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 What Goljan Says !!!  



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  #1

What Goljan Says !!!



Topics


Cell injury --- Page 1
Inflammation --- Page 1
Fluid and hemodynamics --- Page 2
Nutrition --- Page 2
Neoplasia --- Page 3
Hematology --- Page 3
Cardiovascular --- Page 6


Assalam o Alaikum:

Started this thread... hopefully it will help every one.

Note: Better check pictures in Google Images, while listening and reading the lectures. It will help a lot.

Happy studying and Keep Rocking smiling facewinkgrincoolnodgrin


Edited by gik84 on Apr 19, 2009 - 12:33 PM



  #2

hey gik84,
great idea, this wld motivate me to do papi everyday.
i ll squeeze in his lecture in my schedule.
thanq friend


  #3

Day 1, Goljan said he has ADHD. His daughter had gestational diabetes. Oh, and he loves kids, but not teenagers.


  #4

nice idea , i should be starting listening to it soon , and hope i can participate too


  #5

Nice to c u guys here... May be it will take one or two days to start my first post.... Calstudent, JackofKnives and Pyro.... nodnodnodnod thanx for coming here.... if any one wanna start u can shot now... or I will cut the rope coolcoolcoolcool by ma self.

N e ways stay COol. gringringrin
Just Keep Rocking winkwinkwinkwink



  #6

Today I have finnished my Hemo lecs... it got over at 49th minute. So i switched to the Cell injury chap for 11 minz only... Got few points as the introductory minz were there.... N e ways here comes the Post 1 of a long journey... Definitely i will b posting more details from the next posts. winkwinkwink

Just Keep rocking every one ... RIP coolcoolcoolnodnodwinkwink



Cell Injury

Post 1: (Dated: Jan 10 - 2009)
  • If the oxygen partial pressure (O2 dissolved in the plasma) is decreased, the oxygen saturation (O2 attached to Hb) MUST also decrease.... Fe3 cant carry O2.
  • Decrease in Arterial blood flow ---> Ischemia (Not venous)
  • Thrombosis in a muscular artery is the most common cause of ischemia --> Tissue hypoxia



Edited by gik84 on Jan 12, 2009 - 9:56 AM

  #7

Cell Injury

Post 2: (Dated: Jan 12 - 2009)

Hypoxemia (decrease oxygen partial pressure) is a cause se of hypoxia

Respiratory acidosis --> Up CO2 --> pO2 ALWAYS (and vice versa)

In case of ARDS and Hyline membrance disease... massive ventilation defect... 100% cant cure

Hypoxemic patient .... po2 does't increase.... intrapulmanory shunt increase.

Perfusion defect .... increase in dead space.... treatment ....100% increases po2

Sarcoidosis or pulmonary edema .... Diffusion deffect.

J receptors acctivated by fluid in lund interstitium irritation ... J reflex innervated by Tenth Nerve.

Anemia --- normal gas exchange --- Hb low --saturation normal --- excertional dyspnea --- excercise intolerance.

CO poisoning --- House fire u get Cyanide poisoning + Co poisoning = 2 bonuses --- saturation dec, cure 100% O2) ---- cyanide n Co inhibits Cytochrome oxidase.

Cyanosis in Co Poisoning --- decrease in O2 sat --- Red Pigment hides cyanosis.

MtHb poisoning --- O2 Saturation dec --- chocolate colored blood --- Fe3 present not Fe2 (cant carry O2) --- (Question = came from Rocky Mountain - O2 could't cure ??? what is the reason) --- treatment: IV methylene blue, Vitamin C.

Sulfa n nitro containing drugs (Oxidizing agents) ---> produce MetHb ---> Hemolytic Anemia in G6Pd deficiency.

MetHbnemia in HIV??? --- Sulfa methoxazole in pneumocystis crini.

Right shift O2 Curve: 2,3BPG Inc, High altitude, Acidosis, Fever.

Left Shift O2 Curve: Co, MetHb, HbF; 2,3 BBG dec, Alkalosis

Cytochrome oxidase delivers electron to O2 --- Inhibited by Co n Cyanide

Uncoupling Agents (Mitochondrial Membrane permeable protons): Alcohol, salicylates, dinitrophenol. Compensation of NADH, FAD producing systems (which produce protons) ---> increase hyperthermia.

