Composite individual muscles/hybrid muscles	Composite group of muscles
Different origins/2 heads Different innervations for 2 heads §  Adductor magnus-obturator nerve & tibial division of sciatic nerve §  Biceps femoris-long head through tibial division of sciatic nerve,short head through common proneal division of sciatic nerve §  Pectineus-anterior fibres by femoral nerve,posterior fibres by anterior division of obturator nerve	Different individual muscles functioning as one muscle model §  Quadriceps femoris-rectus femoris,vastus medialis,vastus lateralis,vastus intermedius

Digastric muscles

§  Occipitofrontalis

§  Omohyoid -inferior belly & superior belly joined by intermediate tendon

§  Muscle fibres within ligament of Treitz (belly of skeletal muscle fibres & belly of smooth muscle fibres)

Bronchial arteries are direct/indirect branches of descending thoracic aorta

They vary in size,number ,origin

Right side	Left side
1 bronchial artery Arise directly from decending thoracic aorta either from §  3rd posterior intercostal artery or §  Upper left bronchial artery	2 bronchial arteries §  Arise directly from descending thoracic aorta

Blood supply to broncho-pulmonary tree

§  As far as respiratory bronchiole------ pulmonary vessels and bronchial arteries

§  Distal to respiratory bronchiole(alveolar ducts,atria,air saccules,alveoli)------pulmonary vessels alone

o    Ideal/most common  location for peripheral venous cut down---- great sephanous vein(one finger breadth antero-superior to medial malleolus)

o    Skin over this region is supplied by Great saphenous nerve(branch of posterior division of femoral nerve)

Paraduodenal fossa

o    In 20 % of subjects

o    Lies to left of DJ flexure

o    Its orfice looks to right

o    The inferior mesenteric vein lies in free edge of peritoneal fold that forms anterior wall of fossa

o    Incarcerated hernia may thrombose /obstruct the vein

o    Danger of dividing the vein during surgery for incarcerated paraduodenal hernia

§  Superior duodenal fossa-in 50%

§  Inferior duodenal fossa-in 75%

§  Retroduodenal fossa-largest duodenal recess

§  Mesentrico-parietal fossa of waldeyer –in 1%,most usual position of this fossa is in 1^st part of meso-jejunum.Superior mesenteric vessels lie in the fold of peritoneum forming this fossa

Internal iliac artery

Anterior division	Posterior division
Superior vesical artery(gives rise to artery of ductus deferns) Inferior vesical artery(replaced by vaginal artery in females) Obturator artery Middle rectal artery Inferior gluteal artery Internal pudendal artery Uterine artery(only in females)	Iliolumbar artery Lateral sacral artery Superior gluteal artery

Deep middle cerebral veins-àbasal veins-àgreat cerebral veinsàstraight sinus

Cavernous sinus

Incoming channels	Draining channels
Superior ophthalmic veins Inferior ophthalmic vein Central vein of retina Superficial middle cerebral vein Inferior cerebral vein Sphenoparietal sinus Middle meningeal vein	Superior petrosal sinus(drain into transverse sinus) Inferior petrosal sinus(drain into internal jugular veins) Emissary vein(drain into pterygoid plexus of veins) Superior ophthalmic vein(drains into facial vein) Intercavernous vein

Diploic veins

• Develop after birth about 4^th year of life
• Develop within diploe of cranial bones(intervening cancellous & vascular portion)
• Diploe are not present at birth.they develop at 4^th year of life with maximum differentiation at about 35 years.
• At birth cranial vault is unilamellar(one lamina)
• No valves
• Present in cranial bones
• Considerable large veins
• Dilations at regular intervals
• Anastomose externally with pericranial veins & internally with meningeal veins & dural sinuses
• Thin wall lined by single layer of endothelium
• Liable to inflammation after head injury & may give rise to pus in diploe & pyemia
• May give rise to visceral abscess after head injury
• Bleeding after surgical vault fractures or surgical trephination

Major diploic veins

• Frontal
• Anterior temporal/parietal
• Posterior temporal/parietal
• Occipital
• Numerous small diploic veins tributaries of superior sagital sinus

Nasal septum

• Osseous part—vomer,perpendicular plate of ethmoid,nasal spine of frontal bone,rostrum & crest of sphenoid,nasal crest of nasal bone,nasal crest of palatine bone,nasal crest of maxillary bone.
• Cartilagenous part—septal cartilage,septa process of inferior nasal cartilage.

Catalase positive bacteria

§  Staphylococci

§  n.meningitidis

§  atypical mycobacteria

§  pseudomonas

§  coliform

§  h.influenzae

§  h.pylori

§  yersinia

§  pasturella

§  shigella except shigella dysentriae

§  l.monocytogenes

§  nocardia

§  legionella

§  brucella except b.neotomae,b.ovis

§  fungi-aspergillus,candida

streptococci

§  catalase –ive

§  not soluble in 10 % bile, unlike pneumococci

§  hydrolysis of PYR/pyroliddonile naphthlamide

§  failure to ferment ribose

enteerobacteriacae

§  gram –ive rods

§  natural habitat –large intestine

§  aerobic or facultative anaerobes

§  non-sporing

§  non-acid fast

§  grow well on mac-conkey media

§  catalase positive except shigella dysentriae type 1

§  oxidase negative

§  reduces nitrate to nitrite

§  urease negative

§  motile by peritrichate flagella except shigella,klebsiella,salmonella gallinorum-pullorum

§  ferment glucose except shigella

mosquito borne disease

Anopheles	Malaria Filariasis(not in india)
Culex	Bancroftian filariasis Japanese encephalitis West nile fever Viral arthritis
Aedes	Yellow fever Dengue fever Chikungunya fever Rift valley fever
Mansonoides	Malayan/brugian filariasis Chikungunya fever

m.c normal flora of skin----staph. Epidermidis

m.c anaerobic normal flora of skin -----propinobacterium

Site	Normal flora
§  Oropharynx §  Upper respiratory tract §  Nose §  Stomach §  Blood,internal organs §  Gingival crevices §  Colon §  Vagina §  Conjunctiva	Viridians streptococci Non-hemolytic & alpha-hemolytic streptococci Staph. Aureus Bacteroides Babies-breast fed only-bifidobacterium Adults-bacteriodes Lactobacillus Diptheroids??

