Catos 2nd exam

Ectoderm epithelia is all the outside layers. Endoderm epithelia is lining the GI tract. Mesoderm epithelia is lining the CV system, urogenital system and serous cavities.

Over articular surfaces

AVASCULAR, gets it's nutrition from the vascular underlying CT.

Keratin
Endothelium and mesothelium are vimentin

When inside epithelium meets outside epithelium like in the rectum-anus junction

Pericardium, pleura and peritoneum

Alveoli, pleura, pericardium, blood vessels, loop of Henle, lympathics and parietal layer of Bowman's capsule.
Functions: Exchange
Flat nucleus of single layer of cells.

Kidney tubules, thyroid follicles, ducts of secretory unit.
Function: secretion and absorption.
Round nucleus of single layer of cells.

Small and large intestines, GB and large ducts of glands.
Single layer of cells with a basally located oval nucleus and no cilia on the surface. In addition, covered with striated border microvilli and goblet cells.

Oviduct, uterus, efferent ducts and small bronchi.
Single layer of cells with a basally located oval nucleus and the surface covered with cilia.

TRUE!!! Only simple epithelia have cilia. Pseudostratified epithelia are classed as simple epithelia.

Trachea and bronchi
All cells touch the BM but not all touch the surface. Have an oval shaped nucleus and goblet cells

Epididymis
DON'T BE CONFUSED, these have stereocilia to increase absorption. There are also NO goblet cells in the non-ciliated version.

THE SURFACE CELLS ARE THE ONLY ONES THAT ARE IMPORTANT

Dry surface epithelia like skin.
Protection from abrasion
There are no nuclei in the outer layer which usually looks separated from the surface during fixing.

Wet surfaces of the oral cavity, esophagus and vagina.
Protection from abrasion.
Flat nuclei are found in the outer layer.

DESMOSOMES to resist abrasion.

Ducts of sweat glands, male urethra and esophageal glands (VERY RARE).
Protection, limited secretion and absorption.
2 layers of cells with round nuclei

Large excretory ducts of some glands, male urethra and conjunctiva of the eye.
2 layers of cells with oval nuclei

Ureters and urinary bladder.
Permit distention
Binucleated surface cells is defining because this will look like stratified squamous non-keratinized. In addition, the surface is puffy like clouds.

All simple epithelia retain the ability to divide. Only the basal layer of stratified epithelia retain the ability to divide.

When cells of a certain region change into a different but still normal looking type of cells. E.g. stratified squamous in the trachea

Abnormal looking tissue due to damage. This is still reversible.

Non-reversible abnormal looking tissue which is usually cancer.

Glands are classified as epithelium and cancer of the epithelium is called carcinoma, therefore glandular cancer is adenocarcinoma.

Tubular
Acinar
Alveolar
Tubuloalveolar/tubuloacinar

Serous secretion which is watery, protein rich substance

Mucus secretion which is rich in glycoproteins. This secretion is merocrine although it looks like holocrine

They have serous demilunes with intercellular secretory canaliculi.

Sebum which is filled with wax, cholesterol, TGL's and cell debri. Remember this is holocrine secretion.

Apocrine product is similar to eccrine sweat except it is filled with protein and this allows bacteria to thrive. This makes apocrine sweat smelly and these are found in axilla and groin areas.

Sweat which is a hypotonic water solution with very low protein

Milk which contains minerals, electrolytes, carbs, IgA and proteins

Protein portion is released by merocrine but lipid portion is released apocrine.

They are modified ECF spaces
They have microvilli
They are closed off by ZO's
The product eventually gets into a true duct.

Dense irregular CT with type I collagen is found in capsule, septa and trabeculae.
Loose connective tissue with type III collagen is found surrounding each acinus.

Intralobular are lined with simple cuboidal or columnar.
Interlobular are lined with stratified columnar.

Intercalated ducts are lined by simple cuboidal and connect acinus to striated duct.
Striated ducts are simple columnar and have basal infoldings making them striated.

Germ layer of origin is ectoderm so have keratin intermediate filaments BUT THEY ARE SMOOTH MUSCLE CELLS.

YES, they have hemidesmosomes, desmosomes and gap junctions. ON THE EXAM!!!

Na/K pump and K channel in basolateral membrane. Na channel in apical membrane for absorption. In normal cells, these channels are randomly distributed.

1) K channels in basolateral membrane create negative cell interior.
2) With a negative interior, the driving force for Na is an electrical force directed towards the inside of the cell.
3) The Na/K pump is always working and pushes this Na out of the cell.
4) A transluminal potential develops with the lumen negative. This pushes Cl through paracellular pathway into blood.
5) Some Na goes paracellular back to the lumen.

To create an osmotic gradient which favors the absorption of water with the help of aquaporins.

1) K leak channel creates a negative cell interior.
2) Cl is driven out of cell into lumen by electrical gradient.
3) Na/K/2Cl pump in basal membrane replenishes Cl which leaked out apical surface.
4) Transluminal potential with lumen negative draws Na into lumen and water follows.

The pump moves 2Cl and 1Na along their concentration gradients into the cell to replenish the Cl lost from the apical surface. The K moves solely to maintain electrical neutrality but is actually moving against conc. gradient.

Due to cardiovascular hydrostatic pressure, there is always fluid in the alveoli. Our purpose is to reduce this fluid and this is done with electrogenic Na reabsorption.

Type II alveolar cell.

Because the cardiovascular system hydrostatic pressure is insignificant, fluid must be created for the trachea. This is done with electrogenic Cl secretion.

In order to maintain a fluid layer in the trachea, electrogenic Cl secretion occurs. This Cl channel is the CFTR channel which is deficient in CF. W/o the channel, the mucus is very thick.

The Cl channel in the secretory unit of the gland is not a CFTR channel. These patients can still secrete Cl no problem.
The CFTR channel is reversed in the duct and so they can't reabsorb the Cl fast enough.

The sweat duct still reabsorbs Na through the electrogenic method, however Cl does not move paracellular, this is not quick enough. The CFTR channel is inserted into the membrane to make this absorption quicker.
IT IS STILL ELECTROGENIC Na REABSORPTION.

Epithelia only have basal lamina whereas CT have extensive ECM.

Endothelium, mesothelium, mast cells and smooth muscle.

It is very vascular as it provides blood to the avascular epithelium under which it sits.

Gap junctions. Cell junctions are not very numerous in CT.

Areolar, reticular, adipose and lamina propria

Adipose tissue which the primary cell being an adipocyte.

Reticular CT

Bone marrow, spleen and lymph nodes. Reticular CT basically forms the hematopoeitic and lymphoid tissue stroma.
Reticular CT contains reticular cells which make the type III collagen.

As part of the mucosa of respiratory, digestive, reproductive and urinary tracts.