Alcoholics ---> Uncoupling Agent ---> Heatstrokes risk increase

Resp Acidosis --- Hb Normal, O2 Sat dec, Po2 dec

Anemia --- Hb decrease, Saturation Normal, Po2 Normal

Co+ MetHb --- Hb Normal, Saturation dec, Po2 normal

Anaerobic Glycolysis --- all cells can do including. RBC ---> producing 2 ATPs ---> Increase of lactic acidosis ---> acid raised ---> protien denaturation ---> enzymes deatured as well ---> called coagulation necrosis.

Therefore Tissue hypoxia ---> Acidosis ---> coagulation necrosis ultimately

Anaerobic Glycolysis ---> screws all the pumps ---> esp. Na + Water enter cells ---> cell swell up

No ATP ---> irreversible cell damage ---> Ca AtPase dec ---> Intracellular Ca increase ---> Mitochondrial enzymes activated lead to Membrane Damage ---> nuclear enzymes leads to pyknosis ---> Phosphilipase damage to cell membrane ---> Pancreatitis.

Cell death: CK, SGOT, ALT, Amylase increase when cell die

Lipofusin ---> when free radical damage ---> wear n tear pigment ---> brown pigment ---> atrophic organs in elderly ---> pigment cant b digested.

Reperfusion injury is due to O2 Radicals

O2 Radical ---> destroys retina ---> blindness.

O2 Radicals ---> Bronchopulmonary dysplasia (fibrosis)

Iron loves making free radicals ----> cirrhosis, reactive cardiomyopathy, pancreastic failure ---> Malabsorption n diabetes.

Tylenol (Acetaminophen) ---> produce free radicals ---> #1 cause of Fulminant hepatitis (around central vein) ---> kidney damage ----> Treatment : N-Acetyle Cystein (Increases Glutathione)

Superoxide dismutase neutralize superoxide ---> producing peroxide

Pentose phosphate shunt makes Glutathione and NADPH

CCl4 converted in to CCL3 ---> fulminant hepatitis

Acetaminophin (Tylenol) + Aspirin ---> damage kidney (renal medulla) ----> PG dec

Apoptosis ---> genes involved in prog cell death ---> (eg. embryo)

King of our body ---> Y chromosome ---> Mullerian inhibitory factors ---> erase mullerian str ---> caspases wipe them ---> Apoptosis ---> producing lipofusin


Edited by gik84 on Mar 08, 2009 - 3:05 AM

  #8

Cell Injury
Post 3: (Dated: Jan 13 - 2009)

In women ---> X chromosome ---> wolfian duct structures are removed by apoptosis

Anterior mediastenum is smaller in adults as compare to children (Due to thymus) ---> apoptosis in adults

Digeorge syndrome ---> Thymus absent ---> cause tetany

Apoptosis occurs in cancer cells

Apoptotis occurs in neuron cells ---> dec in brain mass ---> pyknotic bodies.

Caspases involves in Apoptosis

Coagulation necrosis ---> Pale infarct - Heart, kidney, spleen, liver

Hemorrhagic infart: Bowel, testicle (torsion), lungs

Its depends on consistency of tissue whether it goes to coagulation or hemorrhagic necrosis.

Left side of heart ---> most of the emboli arises

vegetation of acute rheumatic fever rarely embolize ---> Infective endocarditis does

Clots of emboli or vegetation goes to spleen causing pale infarction

The arrhythmia mostly associated with systemic emboli is atrial fibrillation ---> pieces of emboli travels out and stuck in vessels

Dry gangrene: no pus ---> Diabetics

Most common cause of non traumatic amputation is diabetes ("ATH of popliteal artery)

Popliteal artery a most dangerous artery.

Most common cause of bowel infarction: #1: adhesions of previous surgery, #2: piece of small bowel trapped in an Indirect inguinal hernia in a sac.

Lung: Hemorhagic infarction ---> wedge shape ---> effusion present --> neutrophils present ---> plueretic chest pain

Liquefactive necrosis (liquefy) is related to an infection - neutrophils present - cyctic necrosis - acute inflamation related to neutrophils - damaging the tissues.