Lymphatic filariasis

§  Lymphoscintigraphy-only a research tool,not used for diagnostic purposes

§  Eosinophilia

§  Elevated IgE

§  Antifilarial antibody

§  Definitive diagnosis----demonstration of parasite.                                                                           conc. Of parasite can be done by—                                                                                                         (1) passage of fluid through polycarbonate cylindrical pore filter pore size 3m or                       (2) by knott’s technique-centrifugation of fluid fixed in 2 % formalin

§  PCR

§  ELISA

§  No tests for circulating antigens in brugian filariasis

§  Dorset media and LJ media------------selective media for TB bacilli

§  NNN media-----for leishmania donovani

§  Nutrient agar ----simple media

§  Mac conkey media------------differential as well as indicator media for lactose and non-lactose fermentors.

Pontaic fever-acute febrile self limited illness caised by legionella

Legionella

§  Aerobic

§  Gm –ive

§  Motile

§  Non-encapsulated bacilli

§  Natural habitat-aquatic bodies

§  Outbreaks associated with-----Air conditioning ,cooling towers

§  Multiple modes of transmission-------aspiration(m.c.),aerosolization,direct instillation

§  No man to man transmission

§  No animal reservoir

§  Legionairres disease-----atypical pneumonia(high fever,diarrhea,pneumonia)

§  Pontaic fever

§  m.c extrapulmonary site of ligeonella---heart

§  selective media----buffered charcoal yeast extract(BCYE) agar

§  tmt.-----macrolides(azithromycin),quinolones(gemifloxacin)

resolution of light microscope----200nm

overall magnification----objective lens × eyepiece lens

vaccum is required in-------electron microscope

images in black & white----------electron microscope

light microscope magnifies---------2000 times

electron microscope magnifies----------- 500,000 times

staph. Aureus

§  coagulase positive

§  ferment mannitol

§  clear hemolysis on blood agar

§  liquefy gelatin

§  produce phosphatase

§  potassium tellurite medium----------reduce tellurite to form black colonies

§  produce thermostable nucleases which can be demonstrated by agar diffusion test---ability of boiled culture s to degrade DNA

Nutmeg liver

§  chronic passive congestion of liver eg. In heart failure(cardiac cirrhosis)

§  hepatic lobules are grossly red brown & slightly depressed and are accentuated against surrounding zones of uncongested tan liver.

All blood clotting factors are made exclusively  in liver cells except—factor 8

Serum= plasma — fibrinogen,factor 2,5,8

Serum has high serotonin content because of break down of platelets during clotting

VITAMIN K

For synthesis of Factor 2,7,9,10,protein C, protein S, protein Z.

In coagulation, the procoagulant protein factor X can be activated into factor Xa two ways. Extrinsic and intrinsic ways.

The activating complexes are called tenase. Tenase is a contraction of "ten" and the suffix "-ase", which means, that the complex activate its substrate (inactive factor X) by cleaving it.

Extrinsic tenase complex---- tissue factor, factor VII, and Ca²⁺

Intrinsic tenase complex---- factor IX (IXa), its cofactor factor VIII (VIIIa), the substrate (factor X), and they are activated by negatively charged surfaces (such as glass, active platelet membrane, cell membrane of monocytes.

Factors names

Prekallikrien—fletcher factor(intrinsic)

HMWK---contact activation cofactor; Fitzgerald, Flaujeac Williams factor(intrinsic)

     I.        fibrinogen

   II.        prothrombin

  III.        tissue factor

  IV.        ca2+

   V.        proaccelerin/labile factor

 VI.        old name of factor 5a

VII.        stable factor /proconvertin

VIII.        anti-hemophilic factor A

  IX.        antihemophilic factor B/Christmas factor

    X.        stuart power factor

 XI.        plasma thromboplastin antecedent

XII.        Hageman factor

XIII.        Fibrin-stabilising factor

Not true about apoptosis/irreversible cell injury----cell swelling/shrinking

Reversible cell injury	Irreversible cell injury
Generalized swelling of cell & organelles Loss of microvilli Bleb formation Detachment of ribosomes from ER Myelin figures Clumping of nuclear chromatin	Membrane damage is central factor Severe swelling of mitochondria Large flocculant densities in matrix d/t increased calcium influx Lysosomal swelling:↓basophilia(↓RNP) NUCLEAR protein digestion-pyknosis,karyolysis,karyorrhexis. Severe damage to plasma membrane

Myocardial infarcts <12hrs old are not apparent on gross examination but area of necrosis that first becomes apparent 2-3 hrs after infarct by tri-phenyl-tetrazolium chloride/TTC which imparts brick red colour to non-infarcted myocardiumwhere dehydrogenase enzymes are preserved.

Other stain used---NBT/nitroblue tetrazolium

Other techniques--- autofluoresence staining,immunohistichemical analysis,special DNA stainings

Pseudo-polyp

·         Well differentiated polyp with connective tissue core+inflammatory cell infilterate and smooth muscle cell

·         d/t  re-epithelialization of undermined ulcers & overhanging margins in inflammatory bowel disease.esp . in ulcerative colitis

·         no malignant potential