It has all 3 types of fibers: collagen, elastic and reticular. It also has a crapload of resident cells such as macrophages, fibroblasts, mast cells, plasma cells and adipocytes.

Hyaluronic acid, dermatan, keratan and chondroitin sulfate.

Dense CT has lots of type I collagen fibers and the key resident cell is the fibroblast.

Tendons, ligaments, deep fascia and aponeuroses.

Reticular layer of dermis, periosteum, perichondrium, organ capsules, septa, trabeculae, perineurium and perimysium.

Lack of thyroxine increases the synthesis of GAGS which increases tissue colloid osmotic pressure thereby drawing water into the ISF.

Fibroblasts, mast cells, plasma cells, adipocytes, macrophages, endothelial cells, pericytes and vascular smooth muscle cells.

Secrete procollagen, proelastin, GAGS and all components of the ECM.

Fibroblast growth factor (FGF).
Transforming growth factor.

Syndecan which is chondroitin and heparan sulfate.

Low thyroxine levels.

Fibroblasts - high metabolic activity. Fibrocytes - darker nucleus due to condensed euchromatin.
Fibroblasts - actively secreting, fibrocytes don't secrete.
Fibroblasts - actively dividing, fibrocytes may or may not divide.

A fibroblast with actin and myosin found in areas of wound healing. Have an external lamina

Histiocytes
Alveolar macrophage
Kupffer cells
Osteoclasts
Microglia

Come from monocytes
Have lots of lysosomes, golgi and RER
High phagocytosis
Have Fc receptors for binding of ab and complement

Turn over the old ECM material.
Act as APC's (antigen presenting cells)
Release IL-1, TNF-a, chemotactic factors and enzymes (lysozymes and collagenase)

IL-1

Vimentin and Desmin

Around continuous capillaries and post-capillary venules

Release vasoactive substances to change capillary diameter. Contain smooth muscle to act like muscular layer of bv.

Vascular smooth muscle cells

Lipoblast

The adipocytes are surrounded by a basal lamina which is the only CT cell to have this.

Reticular fibers

Not while they have fat in them.

Last 3 months of fetal life
5 years postnatal
Pre-puberty due to the estrogen

Skin sensory receptors sense cold, send impulse to CNS whereby sympathetics to B3 receptors on Brown adipose are activated by Nepi. This activates hormone sensitive lipase which breaks down TGL's so that they can be used for oxidation. The mitochondria do not use these for energy production but rather heat production.

Thermogenin (UCP-1) is an uncoupling agent which prevents ATP from being made in the mitochondria.

It is found lining endothelial cells but it is made by adipocytes

It inhibits hormone sensitive lipase to prevent TGL breakdown. It also activates the GLUT4 receptor to increase blood glucose uptake. This is because adipose tissue can't use glycerol to synthesize fats.

Inhibit hormone sensitive lipase to prevent TGL breakdown

ACTH, glucagon and Nepi (sympathetics)
They increase levels of cAMP.

Capillaries in adipose tissue are particularly long which causes increased TPR thereby leading to hypertension.

Hormone made by adipose tissue which goes to the hypothalamus to decrease apetite.

Panniculus adiposus

Axilla, neck, mediastinum and kidney hilus

BOTH and both receive sympathetic stimulation

Monocyte

Primary mediators: Histamine, eosinophil chemotactic factor and neutrophil chemotactic factor.

Leukotrienes C4 and D4 - produce vascular and bronchospasm.
Prostaglandin D2 - produce bronchospasm.

The leukotrienes and prostaglandins come from arachidonic acid which came from phospholipase A2 breaking down DAG.

First exposure to antigen (bee venom) binds IgE and causes it to move to mast cell PM.
Second exposure - antigen binds to IgE on the mast cell surface and activates adenylate cyclase. This increases cAMP which causes Ca2+ release. The Ca2+ release causes the granules to fuse and be released.

It is when the granules of the mast cell fuse together before being released.

Phospholipase C converts PIP2 into IP3 and DAG. The DAG is converted into arachidonic acid with phospholipase A2 which can then be converted into leukotrienes C4 and D4 and prostaglandin D2.

Due to RER

Large Golgi apparatus

Lysosomes

Reproductive, respiratory, digestive and urinary systems.

Loose CT with overlying mesothelium

They do not have an epithelium. Contain 2 cell types. Type A - macrophages and Type B - fibroblasts (make synovial fluid)

Hyaluronic acid and lubricin

Stratified squamous keratinized epithelium and dense irregular CT.

Simple columnar or pseudostratified epithelium with lamina propria.

Mesothelium and submesothelial layer (loose CT)

Cartilage is to bone.
CARTILAGE NOT VASCULAR
BONE VERY VASCULAR

Aggrecan (chondroitin and keratan sulfate), and chondronectin (glycoprotein). There is no mineral component like bone

Chondroitin and keratan sulfate, osteocalcin and osteopontin. Finally, hydroxyapatite is the mineralized component of bone.

Type I and II collagen
Type I collagen

Chondroblasts and cytes can divide.
Only osteoprogenitor cells can divide. Osteoblasts and cytes cannot divide.

TRUE

Pinna, auditory tube, vocal cords, epiglottis

Nasal cartilage, thyroid cartilage, tracheal and bronchial cartilage, ARTICULAR CARTILAGE and costal cartilage.
You also find hyaline cartilage in the epiphyseal plates of long bones.

Intervertebral discs, pubic symphysis, muscle insertions and menisci

Because the type II collagen doesn't form fibers, it forms fibrils which make it look glassy. Hyaline means glassy.

Type II collagen

Type II collagen
Integrins of chondroblasts and cytes
Chondroitin sulfate
Hyaluronic acid

2 layers surrounding cartilage. It has a fibrous layer and a chondrogenic layer.

It is dense irregular CT with lots of blood vessels, type I collagen and elastic fibers. The resident cell is a fibroblast.

The chondrogenic layer is where we find chondroblasts which allow for appositional growth of cartilage.

IT HAS NO PERICHONDRIUM
The cells are lined up in rows instead of nests and the only other place that this occurs is the epiphyseal plate.

TYPE III reticular fibers.

1) Begins as mesenchyme with these cells making reticular fibers and hyaluronic acid.
2) Precartilage forms when these cells stop making hyaluronic acid and start making aggrecan. The cells cluster into groups called centers of chondrification.
3) Mesenchymal cells are now chondroblasts which secrete matrix and trap themselves in lacunae. Once this occurs, they are chondrocytes.
4) Chondrocytes divide and form territorial matrix.

Interstitial growth and only happens in young cartilage.

