Biochemistry
Today in Biochemistry, we began to look into lipid metabolism. Lipid metabolism is centrally based around the molecule acetyl-CoA, which can be converted to fatty acids, cholesterol, HMG-CoA, through this pathway.
You see two types of fatty acids: saturated and unsaturated. Saturated fatty acids are long alkyl chains of monocarboxylic acids with an even-number of carbons. Unsaturated fatty acids differ in that they contain C=C double bonds. This results in different melting points; saturated fatty acids are straight chains, meaning they have more surface area and are less likely to be able to flow. Unsaturated fatty acids have kinks in the molecule, and thus have less surface area and more ability to flow. As unsaturation increases, melting point decreases, and as chain length increases, melting point increases.
Two important polyunsaturated fatty acids are linoleic acid and linolenic acid. They are commonly known as omega-3 and omega-6 fatty acids, respectively.
Fatty acids are formed by a number of reactions. The first one to note is the De Novo synthesis. It uses an enzyme with two binding sites: one is an acyl carrier protein, which uses pantothenic acid (found in coenzyme A) to attach fatty acids, and the other is a cysteine residue. The ACP begins by binding malonyl-Coa (an acetyl-CoA with a carboxyl group). The cysteine residue binds an acetyl-CoA. The acetyl is then removed from the cysteine and hooks onto the end of the malonyl-CoA, through the enzyme ketoacyl synthase. This reaction removes the carboxyl group in the form of carbon dioxide. At this point, the cysteine is empty, and the pantothenic acid have a four-carbon chain. The ketone group on the pantothenic acid is then reduced, which uses one NADPH (this is why the hexose monophosphate shunt is so important!). The enzyme hydratase then produces water by removing an OH group and another hydrogen, forming a trans C=C (unsautrated!). The four-carbon molecule is then saturated through the use of another NADPH in a reduction reaction. Extra carbon is then added by transferring the four-carbon molecule to a cysteine residue, addding another malonyl-CoA to the pantothenic acid, and finally transferring the four-carbon molecule onto the malonyl-CoA, releasing another carbon dioxide.
Tuesday, November 2, 2010
#27 What I Learned Today
Introduction to Operative Dentistry
Today in sim lab we performed amalgam restorations on teeth #5, #12, and #14. The type of amalgam that we used for the restoration was Tytin FC (firm condensation) 600 mg, which has modified spherical particles. The alloy material percentage breakdown is:
The amalgam is first brought to the preparation by an amalgam carrier and condensed. Small increments seem to work best, as spillage can occur if you use excess. Start with a small condenser to make sure the pulpal line angles are well condensed and increase in size from there. Remember to also move quickly.
Once the preparation is slightly overfilled, you begin to carve. You can use a number of different hand instruments; personally, I started with a lateral condenser (can be roughly described as christmas tree-shaped) and then used a cleiod side of the cleiod-discoid instrument to clean up the margins. At this time, you make sure to incorporate any occlusal anatomy into the carving as you are trying to replace the initial lost tooth structure. Also of important note, you want to always have part of the carving instrument lying on healthy tooth structure while you are working; this helps simulate proper tooth structure shape.
Towards the end, you can use a ball burnisher to run it along the surface. Another useful tip is to take wet cotton and rub it along the surface of the restoration; it helps give a nice smooth finish. Once you are done carving, you should check the occlusion by having a patient bite down and side-to-side on articulating paper. This will also you to check the contact points and ensure they are restored. If not, modification to the restoration might be necessary. One final go-over of the restoration should be done with a lateral condenser, to ensure a good finish after occlusion is checked.
Also note: In a real patient, dentin sealer should be added to block the dentin tubules and help close up the microscopic space that is found between tooth structure and amalgam (recall: amalgam doesn't bond to tooth!). This should last until the amalgam restoration corrodes from being in the oral environment; the corrosion products help form a better seal. It also helps with post-op sensitivity and discolouration.
Today in sim lab we performed amalgam restorations on teeth #5, #12, and #14. The type of amalgam that we used for the restoration was Tytin FC (firm condensation) 600 mg, which has modified spherical particles. The alloy material percentage breakdown is:
- 61% Ag
- 26% Sn
- 13% Cu
The amalgam is first brought to the preparation by an amalgam carrier and condensed. Small increments seem to work best, as spillage can occur if you use excess. Start with a small condenser to make sure the pulpal line angles are well condensed and increase in size from there. Remember to also move quickly.