Gram + = strep auerues ---> abcess ---> cellulitis ---> infetion spreads thru tissues ---> liquefactive necrosis

Granulomatos necrosis ---> caseous ---> mycobacteria or systemic fungal infection caseous ---> lipid in cell wall giving cheasy appearance

Non caseous ---> Sarcoidosis

Epigastic distress with pain radiating to back ---> pancreatitis (retroperitoneal) ---> Enzymatic fat necrosis

Pendulous breast ---> Traumatic Fat Necrosis ---> Calcification ---> painful (not in cancer) ---> Xray looks like cancer ---> Calcium bound to fatty acid = saponification

Bluish discoloration ---> due to calcium ---> dystrophic calcification

Blue discloration with athromatous plaque = calcium

Lipase specific for pancrease

Alcoholics --> pancrease big time damage

Fibrinoid necrosis ---> immunologic disease (Rheumatoid fever, RA, glomerulonephritis, SLE, Vasculitis)

Palpable purpura ---> small vessel vasculitis ---> type 3 hypersensitivity

Immune complex ---> activates alternative complement system ---> C5a ---> chemotaxis of neutrophils ---> cause actual damage

Sinusoids = charaterstic gaps bw endothelial cells ---> large cells can pass thru them

Rt heart failure ---> backup of blood ---> nutmeg liver

Area around central vien of liver most susecptible to injury normaly ---> Zone 1

Yellow fever (Arbovirus) damage the liver zone 2 (Mid-zone necrosis)

Common cause of fatty change is alcoholics ---> Lactic acidosis (inc NADH shift pyruvate to lactate)

Fasting hypoglycemia ---> ketoacidosis (main ketoacid - B hydroxybutyrate)

Glycolysis provides glycerol 3 phophate, which is the backbone of TAG which is incorporated into VLDL ---> Restricting the carbohydrates will reduce the synthesis of VLDL

Kwashiorkar: reduce protien intake ---> VLDL cant go out of the liver due to dec apo-protiens - huge fatty liver ---> big prutuberant abdomen ---> no oncotic pressure ---> Ascites



  #9

gik wrote:
J reflex innervated by Kent Nerve.


10th nerve ? smiling face


  #10

Thanx but dont worry Unique1 - This is a first session - I will edit everytime I listen to his lecs. cheerz smiling face


  #11

Good idea for you guys to review and learned really well goljan


  #12

Cell Injury
Post 4: (Dated: Jan 15 - 2009)

You need proteins around lipids to dissolve in water.

Ferritin: soluble form of iron ---> best marker for diagnosis of iron dificiency anemia or hemosiderosis, hemochromatosis.

Hemosiderin (Insoluble iron storage), Stored in MP and BM, stained with Prussian Blue Dystrophic calcification: Calcium loves to calcify damaged tissue, normal serum calcium.... (Fat necrosis, ATH, aortic stenosis, hemolytic anemia)

Aortic stenosis: two valves doing job of 3 ---> stenosis ---> Dystrophic calcification

Primary Hyperparathyroidism most common cause of Hypercalcemia

Metastatic calcification: Hypercalcemia or hyperphosphatemia ---> Ca deposits in normal tissue.

Cong bicuspid aortic valve most common cause of aortic stenosis in USA ---> 2 valves instead of 3.

If u cant see a central area of Pallor ---> spherocyte

Spectrin: Needed to keep a bi-concave disc, if its defective ---> spherocytosis.

Ubiquitin: A stress protien

Intermediate filaments: framework of the house ---> when damaged ---> ubiquitin ubiquinate them

A liver with spaces in it ---> fatty liver

Ubiquination: Mallory bodies = alocoholics ---> fatty change

Silver stain Neurofibillary tangles = Alzheimer, Creutzfeld-Jakov disease.

Tau protein associated with Neurofibillary tangles

Parkinsons: lewy bodies in substantia nigra - dompamine decreased

Cell cycle: Labile cell, division via stem cells (BM, Skin, Intestinal crypts) are in cell cycle ---> most affected by drugs ---> specific or non-specific drugs - BM supression, diarrhea, rash on skin (due to presence of stem cells in these tissues).

Stable cells - G0 phase, stimulated to divide (Liver, spleen, Kidney, Smooth muscle, endometium) - stimulated by hormone or growth factor.

Permanent cell can not go in to cell cycle ---> can do hypertrophy only.

Smooth muscle can undergo hypertrophy and hyperplasia as well

The length of the cell cycle is decided by the length of the G1 stage

Proliferative phase can vary the most in menstrual cycle ---> analogous to G1 stage ---> once ovulated it cannot vary

Kinase always means phosphorylation.