ONLY BY INTERSTITIAL GROWTH because there is no perichondrium

Thyroid, testosterone and GH

Cortisone, hydrocortisone and estradiol

Reduced epiphyseal plate width

Accelerated epiphyseal plate ossification stunting growth

Inhibits matrix formation and deforms the epiphyses

Hypovitaminosis D

TYPE II COLLAGEN, don't say elastic fibers although these are very prevalent.

Fibrillin in the elastic cartilage is one of the most thrombogenic substances in the body.

Fibroblasts of dense regular CT mature into chondrocytes. IT MAY AS WELL BE CALLED DENSE REGULAR CT.

No perichondrium
Chondrocytes are in rows
Type I collagen

The organic component of bone which has type I collagen and ground substance (chondroitin sulfate and osteocalcin)

Chondroitin sulfate and osteocalcin.

It binds Ca2+

Hydroxyapatite is CaPO3 crystals.

Mineral confers rigidity and osteoid confers tensile strength.

Osteoprogenitor
Osteoblasts
Osteoclasts
Osteocytes

In the osteogenic layer of the periosteum and in the endosteum.

They are actually mesenchymal cells of the bone.

Alkaline phosphatase

Bone lining cells and they have flat nuclei.

Osteoblasts

Through canaliculi and gap junctions.

PTH stimulates osteocytes to suck up Ca2+ from the lacunar fluid and transfer it through canaliculi to osteoblasts which dump the Ca2+ into the blood.

Carbonic anhydrase to generate protons from CO2.
Acid phosphatase.
Cathepsin K.

It stimulates them to perform slow Ca2+ exchange which is break down of bone to yield Ca2+

Howship's lacunae.

To increase surface area for bone resorption.

Vitamin D and PTH

Because osteoblasts and osteocytes can't divide.

Osteocytic osteolysis

The haversian system (osteon) is made up of concentric lamellae which are alternating left and right hand helices.
A central blood vessel sits in the haversian canal and these are connected through Volkman's canals.
Canaliculi interconnect osteocytes around the rings.

The osteogenic layer of periosteum produces the outer circumferential lamellae and the endosteum produces the inner circumferential lamellae.

Older haversian systems that have been replaced.

Bone is VERY vascular.

Pieces of dense irregular CT from the fibrous periosteum which dip down into the outer circumferential lamellae.

Articular cartilage
Where tendons and muscles insert
On sesamoid bones

1) Blood vessels, nerves and lympathics in the fibrous layer of periosteum.
2) Volkman's canals
3) Nutrient artery in bone marrow
4) Haversian/central canal

Forming, resting and resorbing.

Matrix formation - Osteoblasts lay down osteoid which contains osteocalcin.
Osteocalcin binds Ca2+ in the area and keeps it there.
Osteoblast secretes alkaline phosphatase which increases [Ca2+] and [PO4] in the area.
Osteoblasts secrete vesicles of Ca2+, PO4 and alkaline phosphatase which crystallizes in the matrix.

There is no cartilage model. Mesenchymal cells develop directly into osteoblasts which start making osteoid.
The osteoid binds Ca2+ and starts to mineralize, forming the primary ossification center.

Begin with hyaline cartilage model with perichondrium surrounding except at articulating surfaces.
Perichondrium becomes vascularized and this stimulates osteoblasts to differentiate.
This causes a periosteal collar to form around the bone diaphysis.
Periosteal bud (blood vessel) invades the middle of hyaline cartilage causing chondrocytes to die.
Osteogenic cells come in with blood and differentiate into osteoblasts which form the primary ossification center.

Bone is added to the outer sides of the periosteal collar and cartilage is removed from inner side.

Only after birth is the hyaline cartilage in the epiphysis replaced

At the articular cartilage region.

~25 yrs of age.

Zone of resting cartilage - between epiphysis and epiphyseal plate.
Zone of proliferation - chondrocytes mitosing for interstitial growth.
Zone of hypertrophy - chondrocytes get huge, deposit matrix and die.
Zone of calcification - calcification of the matrix occurs.
Zone of ossification - osteoblasts ossify the matrix.

Pelvic bones, sternum, vertebrae and skull

Yellow marrow is full of fat and is not hematopoietic

Nutrient artery from periosteum splits into central longitudinal arteries which then split into radial arteries. The radial arteries enter Volkman's canals and then central canals.

Adventitial reticular cells support the thin simple squamous endothelium

Endothelium

Reticular fibers.

FALSE! They are for support. THE NORMAL RETICULAR CELLS MAKE THE RETICULAR FIBERS

There are migration pores in the endothelial cells so the blood cells go right through these pores (through the cells).

Macrophages, reticular cells, fibroblasts and endothelial cells.

Macrophages phagocytose RBC nuclei.
Endothelial cells and fibroblasts make growth factors.
Reticular cells make reticular fibers (NOT ADVENTITIAL RETICULAR CELLS) and store fat in some instances.

RBC's develop in erythroblastic islets close to sinusoids.
Here macrophages can recycle the iron and phagocytose pyknotic nuclei.
Neutrophils develop further away.
Megakaryocytes have to be right next to sinusoid walls to release platelets.

In the mesoderm of the yolk sac. These are nucleated RBC's and it is the mesoblastic stage.

In the liver and spleen, these are still nucleated RBC's

At 6th week the primary ossification center develops and is in full swing by 5 month.

Stem cells
Progenitor cells
Precursor cells

Pleuripotential hematopoietic stem cells of bone marrow which can self-renew or give rise to MHSC (multipotential)

Multipotential hematopoietic stem cell which are either CFU-S (myeloid line) or CFU-Ly (lymphoid line)

CFU-GM, CFU-M, CFU-E, CFU-B.
Progenitor cells are committed to a single cell lineage.

Cell in each lineage displaying unique characteristics.

CFU-E. Although so can BFU-E during severe anemia which is why it is called burst forming unit.

Because the primary azurophillic granules form before the secondary specific granules.

Huge cell
Central nucleus with nucleoli
Basophillic cytoplasm due to ribosomes
NO GRANULES
Can mitose

Very dark blue cytoplasm (RIBOSOMES MAKING HB)
Clumped chromatin and more condensed nucleus.
Can mitose

CHECKERBOARD NUCLEUS
Grey cytoplasm due to accumulation of hemoglobin
LAST CELL THAT CAN DIVIDE

The polychromatophillic erythroblast

Cytoplasm is same as mature erythrocyte (ortho means same).
Nucleus is eccentric dark round circle.
CANNOT DIVIDE

No nucleus
Pink cytoplasm
Special stains pick up RNA as black fibers in cell

Hemoglobin
Glycolytic enzymes
Cytoskeleton
Plasma membrane

Due to RER

The promyelocyte stage

Myelocyte

Neutrophil is iliac
Eosinophil is red-orange
Basophil is blue-purple

Myelocyte

Eccentric, kidney-bean shaped nucleus.
Light blue cytoplasm

60-70%

Lysozyme, acid phosphatase, myeloperoxidase and defensins (antibacterial proteins)

Lactoferrin (binds iron away from bacteria)
Lysozyme

3% (1-4%)

Major basic protein (forms holes in parasite PM)
Histaminase (reduce inflammation)

Neutrophils - bacterial infection.
Eosinophils - parasite or worm infection.
Basophils - allergic reaction.

