usually refers to the opening itself while a tracheotomy is the actual operation.

[endtext]

http://www.youtube.com/watch?v=d_5eKkwnIRsendofvid

Examination of Cranial Nerves III, IV, V, VI, VII, VIII, IX, X, XI and XII

2011-04-29T11:30:00.000-07:00

[starttext]

III, IV and VI - Oculomotor, Trochlear and Abducens

Observe for Ptosis
Test Extraocular Movements
1. Stand or sit 3 to 6 feet in front of the patient.
2. Ask the patient to follow your finger with their eyes without moving their head.
3. Check gaze in the six cardinal directions using a cross or "H" pattern.
4. Pause during upward and lateral gaze to check for nystagmus.
5. Check convergence by moving your finger toward the bridge of the patient's nose.
Test Pupillary Reactions to Light

Dim the room lights as necessary.
Ask the patient to look into the distance.
Shine a bright light obliquely into each pupil in turn.
Look for both the direct (same eye) and consensual (other eye) reactions.
Record pupil size in mm and any asymmetry or irregularity.

Test accommodation by making patient to look into distance, then a hat pin 30cm from nose.
If Myasthenia Gravis suspected: Patient gazes upward at Doctor's finger to show worsening ptosis

V - Trigeminal

Test Temporal and Masseter Muscle Strength
1. Ask patient to both open their mouth and clench their teeth.
2. Palpate the temporal and massetter muscles as they do this.
Test the 3 Divisions for Pain Sensation
1. Explain what you intend to do.
2. Use a suitable sharp object to test the forehead, cheeks, and jaw on both sides.
3. Substitute a blunt object occasionally and ask the patient to report "sharp" or "dull."
If you find and abnormality then:
1. Test the three divisions for temperature sensation with a tuning fork heated or cooled by water.
2. Test the three divisions for sensation to light touch using a wisp of cotton.
Test the Corneal Reflex
1. Ask the patient to look up and away.
2. From the other side, touch the cornea lightly with a fine wisp of cotton.
3. Look for the normal blink reaction of both eyes.
4. Repeat on the other side.
5. Use of contact lens may decrease this response.

VII - Facial

Observe for Any Facial Droop or Asymmetry
Ask Patient to do the following, note any lag, weakness, or assymetry:
1. Raise eyebrows
2. Close both eyes to resistance
3. Smile
4. Frown
5. Show teeth
6. Puff out cheeks
Test the Corneal Reflex

VIII - Acoustic

Screen Hearing
1. Face the patient and hold out your arms with your fingers near each ear.
2. Rub your fingers together on one side while moving the fingers noiselessly on the other.
3. Ask the patient to tell you when and on which side they hear the rubbing.
4. Increase intensity as needed and note any assymetry.
5. If abnormal, proceed with the Weber and Rinne tests.
Test for Lateralization (Weber)
1. Use a 512 Hz or 1024 Hz tuning fork.
2. Start the fork vibrating by tapping it on your opposite hand.
3. Place the base of the tuning fork firmly on top of the patient's head.
4. Ask the patient where the sound appears to be coming from (normally in the midline).
Compare Air and Bone Conduction (Rinne)
1. Use a 512 Hz or 1024 Hz tuning fork.
2. Start the fork vibrating by tapping it on your opposite hand.
3. Place the base of the tuning fork against the mastoid bone behind the ear.
4. When the patient no longer hears the sound, hold the end of the fork near the patient's ear (air conduction is normally greater than bone conduction).
Vestibular Function is Not Normally Tested

IX and X- Glossopharyngeal and Vagus

Listen to the patient's voice, is it hoarse or nasal?
Ask Patient to Swallow (bovine cough: recurrent laryngeal)
Examine palate for uvular movement (unilateral lesion: uvula drawn to normal side)
Ask Patient to Say "Ah"
- Watch the movements of the soft palate and the pharynx.
Test Gag Reflex (Unconscious/Uncooperative Patient)
1. Stimulate the back of the throat on each side.
2. It is normal to gag after each stimulus.

XI - Accessory

From behind, look for atrophy or asymmetry of the trapezius muscles.
Ask patient to shrug shoulders against resistance.
Ask patient to turn their head against resistance. Watch and palpate the sternomastoid muscle on the opposite side.

