[postlink]http://tube.medchrome.com/2012/04/electron-transport-chain-and-oxidative.html[/postlink]

[starttext]

Mitochondrial Respiratory or Electron transfer chain is located in inner mitochondrial membrane
Substrate are oxidized and e- released passes from Complex of low redox potential to higher redox potential, eventually being added to O2 at complex IV to form H₂0
At complex I, III and IV, energy generated is used to proton pump (H+) inner mitochondrial membrane (Coupling sites/ Sites of ATP generation coupled with oxidative phosphorylation)
Oxidative phosphorylation: The proton gradient so created is released by passing protons back across inner membrane throught the ATP synthase (Complex V) resulting in ATP generation from ADP (3 for NADH – Complex I, III and IV and 2 for FADH2 – Complex III and IV i.e. Complex I bypassed)

Complex I (NADH dehydrogenase)

Complex II (Succinate dehydrogenase)

Complex III (Cytochrome C reductase)

Complex IV (Cytochrome C Oxidase)

Complex V (ATP synthase)

         NADH → Complex I → Q → Complex III → cytochrome c → Complex IV  → O₂

↑

                        Complex II

↑

                           FADH

Inhibitors of Respiratory chain:

Complex I : Barbiturate, Piericidin
Complex II: Carboxin, M
Complex III: BAL, Antimycin
Complex IV: Cyanide, Carbon monoxide

Cyanide poisoning:

Binds irreversibly to cytochrome a/a3 (complex IV) preventing electron transfer to oxygen, producing many of the same changes seen in tissue hypoxia.
Sources of cyanide include: Burning polyurethane (foam stuffing in furniture and mattresses) and Byproduct of nitroprusside (released slowly; thiosulfate can be used to destroy the cyanide)
Nitrites may be used as an antidote for cyanide poisoning if given rapidly. They convert hemoglobin to methemoglobin, which binds cyanide in the blood before reaching the tissues. Oxygen is also given if possible.

Inhibitors of Oxidative phosphorylation:

Uncouplers (Shunts H+ preventing pumping by ATP synthase) : 2,4 Dinitrophenol (2,4 DNP), thyroxine, thermogenin in brown fat
Inhibitors of ATP translocase: Atractyloside
Inhibitor of ATP synthase: Oligomycin

Respiratory control:

When Oxygen is limited:

↓O₂→ ↓oxidative phosphorylation → ↑[NADH] & [FADH2] → (-)TCA cycle

When Oxygen is adequate:

↑[ADP] → (+)isocitrate dehydrogenase → ↑TCA → ↑[NADH] & [FADH2] →   ↑electron transport → ↑[ATP]

[endtext]
http://www.youtube.com/watch?v=xbJ0nbzt5Kwendofvid

Electron transport chain and Oxidative phosphorylation Animation

[postlink]http://tube.medchrome.com/2012/03/how-to-remember-dukes-criteria-for.html[/postlink]

[starttext]
Mnemonic: Bacterial Endocarditis FIVE PM

Major Criteria

B : Blood culture +ve

Typical micro-organisms in 2 seperate cultures or
Persistently +ve blood cultures drawn 12 hours apart or
Single +ve blood culture for Coxiella burnetti

E : Endocardial involvement

+ve echocardiogram (vegetation, abscess or valve dehiscence) or
New valvular regurgitation

Minor criteria

Fever > 38 oC
Immunologic phenomena (glomerulonephritis, Osler’s nodes, Roth’s spots, Rheumatoid factor)
Vascular phenomena (major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjuntival hemorrhage, Janeway lesions)
Echocardiography findings (suggestive but not definitive)
Predisposition (heart condition or IV drug user)
Microbiologic evidence (Positive blood culture but not meeting major criteria)

Definitive Diagnosis requires 2 Major or 3 Minor + 1 Major or 5 Minor [endtext]

http://www.youtube.com/watch?v=m54F2em4lWwendofvid

How to Remember Dukes Criteria for Infective Endocarditis : Mnemonic

[postlink]http://tube.medchrome.com/2012/03/micturition-reflex-animation-video.html[/postlink]