1%

Both contain IgE receptors on their surface and when this is bound by antigen, both release histamine.

Promonocyte

6% (4-10%)

Largest cell in the blood with azurophillic granules and large eccentric kidney shaped nucleus.

By endomitotic division (64N)

α granules - vWF, PGDF, platelet aggregation factors
δ granules - serotonin and other platelet adhesion factors
λ granules - lysosomes for clot dissolution

α granules are responsible for vessel repair, platelet aggregation and coagulation of blood.

They contain factors that facilitate platelet aggregation, adhesion and stimulate vasoconstriction

Contain hydrolytic enzymes for clot resorption

The platelet demarcation channels

The hyalomere which is the outer light part (microtubules) and the granulomere which is the part containing the 3 types of granules.

Serum is plasma without the coagulation proteins

Heparin
Citrate
EDTA
The latter 2 are Ca2+ chelators

Before birth in the germline cells.

When an antigen binds a specific B cell and stimulates it to tweak it's DNA to bind that antigen specifically

The enzyme γ-glutamyl carboxylase needs Vit. K as a cofactor in order to γ carboxylate factors II, VII, IX and X.

In order for them to interact with Ca2+. Ca2+ binds the negative phospholipids on the endothelial surface (and platelet surface) to the negative γ-carboxyglutamic acid residues on the coagulation factors.
This allows them to interact with each other.

They are on the N-terminus and the carboxylation process forms γ-carboxyglutamic acid residues (Gla)

HMW kininogen, prekallikrein and factor XII all work together to activate XII to XIIa

Mesoderm derived because it is CT without fibers (until clotting occurs)

Made and released by the endothelium

With all the other factors in the liver (except factor III)

They are anticoagulants because they degrade factor V and factor VIII

Once thrombin is formed during coagulation, it stimulates protein C. With the help of thrombomodulin released from the endothelium, protein C is activated 1000 fold. Activated protein C degrades factor V/VIII but also requires protein S as a cofactor to do this.

It is prothrombin before γ-carboxylation by γ-glutamyl carboxylase.

They block epoxide reductase which prevents the conversion of Vit. K epoxide back into the active form of Vit. K.

γ-glutamyl carboxylase requires Vit. K to carboxylate pre-prothrombin. When this happens, Vit. K is converted into Vit. K epoxide (an inactive form). Epoxide reductase converts Vit. K epoxide back into Vit. K.

α2-antiplasmin is an antagonist of plasmin to ensure that the clot isn't broken up too fast.

Stochastic means that progenitor cells randomly decide to form differentiated cells or self renew.
Deterministic means that cytokines and growth factors stimulate the process.

Stem cells can divide to make more of themselves (cells with exactly the same differentiation state)

One daughter cell differentiates, the other self renews.

Cells mature to become more specialized but lose the ability to divide.

1) Colony stimulating factors (GM-CSF, G-CSF, M-CSF, IL-3)
2) Erythropoietin - for RBC's
3) Thrombopoietin - for megakaryocytes.
4) IL-5 and IL-6 - for eosinophillic lineage and lymphoid cells.

Procrit, Epoietin α
Neupogen, Filgrastim
Leukine, Sargramostim

Acute is a lot of blast cells in the peripheral blood.
Chronic is a lot of normal cells and few blast cells.

100-120 days

7 hours in the circulation, 4 days in CT

10 days

V-CAMS and integrins
Collagen, fibronectin and laminin
Growth factors.

They help the cell move from Go into G1 (IL-6, IL-11, IL-12).
OR they keep the cell cycling (GM-CSF, IL-3, IL-4)

Maturation factors like Epo, Tpo, G-CSF, GM-CSF and M-CSF.

Multi-CSF because it stimulates all the cells except RBCs

Neutrophils, eosinophils and macrophages

IL-5

IL-6

Membrane bound proteins with carb side chains, N-acetylneuraminic acid and sialic acid

A bicarb exchanger found in the RBC membrane

It is a side pathway off glycolysis which produces 2,3-DPG during hypoxia

Ferritin

When the cell has a hard time synthesizing DNA such as B12 or folate deficiency (pernicious anemia)

When the ability to synthesize hemoglobin is deficient. W/o Hb, cells continue to divide continuously and get tiny.
This happens with iron deficiency, thalassemias, heavy metal poisoning and anemiochronic disease.

The parietal cells along with HCl.

It binds with B12 in the duodenum preventing proteolytic degradation.

In the terminal ileum with GIF attached by the intrinsic factor-B12 receptor.

Transcobalamin

1) Iron deficiency
2) Thalassemia
3) Chronic diseases (anemiochronic diseases)
4) Porphyrin and heme synthesis defects (lead poisoning and sideroblastic anemias)

When you are unable to form heme so iron deposits in the mitochondria forming cells caused ringed sideroblasts.

Any defect in DNA synthesis of the RBC. Most common one is B12 or folate deficiency.

Acute blood loss
Hemolysis
Bone marrow failure

Increase in RBCs, [hemoglobin] and hct

Absolute is an increase in the number of RBCs
Relative is a decrease in plasma volume thereby leading to polycythemia

Because the macrophages in the spleen are overworked destroying RBCs. This leads to auto-infarction of the spleen and predisposition to infection.

Hydroxyurea or 5-Azacytidine

Mean corpuscular volume (MCV) = hct/RBC count.
MCV tells you the relative size of the RBC (microcytic or macrocytic)

Mean corpuscular hemoglobin (MCH) = [hb]/RBC count and doesn't actually tell you much. MCHC is better test.

90fL

Mean corpuscular hemoglobin concentration (MCHC) = [hb]/hct and it tells you the hemoglobin concentration.
This is useful for hypochromic anemias

30g/dl

85% of people are Rh+ blood

To convert unconjugated (insoluble) bilirubin into lumirubin which is soluble and can be excreted.

Slow bicarb exchange is converting CO2 into HCO3- in the plasma.
Fast bicarb exchange is using carbonic anhydrase in the RBC to convert it.

Neutrophils 60%
Lymphocytes 30%
Monocytes 6%
Eosinophils 3%
Basophils 1%

You are in a neutrophil secondary (specific) granule.