XII - Hypoglossal

Listen to the articulation of the patient's words.
Observe the tongue as it lies in the mouth
Ask patient to:
1. Protrude tongue (unilateral lesion deviates to affected side)
2. Move tongue from side to side[endtext]

http://www.youtube.com/watch?v=PjAghPc9xAQendofvid

12 Lead ECG Placement Video

2011-04-29T10:06:00.000-07:00

[starttext]Electocardiogram(ECG or EKG) is a noninvasive test that is used to reflect underlying heart conditions by measuring the electrical activity of the heart. ECG or EKG leads are attached attached to each extremity (4 total) and to 6 precordial leads on the front of the chest.

Important components of ECG and their representations:

P wave: Depolarization of the right and left atria
QRS complex: Right and left ventricular depolarization
T wave: Ventricular repolarization
U wave: Late repolarization of papillary muscles
PR interval: time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex)
QT interval: duration of ventricular depolarization and repolarization

Leads of ECG:

RA represents right arm
LA represents left arm
LF represents left foot

Bipolar limb leads (frontal plane):
Lead I: RA (-) to LA (+) (Right Left, or lateral)
Lead II: RA (-) to LF (+) (Superior Inferior)
Lead III: LA (-) to LF (+) (Superior Inferior)

Augmented unipolar limb leads (frontal plane):
Lead aVR: RA (+) to [LA & LF] (-) (Rightward)
Lead aVL: LA (+) to [RA & LF] (-) (Leftward)
Lead aVF: LF (+) to [RA & LA] (-) (Inferior)

Unipolar (+) chest leads (horizontal plane):
Leads V1, V2, V3: (Posterior Anterior)
Leads V4, V5, V6:(Right Left, or lateral)

12 Lead ECG Placement

Limb lead placement:
RA: Right forearm or wrist
LA: Leaft forearm or wrist
LL: Left lower leg
RL: Ground lead is generally placed on the right lower leg

Precordial Leads (V1-V6):
V1: 4th intercostal space, right sternal border
V2: 4th intercostal space, left sternal border
V3: midpoint of V2 and V4
V4: 5th intercostal space, left midclavicular line
V5: 5th intercostal space, left anterior axillary line
V6: 5th intercostal space, left mid-axillary line

Contiguous Leads:

Two leads that look at neighbouring anatomical areas of the heart are said to be contiguous.

V1-V2: Septal Leads
V3-V4: Anterior Leads
II, III, aVF: Inferior leads
V5, V6, I, aVL: Lateral leads

Learn more about ECG @ ECG Library
[endtext]

http://www.youtube.com/watch?v=GUIKXnot-1kendofvid

Fetal Circulation Explained with Video

2011-04-28T04:09:00.000-07:00

[starttext]The fetus has 4 circulatory features that are not present in adult circulation:

1. Foramen ovale: oval window between the two atria which covered by a flap of tissue (valve)
2. Ductus arteriosus: a connection between the pulmonary artery and the aorta.
3. Umbilical arteries and vein: vessels that travel to and from the placenta, leaving waste and receiving nutrients.
4. Ductus venosus: a connection between the umbilical vein and the inferior vena cava.

All of these features can be related to the fact that the fetus does not use its lungs for gas exchange, since it receives oxygen and nutrients from the mother’s blood at the placenta. During development, the lungs receive only enough blood to supply their developmental need for oxygen and nutrients.

Most of the blood that enters the right atrium passes directly into the left atrium through the foramen ovale because the blood pressure in the right atrium is somewhat greater than that in the left atrium. The rest of the fetal blood entering the right atrium passes into the right ventricle and out through the pulmonary trunk.

However, because of the ductus arteriosus, most pulmonary trunk blood passes directly into the aortic arch. Notice that, whatever route blood takes, most of it reaches the aortic arch instead of the pulmonary circuit vessels. Blood within the aorta travels to the various branches, including the iliac arteries, which connect to the umbilical arteries leading to the placenta.