[starttext]Micturition (Urination) is the ejection of urine from the urinary bladder through the urethra to the outside of the body. The micturition cycle occurs in 2 phases:

A) Urinary Storage

Mnemonic: Storage = Sympathetic

1. Stimulus: Urine filling until tension in wall of urinary bladder rises above threshold
2. Receptor: Stretch receptors in bladder wall
3. Afferent: Pelvic parasympathetic
4. Center: S2-S4
5. Efferent: Hypogastric sympathetic (lumbar)
6. Effectors:

Detrusor muscle: relaxation
Trigone muscle: contraction (internal urethral sphincter)

B) Micturirion Reflex

Mnemonic: Peeing = Parasympathetic

1. Stimulus: Volume of urine that initiates micturition reflex is 300-400 ml
2. Receptor: Stretch receptors in bladder wall
3. Afferent: Pelvic parasympathetic
4. Centre: S2–S4
5. Efferent: Pelvic parasympathetic
6. Effectors:

Derusor muscle: contraction
Trigone muscle: relaxation (internal urethral sphincter)

Voluntary Control

Because the external urethral sphincter is composed of skeletal muscle, its contraction and relaxation can be consciously controlled until the decision to urinate is made. This control is aided by nerve centers in the brain stem and cerebral cortex that can partially inhibit the micturition reflex. Nerve centers within the pons and hypothalamus function to make the micturition reflex more effective.

Higher control of micturition reflex

1. The reflex is controlled by facilitatory and inhibitory higher centres.

Faciltatory centres: a) Pontine centres b) Post hypothalamus
Inhibitory centres: Midbrain.

2. The higher centers exert final control of micturition

They partially inhibit the reflex except when micturition is desired.
They can prevent micturition by contraction of external urethral sphincter.
When it is time to urinate, the cortical areas: facilitate the sacral centre to initiate micturition reflex and inhibit the external urethral sphincter

[endtext]
http://www.youtube.com/watch?v=v3PRC5H3_mwendofvid

Micturition Reflex Animation: Video

[postlink]http://tube.medchrome.com/2012/03/pathophysiology-of-diabetic.html[/postlink]

[starttext] When the rate of synthesis of ketone bodies exceeds the rate of utilization, their concentration in blood increases, this is known as ketonemia. This is followed by ketonuria – excretion of ketone bodies in urine. The overall picture of ketonemia and ketonuria is commonly referred to as ketosis.

Mechanism:

Hyperglycaemia occurs due to decreased glucose uptake in fat and muscle cells due to insulin deficiency Lipolysis in fat cells now occurs promoted by the insulin deficiency releasing
Free fatty acids (FFA) into the blood which provide substrate to the liver
A switch in hepatic lipid metabolism occurs due to the insulin deficiency and the glucagon excess, so the excess FFA is metabolised resulting in excess production of acetyl CoA
The excess hepatic acetyl CoA (remaining after saturation of TCA cycle) is converted to ketone bodies which are released into the blood
Ketoacidosis and hyperglycaemia both occur due to the lack of insulin and the increase in glucagon and most of the clinical effects follow from these two factors

Summary:

1. ↓ Insulin, ↑Glucogon (glycogen à glucose)

- Glucose 500-700 mg/dl

2. Glucose-derived osmotic diuresis

3. ↑ Glucagon

- ↑ FFA esterfied à ketone bodies à acidosis

Diagnostic tests:

Blood glucose greater than 250 mg/dL
Blood pH less than 7.3
Blood bicarbonate less than 15 mEq/L
Ketones present in blood (exceeds 90 mg/dl)
Ketones excreted in urine exceeds 5000 mg/24 hrs

Signs and Symptoms:

Kussmal's respiration
Fruity odor of breath
Nausea and abdominal pain
Dehydration
Lethargy
Coma
Polydipsia, polyuria, polyphagia

Read more Ketone bodies, Ketosis and Ketoacidosis | Medchrome [endtext]

http://www.youtube.com/watch?v=m0sIW_JTecAendofvid

Pathophysiology of Diabetic Ketoacidosis : Animation

[postlink]http://tube.medchrome.com/2012/02/how-to-remember-portal-vein-anatomy.html[/postlink]

[starttext]
Origin: Hepatic Portal Vein is formed by the union of Splenic vein and Superior mesenteric Vein behind the neck of pancreas at L1 vertebral level.