Term: Phosphorylate = Activation (Glucagon - activate protien kinase) ; Dephosphorylate = De-Activator (Insulin - de-activate protien kinase)

In-active cyclin-D dependant kinase ---> Activated by cyclin-D ---> G1 phase makes cyclin-D

Once Cyclin-D is made in G1 phase it activates Cyclin Dependant kinase

The key area in cell cycle to control is going from G1 to Gs Phase ---> Most critical period ---> if mutation in G1 phase and went in to Gs phase ---> cancer potential

Security check point ---> before going into S phase ---> RB (Ch13) suppressor gene prevents the cell from going into S phase

When phosphorylated by CDK its inactive

P53 #1 for human cancer (Guardian of the cell ---> gives time to cell to correct errors ---> if severe DNA damage ---> apoptosis)

HPV- inactivates Rb n P53 gene (either One of the gene gets mutated ---> cell goes from G1 to S phase)

If no Rb protein ---> Retinoblastoma, osteogenic sarcoma, breast cancer.

Codman’s triangle seen in: osteosarcoma, Ewing sarcoma, subperiosteal abscess.

Vinca Alkaloids works on mitotic spindles(made from periwinkle plant); Paclitaxel on M Phase (chemotherapy,yew tree); Colchicine (use in acute gouty arthritis), Griseofulvin ---> M phase
Etoposide ---> G2 phase
MTX, Bleomycin ---> S phase


MTX, used in rheumatoid arthritis, inhibits DHF reductase ---> can Cause macrocytic anemia.

Atrophy = decrease in tissue mass, decrease cell size, less mitochondria --- does't have enuff organeles to survive.

Hydronephrosis is mostly caused by renal stones ---> increase pressure in cortex n medulla---> ischemia ---> atrophy of renal tubules.

ATH, Alzheimer (B amyloid protein, in layers 3,5,6 destroyed), ALS ---> brain atrophy, neuron degeneration ---> reduction in mass of brain


Casts --> decrease in muscle mass.

Hypopituitarism ---> adrenal gland atrophy (zona reticularis and fasiculata ONLY)

ACTH responsible for glucocorticoid (Z. Fasciculata), and sex hormones (Z. Reticularis); Not aldosterone (zona glumerulosa)

Oral thyroid ---> Natural thyroid goes down ---> thyroid atrophy.

Cystic Fibrosis (defective cystic fibrosis transmembrane regulator at Chr.7) ---> problems with secretions of exocrine part ---> block lumen ---> pancreas atrophy

Atheromatous plaque in renal vessel --->Renal vascular hypertension ---> Renin high ---> diseased kidney get atrophied, other kidney hypertrophy.

If you block G2 phase, you have 4n chromosomes (no mitosis) ---> increase in size of cell ---> copies of structures inside cells

1n - sperm

2n - Diploid cell

3n - Cancer cell or some trisomy disease

Hyperplasia left unchecked is predisposing for cancer (EXCEPT prostate)

Unopposed estrogen (no progesterone) cause endometrial hyperplasia ---> atypical hyperplasia ---> endometrial cancer.

Prostate hyperplasia does not predispose to cancer.


  #13

AWESOME NOTES GIK, cant stop myself without appreciating u.

keep rocking................. w u gl.nodnodnod




  #14

Cell Injury
Post 5: (Dated: Jan 16 - 2009)

Gravid uterus (after delivery): 50% hypertrophy, 50% hyperplasia ---> of smooth muscles.

Normal 3 times many WBC than RBC

RBC hyperplasia in BoneMarrow may be caused by COPD ---> hypoxemia ---> raised Epo

Erythropoetin is made in the endothelial cells of the peri-tubular capillaries

Psoriasis: Silvery Scales is an unregulated proliferation of squamous cells in the skin (hyperplasia).
Treatment: MTX (works on the basal cells from proliferating).


All hormone stimulated glands go through hyperplasia, not hypertrophy.

Urinary bladder goes through hypertrophy of smooth muscle cells related to afterload caused by urethra narrowing due prostate hyperplasia.