Once the preparation is slightly overfilled, you begin to carve. You can use a number of different hand instruments; personally, I started with a lateral condenser (can be roughly described as christmas tree-shaped) and then used a cleiod side of the cleiod-discoid instrument to clean up the margins. At this time, you make sure to incorporate any occlusal anatomy into the carving as you are trying to replace the initial lost tooth structure. Also of important note, you want to always have part of the carving instrument lying on healthy tooth structure while you are working; this helps simulate proper tooth structure shape.
Towards the end, you can use a ball burnisher to run it along the surface. Another useful tip is to take wet cotton and rub it along the surface of the restoration; it helps give a nice smooth finish. Once you are done carving, you should check the occlusion by having a patient bite down and side-to-side on articulating paper. This will also you to check the contact points and ensure they are restored. If not, modification to the restoration might be necessary. One final go-over of the restoration should be done with a lateral condenser, to ensure a good finish after occlusion is checked.
Also note: In a real patient, dentin sealer should be added to block the dentin tubules and help close up the microscopic space that is found between tooth structure and amalgam (recall: amalgam doesn't bond to tooth!). This should last until the amalgam restoration corrodes from being in the oral environment; the corrosion products help form a better seal. It also helps with post-op sensitivity and discolouration.
#26 What I Learned Today
Essentials of Clinical Practice
Today's lecture in ECP focused on how important it is for a dentist to take an accurate and complete medical history. A health assessment begins with a complete history taking of the patient, including:
Finally, we began to look at different medical conditions and how they affect the oral cavity and how you would treat them. An example is dry mouth. It is often a side effect of taking specific medications. Consequently, you often see higher rates of decay as saliva helps remove the oral bacteria and remineralize enamel. Another example is cancer. IV Bisphosphonates are used to treat a number of common cancers, and have been shown to cause jaw bone necrosis in some patients.
Patients often come in with allergies. It's important to probe the specifics of the allergy, such as how the patient feels upon reaction, what happens (rash, swelling). It is important to determine if analphylaxis is a symptom of the allergy. Also, you also have to be aware of latex allergies in a dental office, since there are many latex-based products used including gloves and rubber dams.
Hypertension and its medications can also have side effects which are relevant in a dental setting. Orthostatic hypotension is one, which is low blood pressure occuring when the patient sits up. This can lead to dizziness or a fainting spell, which could cause the patient to fall and injure him or herself. You also tend to see dry mouth, angiodema of the facial region (swelling of the dermis and underlying structures), taste alteration and gingival enlargement.
Fainting situations can also occur to patients who have diabetes, and have a hypoglycemic episode. It is important for a diabetic patient to use a glucometer to take a reading of sugar level before treatment. If the reading is less than 70 mg/dl, then action should be taken.
Finally, asthma can be a factor in a dental office. It is important to probe the patient to determine information such as the severity of attacks, duration, when the last attack was, how they dealt with it (stayed at home, or hospital), what triggers it (odours in dental setting, and stres from appointment often can be a trigger). If the patient does have frequent attack, than an inhaler should be kept close and at the ready.
This is followed up by a physical examination, diagnosis, and finally an assessment of the benefits and risk of performing the treatment in mind.
General and Oral Histology
For histo, we discussed cementum, root and pulp structures of teeth. Cementum is found on the outer surface of the radicular part of a tooth, and is continuous with the periodontal ligament (PDL). It is anchored in the alveolar bone by Sharpey's fibers (type 1 collagen) which span the cementum and PDL. Pre-cementum is secreted by cementoblasts, and is slowly formed throughout life. The pre-cementum is mineralized by the cementoblasts, until its contents are about 50% hydroxyapatite crystals. Over time, cementoblasts may become mineralized in cementum and are called cementocytes. They help by diffusing nutrients from the vascularized PDL to the non-vascularized cementum.