Exchange between maternal and fetal blood takes place at the placenta. Blood in the umbilical arteries is oxygen-poor, but blood in the umbilical vein, which travels from the placenta, is oxygen-rich.

The umbilical vein enters the ductus venosus, which passes directly through the liver. The ductus venosus then joins with the inferior venacava, a vessel that contains oxygen-poor blood. The vena cava returns this mixture to the right atrium.

Changes at Birth Sectioning and tying the umbilical cord permanently separates the newborn from the placenta. The first breath inflates the lungs and oxygen enters the blood at the lungs instead of the placenta. Oxygen-rich blood returning from the lungs to the left side of the heart usually causes a flap on the left side of the interatrial septum to close the foramen ovale. What remains is a depression called the fossa ovalis.

The fetal blood vessels and shunts constrict and become fibrous connective tissue called ligamentums in all cases except the distal portions of the umbilical arteries, which become the medial umbilical ligaments.

1. Ductus arteriosus becomes Ligamentum arteriosum
2. Foramen ovale becomes Fossa ovalis
3. Ductus venosum becomes Ligamentum venosum
4. Umbilical vein becomes Ligamentum teres
5. Umbilical arteries becomes Medial umbilical ligaments

Adapted from Mader: Understanding Human Anatomy and Physiology

[endtext]

http://www.youtube.com/watch?v=uwswhoKfkmMendofvid

Coronary Circulation : Anatomy Demonstration Video

2011-04-26T19:14:00.000-07:00

[starttext]

Coronary circulation is the circulation of blood in the blood vessels of the heart muscle (the myocardium). The vessels that deliver oxygen-rich blood to the myocardium are known as coronary arteries. The vessels that remove the deoxygenated blood from the heart muscle are known as cardiac veins.

The aortic valve has three leaflets, each having a cusp or cup-like configuration. These are known as:

left coronary cusp
right coronary cusp
posterior non-coronary cusp

Just above the aortic valves there are anatomic dilations of the ascending aorta, also known as the sinus of Valsalva.

Arteries of Heart:

Right coronary artery:

Course:

Passes forwards and to the right to emerge on the surface of heart between the root of pulmonary trunk and right auricle.
Runs downwards in right anterior coronary sulcus.
Winds round the inferior border to reach the diaphragmatic surface of heart
Runs backwards and left in the right posterior coronary sulcus to reach posterior interventricular groove
Terminates by anastomosing with left coronary artery

Branches:
Mnemonic: TRaP Me IN

Large:

Marginal
Posterior Interventricular

Small:

Nodal
Right Atrial
Infundibular
Terminal

Area of distribution:

Right atrium
Right ventricle except area adjoining anterior interventricular groove
Small part of left ventricle adjoining posterior interventricular groove
Posterior part of interventricular septum
Conducting system of heart except a part of left branch of AV bundle

Left coronary artery:

Course:

Passes forwards and to the left and emerges between pulmonary trunk and the left auricle
Gives anterior interventricular branch which runs downwards in anterior interventricular groove
After giving off, anterior IV branch, it gives circumflex branch which runs to the left in the left anterior coronary sulcus
Winds round the left border of heart and continues in the left posterior coronary sulcus
Terminates by anastomosing with right coronary artery

Branches:
Mnemonic: LaTe PAD

Large:

Anterior Interventricular
Diagonal branch

Small:

Left atrial
Pulmonary
Terminal

Area of distribution:

Left atrium
Left ventricle except area adjoining posterior interventricular groove
Small part of right ventricle adjoining anterior interventricualr groove
Anterior part of interventricular septum
A part of left branch of AV bundle

Veins of Heart:

Coronary sinus:

Largest vein of heart which opens in right atrium
Situated in the left posterior coronary sulcus
Receives:

Great cardiac vein: Anterior interventricular sulcus
Middle cardiac vein: Posterior interventricular sulcus
Small cardiac vein
Posterior vein of left ventricle
Oblique vein of left atrium
Right marginal vein

Veins opening directly to chambers of heart:

Anterior cardiac veins
Venae cordis minimi (Thebesian vessels)

[endtext]
http://www.youtube.com/watch?v=lScGzpNJEmUendofvid

Development of Heart : Embryology Video

2011-04-26T08:51:00.000-07:00

[starttext]1. Angioblastic cords: Mesenchymal cells in the cardiogenic area form 2 angioblastic cords. These c.ords become canalized to form 2, endothelial heart tubes.