You are in a basophil secondary (specific) granule

You will find eosinophil peroxidase and you are in an eosinophil secondary (specific) granule

1)Adhesion (selectins make granulocyte roll, integrins make them stick and diapedese)
2) Chemotaxis (mast cell released chemotactic agents attract neutrophils)
3) Recognition (bacteria coated with opsonins IgG, IgM, C3 and C3a)
4) Phagocytosis
5) Degranulation (secondary granules fuse with phagosome first, then primary granules)
6) Generation of ROS (O2 respiratory burst)
7) Neutralize spare superoxide (using SOD and catalase)

1) NADPH oxidase uses NADPH to generate superoxide from O2.
2) Superoxide dismutase creates H2O2 from superoxide.
3) Myeloperoxidase adds Cl- to H2O2 and form HOCl (hypochlorite) which destroys bacteria.
4) Glutathione regenerates NADPH for first reaction.

1) Neutrophils show up at pathogen site, phagocytose with O2 burst, release chemoattractants and die. Dead neutrophils, bacteria and myeloperoxidase form green pus.
2) Macrophages show up, also phagocytose and do O2 resp. burst. Also release cytokines (TNF α, IL-1 and IL-12) and eicosanoids (LTB4) which are chemoattractants. Finally, present degraded pathogen antigens on MHC-II surface receptors.

Comes after the innate defense.
3) Macrophages that have destroyed bacteria are presenting antigen on their MHC-II molecules (acting as APCs) in the lymph nodes. Killer T-cells (CD-8+) recognize the MHC-II and destroy the whole macrophage with perforins. They also release more cytokines to recruit B cells. Killer T-cells also recognize MHC-I presented on any non-self cell.
4) B-cells come in contact with pathogen and pump out antibodies.

> 12,000 cells/mm3
Bacterial infection, inflammation, necrosis, metabolic toxins, hemorrhage, splenectomy and stress.

Early infection: Neutrophils diapedese out and leukocyte count drops. Bone marrow reserves drop.
Established infection: Bone marrow ups production to re-establish reserves and increase blood levels.
Recovery: Marrow production decreases and blood levels return to normal
OR Exhaustion: Neutropenia during course of infection, poor sign.

Leukocytes < 4000
Causes: Page 505

F-met-leu-phe

C5a, LTB4, PAF and IL-8

The NBT test turns from blue to black in the presence of superoxide.
It is used to test for NADPH oxidase deficiency (chronic granulomatous disease)

Defect in the NADPH oxidase enzyme preventing the formation of superoxide. Defective respiratory burst reaction.

Neutrophils take out bacteria and NK (T) cells take our virally infected cells.

Motor neurons of ventral horn and autonomic ganglia
Retina, vestibular, cochlea ganglia and olfactory epithelium.
DRG

Neural crest

The dendrites and axon hillock

Dyneins moving vesicles retrograde, Kinesins moving vesicles and organelles anterograde.

Axoplasm, axolemma, periaxonal space, myelin sheath, schwann sheath (neurilemma), external lamina and endoneurium.

Schwann cells

Po is found in the intraperiod lines of the peripheral myelin sheath. The intraperiod lines are E surfaces together.

You are in the major dense lines of a peripheral myelin sheath which is the P surfaces glued together.

Synapsin
Synaptophysin binds it to the active zone and synaptotagmin allows release.

It is activated by Ca rushing into the synaptic bouton and it phosphorylates both synapsin and synaptophysin allow nt to dock with synaptotagmin.

It is MBP and Po artifact, NOT NEUROFILAMENTS

Type A - GSA and GSE

Type B - GVA and pre GVE

Type C - GSA and post GVE

Endoneurium - Loose CT with reticular fibers and capillaries.
Perineurium - DICT with perineurial cells (tight junctions and basal lamina).
Epineurium - DICT

Merkel cells located in the dermis, response to touch
Peritrichial hair cells which wrap around hair follicle.
They are free because they have no myelin, no CT and no Schwann cells

Meissner's corpuscle (touch)
Pacinian corpuscle (pressure)
Muscle spindles
Golgi Tendon Organs

Glutamate

Very vascular
Avascular

Outer layer is dense irregular CT. It is tight on bone so is basically periosteum. The inner layer is fibrous tissue forming the reflections.

Dura is mesoderm
Arachnoid and pia are neural crest.

Arachnoid avascular
Pia vascular

Fibrous astrocyte - found in white matter
Protoplasmic astrocyte - In grey matter and have the feet.

Schwann cells and astrocytes

Very vascular
Avascular

Very vascular
Avascular

Microglia are derived from monocytes which are from mesoderm

Internal glial limiting membrane is astrocytic feet against base of ependymal cells. External is astrocytic feet against pia.

Outer layer is dense irregular CT. It is tight on bone so is basically periosteum. The inner layer is fibrous tissue forming the reflections.

Outer layer is dense irregular CT. It is tight on bone so is basically periosteum. The inner layer is fibrous tissue forming the reflections.

Dura is mesoderm
Arachnoid and pia are neural crest.

Striated border microvilli with cilia.
Attached to each other by tight junctions

Dura is mesoderm
Arachnoid and pia are neural crest.

Arachnoid avascular
Pia vascular

Fibrous astrocyte - found in white matter
Protoplasmic astrocyte - In grey matter and have the feet.

Arachnoid avascular
Pia vascular

Glomerulus
Choroidal cells
Choriocapillaris

Schwann cells and astrocytes

Fibrous astrocyte - found in white matter
Protoplasmic astrocyte - In grey matter and have the feet.

Tight junctions between capillary endothelial cells. This is weird because endothelial cells usually have fascia occludens.

Microglia are derived from monocytes which are from mesoderm

1) CNS myelin has an external lamina surrounding.
2) Axons are so close they share intraperiod lines.
3) Oligo's myelinate multiple neurons.
4) No endoneurium
5) No neurilemma (most important)
6) Proteolipid protein (PLP) is found in intraperiod line instead of Po.

Schwann cells and astrocytes

Internal glial limiting membrane is astrocytic feet against base of ependymal cells. External is astrocytic feet against pia.

Microglia are derived from monocytes which are from mesoderm

Striated border microvilli with cilia.
Attached to each other by tight junctions

Nepi to everywhere except sweat glands of body. Remember: sweat glands of hands and feet are Nepi

Internal glial limiting membrane is astrocytic feet against base of ependymal cells. External is astrocytic feet against pia.

Glomerulus
Choroidal cells
Choriocapillaris

Striated border microvilli with cilia.
Attached to each other by tight junctions

Found in PS and S post cell bodies, sk.muscle end plate and adrenal medulla.
Blocked by hexamethonium (not at NMJ)

Glomerulus
Choroidal cells
Choriocapillaris

All PS end organs and sweat glands of body for S.
Blocked by atropine.

Tight junctions between capillary endothelial cells. This is weird because endothelial cells usually have fascia occludens.