There are a number of different kinds of cementum. Two of them include acellular extrinsic fiber cementum (AEFC) which contains no cementocytes, but has Sharpey's fibers from the PDL. Its function is to anchor the root to the PDL, and is often found in the cervical third of the root. Cellular intrinsic fiber cementum (CIFC) contains cementocytes and is important in repairing resporptive defects in the roots of teeth. Mixed stratified epithelium of both AEFC and CIFC are important in reshaping the tooth surface in order to compensate for drift and shifting of teeth in the alveolar sockets.
Some clinical problems that arise in the cementum include hypercementosis, where you get excessive deposition of cementum on the root surface. This can interfere with tooth extractions. Also, you may see concresence where the roots of two adjacent teeth are joined by cementum. This is often due to sufficient space during tooth development.
I'll finish up with roots and pulp later.
Today's lecture in ECP focused on how important it is for a dentist to take an accurate and complete medical history. A health assessment begins with a complete history taking of the patient, including:
- biographic/demographic/social/family history
- medical history (and current status)
- dental history (and current status)
- medication history
Finally, we began to look at different medical conditions and how they affect the oral cavity and how you would treat them. An example is dry mouth. It is often a side effect of taking specific medications. Consequently, you often see higher rates of decay as saliva helps remove the oral bacteria and remineralize enamel. Another example is cancer. IV Bisphosphonates are used to treat a number of common cancers, and have been shown to cause jaw bone necrosis in some patients.
Patients often come in with allergies. It's important to probe the specifics of the allergy, such as how the patient feels upon reaction, what happens (rash, swelling). It is important to determine if analphylaxis is a symptom of the allergy. Also, you also have to be aware of latex allergies in a dental office, since there are many latex-based products used including gloves and rubber dams.
Hypertension and its medications can also have side effects which are relevant in a dental setting. Orthostatic hypotension is one, which is low blood pressure occuring when the patient sits up. This can lead to dizziness or a fainting spell, which could cause the patient to fall and injure him or herself. You also tend to see dry mouth, angiodema of the facial region (swelling of the dermis and underlying structures), taste alteration and gingival enlargement.
Fainting situations can also occur to patients who have diabetes, and have a hypoglycemic episode. It is important for a diabetic patient to use a glucometer to take a reading of sugar level before treatment. If the reading is less than 70 mg/dl, then action should be taken.
Finally, asthma can be a factor in a dental office. It is important to probe the patient to determine information such as the severity of attacks, duration, when the last attack was, how they dealt with it (stayed at home, or hospital), what triggers it (odours in dental setting, and stres from appointment often can be a trigger). If the patient does have frequent attack, than an inhaler should be kept close and at the ready.
This is followed up by a physical examination, diagnosis, and finally an assessment of the benefits and risk of performing the treatment in mind.
General and Oral Histology
For histo, we discussed cementum, root and pulp structures of teeth. Cementum is found on the outer surface of the radicular part of a tooth, and is continuous with the periodontal ligament (PDL). It is anchored in the alveolar bone by Sharpey's fibers (type 1 collagen) which span the cementum and PDL. Pre-cementum is secreted by cementoblasts, and is slowly formed throughout life. The pre-cementum is mineralized by the cementoblasts, until its contents are about 50% hydroxyapatite crystals. Over time, cementoblasts may become mineralized in cementum and are called cementocytes. They help by diffusing nutrients from the vascularized PDL to the non-vascularized cementum.
There are a number of different kinds of cementum. Two of them include acellular extrinsic fiber cementum (AEFC) which contains no cementocytes, but has Sharpey's fibers from the PDL. Its function is to anchor the root to the PDL, and is often found in the cervical third of the root. Cellular intrinsic fiber cementum (CIFC) contains cementocytes and is important in repairing resporptive defects in the roots of teeth. Mixed stratified epithelium of both AEFC and CIFC are important in reshaping the tooth surface in order to compensate for drift and shifting of teeth in the alveolar sockets.
Some clinical problems that arise in the cementum include hypercementosis, where you get excessive deposition of cementum on the root surface. This can interfere with tooth extractions. Also, you may see concresence where the roots of two adjacent teeth are joined by cementum. This is often due to sufficient space during tooth development.
I'll finish up with roots and pulp later.