2. Heart Tube: Tubes fuse to form a single endothelial heart tube. The surrounding mesoderm form the primitive myocardium.

3. The heart is composed of an endothelial tube separated from the primitive myocardium, by gelatinous connective tissue called cardiac jelly.

4. Endocardium: The endothelial tube becomes the lining of the heart, the endocardium

5. Myocardium: The primitive myocardium becomes the muscular wall or myocardium

6. Epicardium: The visceral pericardium or epicardium is derived from mesothelial cells of the sinus venosus and spread over the myocardium

7. Dextral looping: The primitive heart tube undergoes dextral looping (bends to right)

The tubular heart develops and the adult sturctures derived from them are:
a. Truncus arteriosus :

Aorta
Pulmonary trunk

b. Bulbus cordis :

Smooth part of right ventricle (Conus arteriosus)
Smooth part of left ventricle (Aortic vestibule)

c. Primitive Ventricle :

Trabeculated part of right and left ventricle

d. Primitive Atrium :

Trabeculated part of right and left atrium

e. Sinus venosus :

Right horn: Smooth part of right atrium (Sinus venarum)
Left horn: Coronary sinus, Oblique vein of left atrium

The sinus venosus receives
a. The umbilical vein, from the chorion
b. The vitelline vein from the yolk sac
c. The common cardinal veins from the embryo

Partitioning of the Primitive Heart:

Endocardial cushions form on the dorsal and ventral walls of the atrioventricular canal.
The atrioventricular endocardial cushions fuse, dividing the atrioventricular canal into right and left atrioventricular canals.

Partitioning of the Primitive Atrium
It is divided into right and left atria by two septa:

Septum primum
Septum secundum

Septum primum unites with the Atrioventricular septum (endocardial cushions).
Foramen primum forms and then disappear.
Perforations appear in the central part of the septum primum. The perforations form foramen secundum.
Septum primum fuses with the endocardial cushions, obliterating the foramen primum.
Septum secundum overlaps the foramen secundum in the septum primum.
Septum secundum forms foramen ovale, opening between the atria.
Part of septum primum, forms valve for foramen ovale.
During fetal life, blood is shunted from the right atrium to the left atrium via the foramen ovale and foramen secundum.
Closure of the foramen ovale normally occurs immediately after birth and is caused by the increased atrial pressure that result from the changes in the pulmonary circulation and decreased right atrial pressure caused by the closure of the umbilical vein.

The septum primum forms the floor of the fossa ovalis. The inferior edge of the septum secundum forms a rounded fold, the limbus fossae ovalis (anulus ovalis).

Interventricular (IV) Septum:
IV septum develops in the floor of the ventricle and grows toward the Atrioventricular cushions but stops short leaving the interventricular(IV) foramen.
The membranous IV septum (closes the IV foramen) forms by the fusion of:

Right bulbar ridge
Left bulbar ridge
AV cushions

Aorticopulmonary septum:
Neural crest cells migrate into the truncal and bulbar ridges of the truncus arteriosus, which grow in a spiral fashion snd fuse to form the aorticopulmonary (AP) septum. The AP septum divides truncus arteriosus into the aorta and pulmonary trunk.
[endtext]
http://www.youtube.com/watch?v=aZUDePgRQqIendofvid

How to draw brachial plexus : Video

2011-04-25T09:26:00.000-07:00

[starttext]
1. Write the Root values C5, C6, C7, C8 and T1 leaving almost equal space between the 2 consecutive points.

2. Join C5 and C6 like in the video to get image similar to greater than sign. Join C8 and T1 in the same manner. Leave C7 alone in between.

3. As demonstrated in the video, from green, blue and orange figures obtained from step 2, extend 3 curved parallel lines that drop into the same imaginary horizontal line.

4. From the end of the green line extend a line (brown) to the orange line slightly above the end of the orange line as shown in the picture below.