Barrets esophagus(Metaplasia) = glandular cells, mucus secreting, goblets cells instead of squamous cells ---> precursor of adeno.ca

Mid esophageal Ca ---> most common Ca in USA

Lining of main stem bronchus ---> psuedost. columnar ---> smoker ---> undergo sq metaplasia

Inc Goblet cells in main stem bronchus ---> hyperplasia

Also smookers have goblet cells in terminal bronchioles ---> metaplasia (normally no goblet cells in this place)

If goblet cells in stomach = abnormal ---> should be present in s.intestine ---> glandular metaplasia ---> precursor for adenocarcinoma of stomach

H. Pylori is the most common cause of adenocarcinoma of the stomach ---> produce damage to the pylorus and antral mucosa ---> chronic atrophic gastritis with intestinal glandular metaplasia ---> precursor lession for adenocarcinoma

Lung: Cilliated columnar epithelium ---> sq metaplasia ---> sp dysplasia ---> Cancer Sq Carcinoma

Distal Esophagus: Sq ---> glandular epithelium, mucus secreting ---> defense against acid injury ---> may go into atypical metaplasia ---> adenocarcinoma

Clonorchissinensis (Chinese liver fluke) is associated with cholangio carcinoma Schistosome Haematubium causes squamus metaplasia (instead of transitional) in the urinary bladder --->SCC.

Dysplasia = atypical hyperplasia, precursor for cancer.

Actinic (solar) keratosis premalignant to SCC of the skin, related to chronic sun exposure (UV light) and excess keratin. If scraped off, it grows back.

No premalignant lesion to basal cell cacinoma. It is more common.

---------------------------------------- END Cell Injury ---------------------------------------------


  #15

Inflammation
Post 6: (Dated: Jan 16 - 2009)

Histamine is responsible for the rubor, calor (both: vasodilatation on arterioles) and
tumor ("permeability on venioles) of acute inflammation.


Bradykanin: part of kininogen system which is between Hageman factor 12 and 11; when u activate intrinsis pathway u automatically activates the kininogen system ---> end product bradykinin.

Angioadema ---> complication of ACE inhibitor ---> inhibits metablolism of bradykinin which increases vesel permeability and producing angioedema , swelling of tissues.

Bradykinin also produces cough ---> mechanism unknown.

Bradykinin degraded by ACE

ACE and PGE2 are responsible for the dolor.

Neutrophils in small vessels gets sticky because of adhesion molecules synthesis ---> neutrophils stick to endothelial cells (pavementing or margination) ---> type 4 collegenase ---> drill hole in BM.

Cancer cells also contain Type4 Collegenase like neutrophils---> stick to endothelial cells through adhesion molecules usually against laminin in BM ---> pass through the BM by using collegenase ---> Get out of the vessels dont know the directions because of no chemotaxis

C5A, LTB4 ---> Involves in chemotaxis and make adhesion molecules in neutrophils.

IgG, C3B ---> opsonization recognized by Neutrophils, monocytes and macrophages.

Hypogammaglobulinemia: sex linked disease ---> Infections due to lack of opsonization.

Neutrophils must have receptors for IgG and C3b like monocyte machrophages.

Neutrophils for acute inflamation; for chronic monocytes and machrophages.

Monocytes: When get tired becomes machrophages

I-cell disease (lysosomal storage disease): can’t add mannose 6 phosphate residues to lysosomal enzymes ---> no proper trafficking ---> empty lysosomes.



  #16

Inflammation
Post 7: (Dated: Jan 17 - 2009)

Chlamydia can come out of phagolysosome

C3A, C5A ---> anaphylatoxins (stimulate mast cells to release histstamine)

Oxygen dependant myeloperoxidase system: O2 is converted by NADPH oxidase in cell membrane of neutrophils + monocytes (not Macrophages ---> they loose this system).

NADPH: Synthesized in P.P shunt ---> G6Pd converts G6P in to 6-phosphogluconate --> you get NADPH, Glutathione (Neutralizing factor for free radical).

NADPH converts molecular O2 into superoxide (free radical - having unpaired electron in its outer orbit), that gives off energy --> respiratory burst ---> Can be measured by radiation detector or NBT dye test: if working ok ---> bluish color, if not ---> chronic granulomatous disease of childhood (X-linked, no NADPH oxidase).


Superoxide is converted to peroxide which together with chloride (catalyzed by myeloperoxidase) to form bleach (kills bacteria)

Microglial cells are the Macrophages of the CNS ---> reservoirs of CNS Aids ???

Reservoir of Aids outside CNS are dendritic cells (Macrophages outside CNS) are re located in lymph nodes.