#25 What I Learned Today
Professionalism and Ethics
We broke into groups today and worked at putting together a code of ethics that we wanted our class to follow. It was pretty open-ended, ranging from things like specific do's-and-do-not's, to personal characteristics to follow.
When the code is put together and made available on-line, I'll be sure to post it here.
Biochemistry
We continued our look at energy metabolism by moving from the Kreb's cycle to oxidative phosphorylation and the electron transport chain. In summary, this step takes the hydrogen transporters, releases their hydrogens via oxidative phosphorylation. This sets up a hydrogen gradient, which the enzyme ATP synthase uses to produce ATP molecules.
The first step is to get NADH produced outside the mitochondria by glycolysis into the cell so that it can be processed by the enzymes in oxidative phosphorylation. Since the transporters cannot move freely across the membrane, two specific shuttles are put to good use:
Glycerol Phosphate Shuttle
Both the cytoplasm and mitochondria share an identical reaction: dihyroxyacetone phosphate can be converted to glycerol phosphate. In the cytoplasm, this oxidizes NADH to NAD+. Glycerol phosphate in then shuttled across the membrane and into the mitochondria, where it is converted back to dihydroxyacetone phosphate. This reaction reduces FAD+ to FADH2. However, as you probably know, FADH2 generates less ATP than NADH, so some energy is lost in this shuttle. The better way is to transfer the hydrogen from an NADH cytoplasm to a mitochondrial NADH. This is what the malate shuttle does.
Malate Shuttle
In the cytoplasm, oxaloacetate is reduced to malate, which converts an NADH to NAD+. Malate is then transported into the mitochondria, using a transporter which also sends alpha-ketoglutarate into the cytoplasm. Once in the mitochondria, malate is oxidized back to oxaloacetate, which converts NAD+ to NADH. Oxaloacetate then undergoes transamination with glutamate to become aspartate, where it is shuttled out to the cytoplasm. The aspartate then undergoes transamination with alpha-keoglutarate to regenerate the oxaloacetate and convert the A-K to glutamate.
Electron Transport Chain
Energy from the electron transporters then form the electrochemical hydrogen gradient by releasing H+ in a step-by-step oxidative phosphorlation process. The five components of the process include 4 oxidoreductases, and ATP synthesis.
Step 1: NADH transfers electrons to ubiquinone
Step 2: FADH2 transfers electrons to ubiquinone
The ubiquinone from these two separate steps come together to continue with grouped oxidative phosphorylation:
Step 3: ubiquinone transfers electrons to ferricytochrome b
Step 4: ferricytochrome transfers electrons to oxygen (to form water)
Step 5: ATP Synthesis
With ATP syntheis, hydrogen binds to the 'stalk' portion of ATP synthase, which is embedded in the membrame. This changes the shape and makes the 'wheel' portion go from wanting to bind ADP and inorganic phosphate to wanting to bind ATP. This shape changes produces sufficient energy to force ADP and Pi together to form ATP. As more hydrogen molecules pass through, the shape changes again and favours ADP and Pi binding again.
We broke into groups today and worked at putting together a code of ethics that we wanted our class to follow. It was pretty open-ended, ranging from things like specific do's-and-do-not's, to personal characteristics to follow.
When the code is put together and made available on-line, I'll be sure to post it here.
Biochemistry
We continued our look at energy metabolism by moving from the Kreb's cycle to oxidative phosphorylation and the electron transport chain. In summary, this step takes the hydrogen transporters, releases their hydrogens via oxidative phosphorylation. This sets up a hydrogen gradient, which the enzyme ATP synthase uses to produce ATP molecules.
The first step is to get NADH produced outside the mitochondria by glycolysis into the cell so that it can be processed by the enzymes in oxidative phosphorylation. Since the transporters cannot move freely across the membrane, two specific shuttles are put to good use:
Glycerol Phosphate Shuttle
Both the cytoplasm and mitochondria share an identical reaction: dihyroxyacetone phosphate can be converted to glycerol phosphate. In the cytoplasm, this oxidizes NADH to NAD+. Glycerol phosphate in then shuttled across the membrane and into the mitochondria, where it is converted back to dihydroxyacetone phosphate. This reaction reduces FAD+ to FADH2. However, as you probably know, FADH2 generates less ATP than NADH, so some energy is lost in this shuttle. The better way is to transfer the hydrogen from an NADH cytoplasm to a mitochondrial NADH. This is what the malate shuttle does.