5. In between the green and blue line draw a cross touching both lines. Draw a branch from orange line on the blue line such that it meets the green line of the cross.

6. For branches and labelling, follow the video or picture.

Mnemonic: Real Teenager Drinks Cold Beer (R=Root, T=Trunk, D=Division, C=Cord and B=Branches)
[endtext]
http://www.youtube.com/watch?v=9E1eIAKLxNsendofvid

Hemostasis Animation Video

2011-04-24T03:28:00.000-07:00

[starttext]Blood normally circulates through endothelium lined blood vessels. When a blood vessel is severed, a blod clot (thrombus) forms as a part of hemostasis, the physiologic response that stops bleeding.

Summary of the Steps involved in Hemostasis:

Vasoconstriction mediated by serotonin (5-HT), thromboxane (TXA2),etc.
Exposure of collagen on the wall of blood vessel leading to platelet aggregation and formation of white plug or primary hemostatic plug.
Adhesion of platelet to blood vessel wall leads to activation of platelets resulting in release of ADP and TXA2.
ADP and TXA2 further facilitates aggregation of platelets by increasing platelet stickiness.
Platelet activation also leads to initiation of blood clotting (injured tissue also releases thromboplastin)
Fibrinization of primary platelet plug leads to formation of strong secondary platelet plug.

[endtext]

http://www.youtube.com/watch?v=HFNWGCx_Eu4endofvideo

Mechanism of cough reflex

2011-04-17T04:17:00.000-07:00

[starttext]
Mechansim:

Deep inspiration, closed glottis
Increased intrapleural pressure then glottis opens suddenly with outflow of air at high velocity
Leads to the expulsion of irritants from mouth only

Pathway:

Receptors in nose, paranasal sinuses, pharynx, trachea, pleura, diaphragm, perichondrium, stomach, ex.auditory canal and tymphanic membrane
Stimulus pass via V,IX,X cranial nerves and phrenic nerves. And reach to
Cough centre in medulla
Efferent nerves from medullary centre, X cranial nerve, phrenic nerve, spinal motor nerve
Activation of primary and accessory respiratory muscles

Read more Mechanism of Cough and Sneeze | Medchrome
[endtext]

http://www.youtube.com/watch?v=2hrcH240SgQendofvid

Pathogenesis of AIDS and Replication of HIV

2010-11-06T05:12:00.000-07:00

[starttext]

HIV-1 initially infects T cells and macrophages directly or is carried to these cells by dendritic cells.
Viral replication in the regional lymph nodes leads to viremia and widespread seeding of lymphoid tissue.
The viremia is controlled by the host immune response, and the patient then enters a phase of clinical latency. During this phase, viral replication in both T cells and macrophages continues unabated, but there is some immune containment of virus.
There continues a gradual erosion of CD4+ cells by productive infection or other mechanisms.
When the CD4+ cells that are destroyed cannot be replenished, CD4+ cell numbers decline and the patient develops clinical symptoms of full-blown AIDS.
Macrophages are also parasitized by the virus early; they are not lysed by HIV-1, and they can transport the virus to various tissues, particularly the brain.

WHO New Recommendation for HIV/AIDS @ Medchrome

[endtext]

http://www.youtube.com/watch?v=9leO28ydyfUendofvid

Nasal Myiasis Removal Video

2010-11-05T02:23:00.000-07:00

[starttext]This post includes a video of maggots in nose and the removal of maggots using ether.

Myiasis is the infestation of tissue with fly larvae, commonly referred to as maggots. Maggots infest nose, nasopharynx and paranasal sinuses causing extensive destruction and obvious deformity.

Treatment:

Visible maggots should be picked up with forceps
Instillation of chloroform water/ether and oil (liquid paraffin) kills them
Nasal docuhe with warm saline is used to remove slough, crusts and dead maggots
Avoid contact of the patient with flies by use of mosquito nets
Nasal hygiene for prevention

For complete information about nasal myiasis: http://medchrome.com/minor/ent/nasal-myiasis-maggots-in-nose/

[endtext]

http://www.youtube.com/watch?v=BYXcZpGS164endofvid

Tumorman and Pathology of Neurofibromatosis

2010-10-31T05:49:00.000-07:00

[starttext]

Neurofibromatosis was described by von Recklinhausen in 1882. Neurofibromas may arise in any part of the body including axilla, thigh, buttock, deep lying soft tissue, orbit, mediastinum, retroperitoneum, tongue, gastrointestinal tract.