G6Pd deficiency: Infection prrecipitates hemolysis ---> No NADPH ---> No Functioning O2- dependant Myeloperoxidase system ---> susceptible to infections ---> hemolysis

All females of male dominant disease ---> a-symptomatic carriers of disease ---> transmit disease to 50% of sons.

CGD of childhood ---> X-linked recessive ---> boy gets from Mom

CGD: NADPH oxidase missing ---> no color in NBT dye test ---> lacking respiratory burst
Superoxide --> No
Peroxide ---> No
Myeloperoxidase ---> yes
Chloride ---> Yes


All living organisms make Peroxide including all bacterias

Not all bacterias contain catalase.

In CGD patients: They cannot kill staph; They can kill strep

Catalase + Coagulase positive (Staph. Aureus) breaks down peroxide and prevent its utilization in CGD.

Strep doesn’t have catalase, so it can be killed even in CGD patient.

In Myeloperoxide deficiency (AR),
Respiratory burst = Yes
Peroxide = Yes
Superoxide Free radicle = Yes
Chloride = Yes
Myeloperoxidase = No,
but no bleach ---> cant kill bacteria.


Opsonization defects (eg. Brutons agamaglobulinemia ---> missing IgG; C3 deficiency).

CGD of childhood (Cant make bleach + absence of repiratory burst ) and Myeloperoxidase deficiency (cant make bleach + autosomal recessive disorder) are both microbiocidal defects ---> cant kill bacteria.

Adhesion/B integrin defect ---> impaired adhesion, phagocytosis ---> umbilical cord doesn’t fall off (removed surgically), no neutrophils lining the small vessels.

Histamine: King of chemical mediators of acute inflamation ---> atrioles: vessodilate ---> Venules: increase vessel permeability.

Serotinin (made by tryphan) ---> a neurotransmitter ---> deficiency ---> depression

Anphylotoxins: C3A and C5a ---> stimulates mast cells to release histamine ---> vesodilation and increase vessels permeability.

In shock: if you activate complement system ---> anaphylotxins will be there.

NO: mainly made in endothelial cells ---> potent vesodilator ---> used in treatment of pulmonary hypertension; big role in septic shock.


IL-1 (pyrogen)---> stimulate hypothalamus to produce PG ---> stimulate thermoregulatory centre to produce fever (reduced by aspirin ---> inhibits PG).

Corticosteroids (supreme anti-inflamatory agent) inhibit PLA2 ---> no release of retinoic acid from PL ---> no PG, IL.

Omega-6 ??? fatty acids that can make arachidonic acid (linoleic acid) in Wallnuts and tissue oils ???: acts like aspirin ---> blocks platelet aggregation.

Omega 3 (like aspirin) inhibits platelet aggregation ---> protects heart.


  #17

Guys if any one... who accidentaly or intentionally visits this thread.... as the core template m following is from the previous PDF file ... link given at the top of the page...as at many places there were gaps of lectures... so m filling those gaps and expanding the great work already been done... so m placing Question Marks "???"... in my editions ... if some one knowns them or wanna make corrections ... do let me know ... may be it will help others a lot ...take care...

nodnodnodnodnodnodnod

Just Keep Rocking grin


  #18

Inflammation
Post 8: (Dated: Jan 18 - 2009)


Zileuton blocks 5-Lipoxygenase.

LTC4, -D4, E4: the slow reacting substance of bronchial asthma ---> potent broncho-constrictors

Zileuton works great in asthma ---> blocks all Leukotrienes ---> including LTB4 (adhesion molecules and chemotaxis)

Aspirin blocks cycloxygenase irreversibly if we are talking about platelet

TXA2 made in platelets ---> vasoconstrictor, brochconstrictor, platelet aggregation.

PGI2 made in endothelial cells ---> vasodilator, inhibits platelet aggregation.

PGE2 ---> vasodilator in kidney, keeps the fetus's patent ductus patent, mucus barrier in stomach, primary dysmenorrhea, increase uterine contractility (abortificant to express fetal material).

Dipyridamole inhibits TX synthase, used in stress test in coronary artery disease.

Coticosteroids: Anti-inflamatory agent ---> block phospholipase A2; decrease adhesion molecules synthesis along with other steroids like Epi and N.Epi

White person: 50% of neutrophils already stuck to endothelium of small vessels; 50%circulate.