Malate Shuttle
In the cytoplasm, oxaloacetate is reduced to malate, which converts an NADH to NAD+. Malate is then transported into the mitochondria, using a transporter which also sends alpha-ketoglutarate into the cytoplasm. Once in the mitochondria, malate is oxidized back to oxaloacetate, which converts NAD+ to NADH. Oxaloacetate then undergoes transamination with glutamate to become aspartate, where it is shuttled out to the cytoplasm. The aspartate then undergoes transamination with alpha-keoglutarate to regenerate the oxaloacetate and convert the A-K to glutamate.
Electron Transport Chain
Energy from the electron transporters then form the electrochemical hydrogen gradient by releasing H+ in a step-by-step oxidative phosphorlation process. The five components of the process include 4 oxidoreductases, and ATP synthesis.
Step 1: NADH transfers electrons to ubiquinone
Step 2: FADH2 transfers electrons to ubiquinone
The ubiquinone from these two separate steps come together to continue with grouped oxidative phosphorylation:
Step 3: ubiquinone transfers electrons to ferricytochrome b
Step 4: ferricytochrome transfers electrons to oxygen (to form water)
Step 5: ATP Synthesis
With ATP syntheis, hydrogen binds to the 'stalk' portion of ATP synthase, which is embedded in the membrame. This changes the shape and makes the 'wheel' portion go from wanting to bind ADP and inorganic phosphate to wanting to bind ATP. This shape changes produces sufficient energy to force ADP and Pi together to form ATP. As more hydrogen molecules pass through, the shape changes again and favours ADP and Pi binding again.
#23 What I Learned Today
Introduction to Operative Dentistry
No lecture; we had an exam and a rubber dam isolation practical. However, I don't want to leave you empty handed, so here is some bonus content on the physiological characteristics of enamel!
General and Oral Histology
Enamel is formed from ameloblasts, which differentiate from inner enamel epithelium of the enamel organ. This differentiation occurs to the cells on the other side of the basement membrane, adjacent to the dental papilla cells. The ameloblasts begin to deposit enamel shortly after odontoblasts begin depositing dentin (layering process in both is referred to as apposition).
Enamel is one of the hardest substances in the human body, and consists of rods made of hydroxyyapatite (HAP) crystals from calcium and phosphates. Also find some proteins called alemogenin, ameloblastin, and enamelin
You commonly see six different life stages in ameloblasts:
Enamel rods are arranged in rows that extend from the DEJ to the outer surfaces. They form 'S' like paths, with the most oblique angles (as compared to the DEJ) occuring towards the incisal edge. Clinically, this is important, as isolated enamel rods, or parts of enamel rods are brittle and break easily. The strength of the enamel is dependent on the dentin support underneath.
No lecture; we had an exam and a rubber dam isolation practical. However, I don't want to leave you empty handed, so here is some bonus content on the physiological characteristics of enamel!
General and Oral Histology
Enamel is formed from ameloblasts, which differentiate from inner enamel epithelium of the enamel organ. This differentiation occurs to the cells on the other side of the basement membrane, adjacent to the dental papilla cells. The ameloblasts begin to deposit enamel shortly after odontoblasts begin depositing dentin (layering process in both is referred to as apposition).
Enamel is one of the hardest substances in the human body, and consists of rods made of hydroxyyapatite (HAP) crystals from calcium and phosphates. Also find some proteins called alemogenin, ameloblastin, and enamelin
You commonly see six different life stages in ameloblasts:
- morphogenic: begin to see IEE cells differentiate into pre-ameloblasts
- organizing: odontoblasts sectrete growth factors which leads to further differentiation into columnar secretory cells, or ameloblasts.
- formative: basement membrane between ameloblasts and odontoblasts disappears, and enamel crystals are secreted along mantle dentin to form the DEJ
- secretory: ameloblasts secrete enamel from Tomes' processes and move away from DEJ
- maturative: ameloblasts undergo structural changes. These include the loss of the Tomes' processes, and the ameloblasts are no longer able to secrete enamel.