Plexiform Neurofibroma

Age: Usually occurs in children and young adults.

Site: Head and neck region

Clinical presentation: The expanded nerves form irregular, convoluted cords and nodules.

Gross: Plexiform neurofibroma is associated with

hyperpigmented skin
thickening of soft tissue
hypertrophy of bone

Microscopic features:

Nodules of tortuous, expanded nerve branches cut in various planes of section.
There is prominent myxoid change. In some cases cells spill out from the nerve into the soft tissue.
In early stage, the affected nerve displays increase in endoneurial matrix. In the late stage the nerve fibres are replaced by proliferation of Schwann cells together with thick wavy collagen bundles
Presence of mitotic figures is indicative of malignancy.

Immunohistochemistry:

Axon- Neurofilament positive
Schwann cells- S100 protein positive
Perineurial cells- EMA positive

Read a case about the TUMORMAN
[endtext]

http://www.youtube.com/watch?v=pwfdTndbNfAendofvid

Fate of RBC / Hemoglobin Video

2010-10-20T23:00:00.000-07:00

[starttext]When the RBCs become old, their wall become weak and the shape is changed due to slowing of enzyme activities. Some of these RBCs are then broken down by the force of the circulation. The hemoglobin released combines with haptoglobin (a plasma protein) and is carried to the RE cells. But most of the RBCs are phagocytosed by the RE cells and broken down. The Hb is released inside the RE cells. Th RE cells are situated mainly in the spleen and also the liver, bone marrow, etc. and these cells do not phagocytose the normal RBCs as the normal RBCs are flexible and can pass easily through the splenic filter. The old RBCs are deformed and stiff hence fail to pass through the filter and are phagocytosed by the RE cells situated near the filter.

There may be other mechansims for the detection of senile RBCs by the RE cells.

Some Hb in plasma is split into haem and globin. This haem is carried to the RE cells by another plasma protein known as haemopexin.

First step of the process is opening of tetrapyrrole ring. This is catalysed by the enzyme haem oxidase with liberation of one molecule of carbon monoxide (only reaction on the body producing CO). Then the globin is separated and added to the amino acid pool. THe Fe liberated is either stored in the RE cells as ferritin or used again. The other portion i.e. the opened up tetrapyrrole structure, forms the biliverdin which is reduced to bilirubin and is carried to hepatocytes (liver cells).

Inside the hepatocytes the billirubin is bound to the cytoplasmic proteins called ligandins. There, with the help of the enzyme gluconyl transferase it is conjugated to form bilirubin mono or diglucuronides in the smooth endoplasmic reticulum. Deficiency of this enzyme in neonates leads to physiological jaundice. Now this is called conjugated bilirubin (soluble) and is excreted through the bile in intestine. A small amount of bilirubin sulphate, etc. are also formed. If bilirubin accumulates inside the body, jaundice occurs and jaundice may occur due to increased destruction on RBCs, due to decreased glucuronyl transferase activity or other problems in the liver, or due to obstruction of the bile flow to the intestine.

In the intestine the bilirubin is acted upon by bacteria to form urobilinogen. SOme of the urobilinogen which passes through stool is called stercobilinogen which gives yellow color to the stool. This stercobilinogen on oxidation, outside the body, is converted into stercobilin which then gives stool a brown color.

Part of the urobilinogen formed in the intestine is reabsorbed and re-excreted through bile (entero-hepatic circulation). A part of this urobilinogen is also excreted through urine. On oxidation tis is converted to urobilin.

It is clear thar from e above discussion that bilirubin is formed from the dead RBCs and is excreted with bile, so bilirubin is purely an excretory product. But as stated before, the bilirubin level in the body increases either due to increased hemolysis or due to decreased excretion by the liver, hence its plasma level is a good indicator of liver disease and also hemolysis.

[endtext]

http://www.youtube.com/watch?v=g97zy_G_mYkendofvid