Decrease in adhesion molecules synthesis ---> remaining 50% stuck ---> start to circulate ---> Neutrophils count increase in CBC.

Corticosteroids: Stimulate caspases of B-Cells ---> Apoptosis; Eosinophils decreased; Only neutrophils increase ---> decrease adhesion molecules.

Addison's disease: Decrease cortisol ---> Neutrophils count decrease; Eosinophil count increase.

MI: Epinephrine ---> decreases adhesion molecules ---> Raised adhesion molecules in CBC

Alveolar MP have a lot of lysosomes which are seen as black dots on EM.

Lamellar bodies (where lechitin is located) are seen in pneumocyte type 2.

Monocyte grayish cytoplasm, single nucleus, garbage in cytoplasm, on Em.

Vitamin E neutralizes oxidized LDL

EM: All nucleus with very little cytoplasm = Lymphocyte

T-lymphocytes Vs B-lymphocytes: 60% T-lymphocytes in peripheral blood

60% of lymphocytes are Th:Tc ratio is 2:1.

Slide: Thumb print ---> RER --> Ribosomes --> immonuglobullins ---> Plasma cells (M.Myeloma)

Plasma cell has a lot of ribosomes, because of Ig production. It is located in germinal follicle.

Basophils: Granules ---> more purplish and darker

Eosinophils: Granules of color same as RBC

Eosinophils have crystals in their cytoplasm. In asthma: degenerating eosinophils form Charcot-Leyden crystals seen in sputum.

Major basic proteins are released by eosinophils in type 2 HyperSensitivity to kill helminths.

Shisto ???: Eggs coated by IgE antibodies ---> Eosinophils have receptors for IgE antibodies --->release chemicals ---> MBP Kill helminths

T-2 Hypersensitivity: Cell hooking in to antibody on a target cell (Eosinophils = effector cells).


T-1 Hypersensitivity: Mast cells = effector cells

Mast cells release histamine and eosinophil chemotactic factor in type 1 H-S.(from purple granules) ---> Eosinophils here release histaminase and leukotriene neutralizing agents.

Eosinophils: T1 hypersensitivity = Knock off mediators producing hypersensitivity; T2 hypersensitivity = kills helminths.



  #19

Inflammation
Post 9: (Dated: Jan 20 - 2009)

CD3 = marker in antigen recognition site for all T cells
CD1 = antigen marker for histiocyte including langerhan cells.
CD10 = CALLA antigen (common ALL antigen), common marker of leukemia in children
CD15, 30 = Reed Sternberg
CD21 = B cell, EBV hooks on it
CD45 = all leukocytes


Burkits lymphoma is a B cell lymphoma

IL1 responsible for fever most of the time.

Fever right shifts O2 dissociation curve

During fever lots of O2 is needed in inflamation for O2 dependant myeloperoxidase system.

Antipyretics reduce the oxygen in neutrophils (disturbs O2 dep. myeloperoxidase system)

Fever is not good for viral and bacterial reproduction.(at 103 - 104 F)

Pus coming out of lactiferous duct in post partum ---> Staph. Aureus.

Osteomyelitis ( yellowish absscess) ---> Staph. Aureus. In Sickle cell anemia, it is usually cause by Salmonella Typhimurium --->Hematogenous spread.

Hot ---> spread all over the face ---> Cellulitis ---> Strep. Pyogens

C. dyphteria toxin damages the sub/mucosa ---> psedomembrane (like ke C. difficile); gram + rod ; exotoxin disturbs riboxylation of proteins (elongation factor II) ---> damages the mucosa + submucosa producing a pseudomembrane; does't invades but produces the toxin that damages the membranes; Endotoxin is for diagnosis in stool.

Bread and butter pericarditis = fibrinous inflammation ---> Usually due to increase vessel permeability ---> SLE, MI, coxsackie

Dressler’s syndrome: pericarditis which develops about 6 weeks after an MI or heart surgery.

Most common organism causing infection in 3rd degree burn is Pseudomonas Aeruginosa. Pus color is green due to pyocyanin.

The basal cell layer on both sides of the cut proliferate and go underneath the clot and seal it; not over the clot.

Appendicectomy: by 48 hours the wound is sealed off because of basal cells.

The key for the healing of the wound is presence of granulation tissue + fibronectin.

Fibronectin is an adhesion molecule and fibroblast chemotactic in healing process.