Termination: The portal vein terminates by branching into right branch (entering right lobe of liver) and left branch entering (left lobe of liver).

Tributaries:

Splenic vein
Superior mesenteric vein
Cystic vein
Paraumbilical vein
Right and Left gastric vein
Superior pancreaticoduodenal vein

Points to remember:

Tributaries of splenic vein:

Veins corresponding to the branches of splenic artery
Inferior mesenteric vein

Tributaries of inferior mesenteric vein:

Veins corresponding to the branches of inferior mesenteric artery

Tributaries of superior mesenteric vein:

Veins corresponding to the branches of superior mesenteric artery
Inferior pancreaticoduodenal vein
Right gastroepiploic vein

Sites of Portocaval Anastomoses

Site	Portal vein	Systemic vein
Abdominal esophagus	Esophageal tributaries of left gastric vein	Esophageal tributaries of acessory hemiazygos vein
Umbilicus	Paraumbilical vein	Superior and Inferior epigastric vein
Anal canal	Superior rectal vein	Middle and Inferior rectal vein
Bare area of liver	Hepatic venules	Phrenic and intercostal veins
Posterior abdominal wall	Twigs of colic vein	Retroperitoneal vein

[endtext]

http://www.youtube.com/watch?v=8V3dXPNcnUoendofvid

How to remember Portal vein anatomy?

[postlink]http://tube.medchrome.com/2011/11/development-of-pituitary-gland.html[/postlink]

[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

Development of Pituitary Gland : Embryology Video

[postlink]http://tube.medchrome.com/2011/11/elisa-test-antibody-detection.html[/postlink]

[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

ELISA test : Antibody Detection

[postlink]http://tube.medchrome.com/2011/10/lifecycle-of-chlamydia-animation-video.html[/postlink]

[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

Lifecycle of Chlamydia : Animation Video

[postlink]http://tube.medchrome.com/2011/10/mechanism-of-action-of-steroid-hormones.html[/postlink]

[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

Mechanism of Action of Steroid Hormones: Animation

[postlink]http://tube.medchrome.com/2011/07/gastric-acid-secretion-physiology.html[/postlink]

[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

Gastric Acid Secretion Physiology Animation: Video

[postlink]http://tube.medchrome.com/2011/06/zn-staining-technique-for-acid-fast.html[/postlink]

[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

ZN staining technique for Acid Fast Bacilli: Demonstration Video

[postlink]http://tube.medchrome.com/2011/06/how-to-remember-branches-of-external.html[/postlink]

[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

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

[postlink]http://tube.medchrome.com/2011/05/draw-to-know-it-branches-of-celiac.html[/postlink]

[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

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

[postlink]http://tube.medchrome.com/2011/05/pathogenesis-of-atherosclerosis-video.html[/postlink]

[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

Pathogenesis of Atherosclerosis : Video Animation

[postlink]http://tube.medchrome.com/2011/05/baroreceptor-reflex-animation-video.html[/postlink]

[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

Baroreceptor Reflex Animation Video

[postlink]http://tube.medchrome.com/2011/05/lipoprotein-metabolism-animation-video.html[/postlink]

[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

Lipoprotein Metabolism : Animation video

[postlink]http://tube.medchrome.com/2011/05/lecture-video-cell-adaptation-cell.html[/postlink]

[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

Lecture Video: Cell Adaptation, Cell Injury and Cell Death

[postlink]http://tube.medchrome.com/2011/05/tracheotomy-procedure-animation.html[/postlink]

[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