1) CNS myelin has an external lamina surrounding.
2) Axons are so close they share intraperiod lines.
3) Oligo's myelinate multiple neurons.
4) No endoneurium
5) No neurilemma (most important)
6) Proteolipid protein (PLP) is found in intraperiod line instead of Po.

Tight junctions between capillary endothelial cells. This is weird because endothelial cells usually have fascia occludens.

Nepi to everywhere except sweat glands of body. Remember: sweat glands of hands and feet are Nepi

Very vascular
Avascular

Very vascular
Avascular

Found in PS and S post cell bodies, sk.muscle end plate and adrenal medulla.
Blocked by hexamethonium (not at NMJ)

All PS end organs and sweat glands of body for S.
Blocked by atropine.

Outer layer is dense irregular CT. It is tight on bone so is basically periosteum. The inner layer is fibrous tissue forming the reflections.

Outer layer is dense irregular CT. It is tight on bone so is basically periosteum. The inner layer is fibrous tissue forming the reflections.

1) CNS myelin has an external lamina surrounding.
2) Axons are so close they share intraperiod lines.
3) Oligo's myelinate multiple neurons.
4) No endoneurium
5) No neurilemma (most important)
6) Proteolipid protein (PLP) is found in intraperiod line instead of Po.

Dura is mesoderm
Arachnoid and pia are neural crest.

Dura is mesoderm
Arachnoid and pia are neural crest.

Arachnoid avascular
Pia vascular

Arachnoid avascular
Pia vascular

Nepi to everywhere except sweat glands of body. Remember: sweat glands of hands and feet are Nepi

Fibrous astrocyte - found in white matter
Protoplasmic astrocyte - In grey matter and have the feet.

Found in PS and S post cell bodies, sk.muscle end plate and adrenal medulla.
Blocked by hexamethonium (not at NMJ)

Schwann cells and astrocytes

All PS end organs and sweat glands of body for S.
Blocked by atropine.

Microglia are derived from monocytes which are from mesoderm

Fibrous astrocyte - found in white matter
Protoplasmic astrocyte - In grey matter and have the feet.

Internal glial limiting membrane is astrocytic feet against base of ependymal cells. External is astrocytic feet against pia.

Striated border microvilli with cilia.
Attached to each other by tight junctions

Schwann cells and astrocytes

Microglia are derived from monocytes which are from mesoderm

Glomerulus
Choroidal cells
Choriocapillaris

Internal glial limiting membrane is astrocytic feet against base of ependymal cells. External is astrocytic feet against pia.

Tight junctions between capillary endothelial cells. This is weird because endothelial cells usually have fascia occludens.

Striated border microvilli with cilia.
Attached to each other by tight junctions

Glomerulus
Choroidal cells
Choriocapillaris

1) CNS myelin has an external lamina surrounding.
2) Axons are so close they share intraperiod lines.
3) Oligo's myelinate multiple neurons.
4) No endoneurium
5) No neurilemma (most important)
6) Proteolipid protein (PLP) is found in intraperiod line instead of Po.

Nepi to everywhere except sweat glands of body. Remember: sweat glands of hands and feet are Nepi

Tight junctions between capillary endothelial cells. This is weird because endothelial cells usually have fascia occludens.

Found in PS and S post cell bodies, sk.muscle end plate and adrenal medulla.
Blocked by hexamethonium (not at NMJ)

1) CNS myelin has an external lamina surrounding.
2) Axons are so close they share intraperiod lines.
3) Oligo's myelinate multiple neurons.
4) No endoneurium
5) No neurilemma (most important)
6) Proteolipid protein (PLP) is found in intraperiod line instead of Po.

All PS end organs and sweat glands of body for S.
Blocked by atropine.

Nepi to everywhere except sweat glands of body. Remember: sweat glands of hands and feet are Nepi

Found in PS and S post cell bodies, sk.muscle end plate and adrenal medulla.
Blocked by hexamethonium (not at NMJ)

All PS end organs and sweat glands of body for S.
Blocked by atropine.

Gi which inhibits adenylate cyclase in heart causing hyperpolarization and decrease HR.

Gq which increases IP3 through PLC and thereby increases Ca2+

alpha 1 and beta 1

alpha 2 and beta 2

Thermogenesis

alpha's
beta's

Most blood vessels
Radial muscle of eye
Stomach and bladder sphincters
Salivary glands
Sweat glands on palms and soles.

Pancreatic beta cells
Pancreatic acinar cells
Blood platelets
Presynaptic membrane

Cardiac muscle cells
JG cells of kidney
Posterior pituitary
Adipocytes

Airways.
Coronary, sk.muscle, adipose tissue and liver blood vessels.
Ciliary muscle of eye.
Hepatocytes of liver.

Agonists: Nepi and phenylephrine
Antagonists: Phenoxybenzamine, phentolamine, prazosin

Clonidine
Yohimbine

Agonists: Nepi, Isoproterenol, Dobutamine.
Antagonists: Propranolol and metoprolol

Agonist: Isoproterenol, Albuterol
Antagonist: Butoxamine, Propranolol

Agonist: Carbachol
Antagonist: Curare, Hexamethonium

Agonist: Carbachol
Antagonist: Atropine

Ach: small clear vesicles
Nepi: small dense vesicles
Neuropeptide Y and VIP: Large dense core vesicles.

Conversion of GTP into cGMP which activates protein kinase G (cGMP dependent protein kinase)

1) It phosphorylates K channels activating them, allowing hyperpolarization of the smooth muscle cell.
2) It prevents Ca2+ channels from opening.
3) It inhibits IP3 activated Ca2+ channels.
4) It activates myosin light chain phosphatase by phosphorylating it.

Nitric oxide

Certain cells use nitric oxide synthase and convert Arg into Citrulline and NO.

Reacts with tissue thiols to generate s-nitrosothiols which liberate NO.

Inflammation causes release of bradykinin, prostaglandins, serotonin and substance P.
Prostaglandins in particular bind to 7-transmembrane G-protein coupled receptor. This causes phosphorylation of a Na channel in the DRG resulting in activation.
In the CNS, the prostaglandins cause phosphorylation of non-selective cation channels and inhibit glycinergic activity.

Phospholipase A2 creates arachidonic acid from DAG. The arachidonic acid is converted into PGH2 by COX enzymes.

Corticosteroids and cortisol block PLA2.
NSAIDS block Cox.
Aspirin is an irreversible blocker of COX1/COX2
Ibuprofen is a reversible blocker of both.
Vioxx is a selective COX2 blocker.

Because it adds a serine group to the enzyme.

Kd is the [] of drug required to bind half the receptors
Bmax is the total number of receptors.

Epilepsy is attributed to inability to control ECF K.
Serum K is 1.6X higher than CSF K so bleeding also causes hyperkalemia.