Granulation tissue starts at day 3, peak on day 5.

No granulation tissue ---> no healing of wound

Type 4 collagen in basement membrane.
Type 1 collagen is in bone, skin, tendons and ligaments
Typ 3 collagen is in the initial stages of wound repair. Broke by type 3 collagenase.


Metallo enzyme (need zinc) helps turn type 3 into type 1

Maximal tensile strength in a wound by 3 months is 80%.

Most common cause of poor wound healing is infection.

Ehlers danlos syndrome: defect in collagen.

Marfan syndrome: defect in fibriLlin.

Scurvy: defect in hydroxylation of proline and lysine by ascorbic acid ; Normally triple helix stick together and forms tensile strength by cross bridges ---> cross bridges anchors into places where hydroxylated proline and lysine ; No cross bridges ---> cannott attach to anything ---> weak abnormal collagen ---> hemorrhage, no wound healing, hemoarthrosis.

Keloid: (hypertrophied scar) = excess of type 3 collagen deposition ; genetic predisposition in blacks.

SCC is common in the setting of scars related to 3rd degree burns or chronically draining sinus tract (in osteomyelitis).

IgM is the most potent activator of the complement system, because it has 10 antigen recognition sites. Main Ig of Acute inflammation.

IgG complement activation doesn’t go beyond C3 (no C5A and so on). Main Ig of chronic inflammation.

After 10 days to 2 weeks there is a isotype switching: Same plasma cell making Igm ---> splice out the "Nu"-Heavychain (Heavy chain that defines specificities of an Ig) and it splices in a gamma heavy chain.



  #20

Inflammation
Post 10: (Dated: Jan 21 - 2009)

Acute Allergic reactions: Key cell eosinophil

Viral infection: Key cell Lymphocytes

Chronic inflammation: Key cells Monocytes, machrophages, raised plasma cells, raised lymphocytes.

Pus is not a charactristic of chronic (only of acute) inflammation: Increased vessels permeability ---> neutrophils immigration in interstitial tissue ---> protein rich fluid (exudate: 3gm protien/dl ), cell rich fluid called PUS ---> produces tumor in acute inflammation.

Granuloma: roundish and pink, multinucleated giant cells. Type 4 H-S.

Sometime gets calcified. Epitheloid cells are activated MP, when they die they form multinucleated giant cells which are seen in granulomas.

Tc killing neoplastic cells or virally infected cells is also Type 4 H-S (no antibodies)

Poison ivy: Type 4 H-s

MP and Th CD4 are the key cells of TB.

Key actors in delayed reaction H-S ---> MP processes antigens ---> presents antigen to Th cels ---> Th cells releases cytokines ---> Gamma interferon and MP inhibitory factor (involved in granuloma) ---> activates the MP to kill TB, cryptoccocus, Histoplasma etc.

Subset1 Th cells ---> Type 4 H-S


MP release IL-12 ---> activates and presents antigens to subset1 Th cells ---> turns into subset1 Cd4 Th cells (memmory T cells of the event)

Marker of all histiocytes and MP have ---> cluster designation 1 ???

Langerhans cells (EM: birbeck granules looks likes tennis rackets) are the MP of the skin, phagocytose PPD, proceses it and present it to Th type 1 that has memory of previous exposure ---> release cytokines that produce the inflammatory reaction which is part of the positive PPD.

Old people usually don't have Type4 H-S. they have lesser than brisk response to PPD. Some times they need double type of PPD, because of decreased immune response.

HIV: less/no type 4 H-S (Th dec.), no granuloma formation in HIV ; No Th cells.

PPD of 5 mm indurtion is enough to say positive in HIV ---> that would be pretty good immune response.

Reaction to injury in permanant tissues ---> scar tissue (no contraction)

Scar tissue: heart muscle, kidney (especially straight portion of PT, TAL)

Damage to free wall of left ventricle ---> firbrous tissues does't contract ---> EF goes down

Kidney Medulla most susceptible to ischemia.
Most suceptible to ishemia of kidney Nephron: 1) straight portion of proximal tubule (most of oxidative metabolism located, most of the reabsorption of Na and HCO3) ; (2) Medullary segment of the thick ascending limb (Na-K-Cl pump located)


Na-K-Cl pump generates free water (80ml for those 4 ions). Blocked by lasix (Loop diuretic)





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