The K channel

Na/K channels

TEA, 4-amino-pyridine and dendrotoxin

Phenytoin is a Na channel blocker used to prevent overexcitability.

It opens special K channels to hyperpolarize neurons.

Place electrodes over muscle and tell patient to move. Measure electrical activity in the muscle.

Stimulating a peripheral nerve and measuring the activity in the cortex.

Electroencephalogram which is constant measurements of overall brain activity during sleep or coma.

Asking a patient to perform a task while you measure activity in the cortex.

Stratified columnar with goblet cells

Modified sebaceous glands in eyelid

Modified sebaceous glands in eyelid

Apocrine sweat glands in the eyelid

Begins in lacrimal gland then to lacrimal duct and medially across eye to lacrimal puncta. The puncta drain into the lacrimal sac which drains through the nasolacrimal duct into the inferior meatus of the nose.

DICT with Type I collagen
AVASCULAR, the blood vessels seen here are in the conjunctiva

It is avascular but does contain nerves.

Spaces of Fontana which drain aqueous humor into the canal of Schlemm

1) Anterior epithelium - stratified squamous non-keratinized.
2) Bowman's membrane - basal lamina of anterior epithelium.
3) Substantia propria - DICT with type I collagen fibers
4) Descemet's membrane - Thick basement membrane of posterior epithelium
5) Posterior epithelium - simple squamous with tight junctions.

The anterior epithelium

Na/K pumps in the posterior epithelium and tight junctions as well.

Highly vascular pigmented layer of loose CT and melanocytes

Choriocapillaries which are fenestrated capillaries.

Basal lamina of choriocapillaries
Type III collagen
Elastic fibers
Type III collagen
Basal lamina of pigmented cells of retina.

It is an extension of the choroid.
It is a 2 layered epithelium with the inner layer being non-pigmented and the outer layer being pigmented

It is non-pigmented and it secretes aqueous humor

Tight junctions of the inner epithelial layer of the ciliary body.

Fibrillin

It is a continuation of the choroid. It is loose CT with NO ANTERIOR EPITHELIUM. The posterior epithelium is a double pigmented layer of cells continuing on from the ciliary body.

Activate the a1 receptor on the myoepithelial cells of the dilator pupillae thereby opening up the pupil

Activate the muscarinic receptor on the muscle which encircles the pupil

An avascular epithelium with no CT. (good for transplant)

Crystallins which increase refractive power

Hyaluronic acid
No, you are born with vitreous
It is avascular

Cones

The tight junctions btw the pigment epithelium of the retina

In the apical microvilli

Phagocytose shed tips of rods and cones.
Synthesize melanin.
Esterify Vit. A and transport it to rods and cones.

There is an inner segment where the rhodopsin is made and an outer segment that contains the membranous disks.

Activated opsin transfers GTP to G-protein transducin which activates cGMP phosphodiesterase. Decreases in cGMP closes Na channels which hyperpolarizes the cell.

It is the outer limiting membrane which is tight junctions between Muller cells and photoreceptors

The outer nuclear layer is the nuclei of the rods and cones.

It is the outer plexiform layer which is synapses between photoreceptors and bipolar cells.

Inner nuclear layer which is nuclei of bipolar cells, horizontal cells, Muller cells and amacrine cells.

Inner plexiform layer which is synapses between bipolar cells and ganglion cells.

Ganglion cell layer and it is what it says. You do not find this layer in the fovea.

Optic nerve fiber layer which is unmyelinated fibers of ganglion cells.

Inner limiting membrane and it is basement membrane of the Muller cells

They are the same except perilymph has no protein

The endolymphatic duct which drains into the endolymphatic sac in the cranial cavity

A kinocilium which is a modified cilium and stereocilia which are microvilli.

The macula are found in the utricle and saccule and have an otolithic membrane with otoliths on top.
The function is static equilibrium and linear acceleration.

Depolarizes the neuroepithelial cells. Bending away hyperpolarizes them.

In the ampulla of the semicircular ducts.
Function: Rotational (dynamic) motion and angular acceleration.

Glutamate

The ductus reuniens

It is a pseudostratified epithelium that is VASCULAR. This is abnormal and this is the site of endolymph production.

Ligament is compact bone opposite tectorial membrane. Limbus is screw shelf on same side.

The hair cells of the cochlea do not have a kinocilium, just have a taller stereocilium.

Bending stereocilia towards the taller one, leads to opening of K channels and influx of K from the high endolymph [K]. This causes depolarization which leads to the release of glutamate which activates the axon of the bipolar cells.

It is tight junctions btw the phalangeal processes of the outer phalangeal cells and the apex of the outer hair cells.

Low freq heard at apex, high freq heard at base

The myotubes which developed from fusion of myoblasts.

It is the dilation of 2 SR's on either side of the T-tubule.
It is characteristic of sk. muscle and calsequestrin is found in the dilated ends.

α-actinin which binds thin filaments to Z line with help of nebulin.

Cap Z caps the plus end of actin in the Z disc.
Tropomodulin caps the negative end at the A-I junction.

Myomesin

No, only hypertrophy. Satellite cells can divide and add to the muscle fibers but cannot synthesize more myofibrils.

They are the organelles.

Fascia adherens and desmosome at the perpendicular portions. The tonofilaments that insert into the desmosome are desmin and vimentin.
Gap junctions at the parallel portions.

Excrete Na and H2O
Prevent renin release
Decrease BP

Endomysium with capillaries

It is a protein that controls the SR Ca pump in cardiac muscle. Thyroid hormone can change phospholamban activity.

NO, only hypertrophy and scar tissue after damage.

Vas deferens, arrector pili, iris muscles, large arteries and lung airways.

External lamina and type III collagen (reticular fibers)

No troponin
No T-tubules (caveolae)
SR doesn't store Ca2+
Z-discs are actually round and form dense bodies.
Ca-Calmodulin needed for contraction.
Thick filaments regulate the contraction by being phosphorylated.

Nerve impulses in vascular smooth muscle.
Stretching in visceral smooth muscle.
Oxytocin in uterine smooth muscle.
Epinephrine in other places.

A fibroblast that can contract and is prominent during wound healing.

1) The kinetics of the delayed rectifier K channel are slower
2) T-tubules trap ECF K which prevents outward flux of K.

SR is connected to T-tubules by a link between calcium release channels and dihydropyridine receptor.
Depolarize the T-tubule and the conformation of the dihydropyridine receptor changes opening the CRC.

You have to get rid of all Ca2+. Use Na/Ca exchanger (predominant) and Ca pump.
Digitalis blocks the Na/K pump which leaves Na high in cell thereby inhibiting Na/Ca exchanger.

Endothelial nuclei run with blood flow. Smooth muscle nuclei are perpendicular.

vWF
They secrete basal lamina and endothelin 1 which is a vasoconstrictor

It is secreted by endothelial cells and it is arranged as a sheet not as fibers.

Smooth muscle walls
Sympathetic innervation

cardiac muscle

Make type I and type III collagen as well as elastin. However, the elastin here is in fibers not sheets.

Chondroitin sulfate
Dermatan sulfate

It is an endothelium with subendothelial layer.
In the heart, it is endocardium and in capillaries it is just endothelium.
It has an internal elastic lamina which is type I, type III and elastin.

Myocardium

Tunica media is thicker in arteries, tunica adventitia is thicker in veins.

Epicardium and really isn't an adventitia but a serosa.

Type I and elastic fibers.

In the tunica adventitia of large arteries and veins.

Also called conducting arteries
Very thick tunica intima and media. Media has a lot of elastin in it.
Locations: All branches off aorta.
Possess vasa vasorum.
Function: Secondary pump and pressure reservoir.

Also called distributing arteries.
1 place where internal elastic laminae is VERY THICK.
Thick tunica media with more muscle than elastin and is equal to adventitia.
Locations: All the named arteries of the body.

2nd site of thick internal elastic laminae.
Function: Regulates peripheral resistance and is site of greatest pressure drop.
Site of vasoconstriction through α1.

1) Thicker in lower extremity arteries
2) Thicker in coronary arteries
3) Thin in pulmonary arteries
4) Smooth muscle cells are longitudinal in joint capillaries
5) Composed of cardiac muscle in roots of great vessels.

Active transcytosis
Pericytes are common
Continuous basal lamina.

Loaded with pores bridged by diaphragms
No pericytes
Continuous basal lamina
Locations: Choroid plexus, choriocapillaries, glomeruli of kidney, pancreas, endocrine glands, intestinal mucosa.

Pores w/o diaphragms
Gaps btw endothelial cells
Discontinuous basal lamina
Locations: Anterior pituitary and adrenal cortex

Deactivate bradykinin and serotonin
Breakdown lipoproteins
Release prostacyclins
Convert Ang I into Ang II

Also called capacitance vessels
Contain 60% of blood volume (reservoir)
Very thick adventitia and no obvious demarcation between layers.

Pericytes in the walls
Run by themselves
Main site of diapedesis (therefore no smooth muscle wall)
Sensitive to temp change, inflammation and allergic reactions

Muscular venules

Cardiac skeleton is DICT
Valves are fibrous CT lined by endothelium.

Phase 4 - Inward rectifying K channel opens at hyperpolarized potentials.
Phase 0 - Fast Na channel
Phase 1 - IR K channel closes, transient opening K channel opens.
Phase 2 - L-type Ca channels open (Delayed rectifying K channels open but slowly)
Phase 3 - Delayed rectifier K channel opens all the way.

Tetrodotoxin

K permeability is much higher at rest (phase 4) than phase 2

Only 3 phases
Phase 4 (unstable) - Na and Ca channels open.
Phase 0 - Ca channels depolarize (MUST KNOW).
Phase 3 - Same delayed rectifier K channel.

Nepi/sympathetics increase Ca and Na conductance thereby speeding up HR.
Ach opens K channels to hyperpolarize phase 4.
Ca channel blockers slow HR by slowing phase 4.

Preload

The length-tension relationship

a wave represents atrial systole causing increased pressure.
c wave represents atrial pressure increase due to blood forcing out of ventricle.
v wave represents atria filling up during ventricular systole.

Stroke volume x afterload

Increased HR prevents the full relaxation of ventricles due to residual Ca2+ which increases contractility.

1) Myogenic control - Minor control. If you stretch the bv, then it reacts and contracts.
2) Metabolic regulation - Major control. Accumulation of metabolic byproducts results in vasodilation to restore perfusion.
3) Endothelium releases factors (nitric oxide) to control diameter.

Heart, brain and kidney is intrinsic control.
Sk. muscle is extrinsic control during rest.

Primary epidermal ridges.

1) Has unipotential stem cells.
2) These stem cells only divide at night and only give rise to keratinocytes. This is stimulated by EGF from dermis.
3) Attached to basal lamina by hemidesmosomes and desmosomes.
4) Only layer with hemidesmosomes.
5) Have keratin IF's as tonofilaments.
6) Contain melanocytes and merkel cells.

1) 8-10 layers of keratinocytes attached by desmosomes.
2) Contain Langerhans cells.
3) Lots of keratin tonofilaments.
4) Keratinocytes contain membrane-coating granules and lamellar bodies.

1) Has keratohyalin granules (fillagrin) which give it it's name.
2) The membrane-coating granules are released in this layer.
3) Apoptosis begins forming stratum corneum.

Contain and release fillagrin which bundles tonofilaments and deposits on P surface of cell PM forming waterproof barrier.

Involucrin, fillagrin, tonofilaments and glycolipid from lamellar bodies.

In the stratum corneum

Autoantibody against desmocolin/desmoglein of skin desmosomes. Skin blisters as fluid leaks into the stratum corneum.

Found in stratum basale and are from neural crest.

They are melanocytes and they are like this because they are attached to basal lamina with hemidesmosome but not to other cells with desmosomes.

In the keratinocytes of the stratum spinosum released by melanocytes from stratum basale.

Mesoderm - Monocyte precursor system.

Langerhans cells with no cell junctions.

In langerhans cells of the stratum spinosum.

In the stratum basale

Neural crest

Thick skin - Eccrine sweat glands
Thin skin - Hair follices, sebaceous glands and sweat glands.
No stratum lucidum in thin skin, thinner spinosum and thinner corneum.

Epidermis is from ectoderm.
Dermis is from mesoderm.

Loose CT
Continuous capillary loops
Meissner's corpuscles

DICT with type I collagen, elastic and reticular fibers.
Contains Pacinian corpuscle

1) Subpapillary plexus - most important, runs parallel to papillary layer and gives off capillary loops into papillae. Has an excess of venules and uses these for thermal regulation.
2) Subcutaneous plexus - in hypodermis
3) Cutaneous plexus - between papillary and reticular layers.

Eumelanin - imparts black and brown color.
Pheomelanin - imparts red color.
Oxyhemoglobin
Carotenes - in fat, give yellow color.

Eccrine sweat gland

Aldosterone to decrease NaCl secretion.

Axilla, hands and feet.

Axilla, areola, perianal region, eyelids and ear.

Androgens

No, only thin

Onto the hair follicle

Face, forehead, scalp

Through hormones like androgens not through ANS.

Internal root sheath, cortex and medulla of hair.

It is where the arrector pili muscles insert. It has stem cells which regenerate the epidermis, hair shaft and sebaceous glands. Some of the cells also migrate down and replace the matrix stem cells.

The outer root sheath