- protective/desmolytic: ameloblasts collapse to form the reduced enamel epithelium
Enamel rods are arranged in rows that extend from the DEJ to the outer surfaces. They form 'S' like paths, with the most oblique angles (as compared to the DEJ) occuring towards the incisal edge. Clinically, this is important, as isolated enamel rods, or parts of enamel rods are brittle and break easily. The strength of the enamel is dependent on the dentin support underneath.
#22 What I Learned Today
Biochemistry
Today in Biochemistry, we looked at regulation methods for the citric acid cycle. The cycle can be regulated a number of ways.
Today in Biochemistry, we looked at regulation methods for the citric acid cycle. The cycle can be regulated a number of ways.
The first method uses the products of the cycle to perform allosteric inhibition. Two of the products of the reaction, NADH and acetyl-CoA, inhibit the initial step where pyruvate is converted to acetyl-CoA by pyruvate dehydrogenase.
The cycle can also be covalently regulated by the addition or removal of a phosphate group. When phosphorylated, the enzyme is inactivated. When dephosphorylated, the enzyme is activated. With that in mind, two products of CAC, NADH and acetyl-CoA, activate the activity of protein kinase. Thus, the formation of lots of product results in the shutting down of the cycle. Protein kinase is inhibited by high levels of pyruvate and ADP. Thus, lots of reactants leads to the subsequent production of ATP through the running of Kreb's cycle, and ultimately the electron transport chain.
Finally, the citric acid cycle can be regulated by controlling the activity of enzymes in irreversible steps of CAC. This includes the steps with the following enzymes:
- citrate synthase
- isocitrate dehydrogenase
- alpha-ketoglutarate dehydrogenase
Deficiencies in pyruvate dehydrogenase complexes can have devastating results as it becomes difficult to get energy from pyruvate and glucose. It tends to affect neural tissues since the brain is essentially only able to use glucose for energy.
Principles of Dental Materials
In dental materials, we began to look at the composition and structure of dental amalgam. This lecture is a re-hash of what we learned in Operative class last week. To summarize, amalgam is a setting procedure where amalgam alloy (powder) reacts with mercury (liquid) to form set amalgam (solid).
In dental materials, we began to look at the composition and structure of dental amalgam. This lecture is a re-hash of what we learned in Operative class last week. To summarize, amalgam is a setting procedure where amalgam alloy (powder) reacts with mercury (liquid) to form set amalgam (solid).
Advantages of amalgam include:
- high durability (lasts longer than most direct restorative materials)
- setting material (allow for easier placement by the dentist)
- good consistency (easy placement and shaping)
- low cost
- gray-metallic luster (unnatural appearance)
- contains mercury (very small amount released during chewing; greatest exposure comes from the setting and removal of the amalgam)
- low tensile, ductility and toughness (brittle alloy that cannot be used in thin sections)
- setting reaction takes time (strength builds over 24 hours, patient needs to be careful about mastication initially)
- Creep, dimensional change (can lead to marginal breakdown, but vary rarely seen in new copper amalgams)
- tarnish (the darkening of metal in oral cavity. Rarely seen in newer amalgam, but some patient's saliva content may still cause it)
- corrosion (due to gamma-2 phase, but rarely seen in newer amalgam)
Dental Anatomy
We had a practical examination today, which consisted of stations of Fuller & Denehy drawings and Kilgore teeth. Some of the questions asked for tooth identification, while others asked for specific tooth structures. It's important to know 'standard' (understanding that there is quite a bit of variation, especially within root structures) anatomical dentition in order to detect anomalies and be able to restore teeth to working form.
We had a practical examination today, which consisted of stations of Fuller & Denehy drawings and Kilgore teeth. Some of the questions asked for tooth identification, while others asked for specific tooth structures. It's important to know 'standard' (understanding that there is quite a bit of variation, especially within root structures) anatomical dentition in order to detect anomalies and be able to restore teeth to working form.
#21 What I Learned Today
Essentials of Clinical Practice
Exam today; no lecture.
Gross Anatomy I
Today we discussed anatomical structures found in the anterior body wall and peritoneal cavity. The muscles of the anterior body wall consist of three major layers, from external to internal: external oblique muscle, internal oblique muscle, and transversus abdominis muscle. Each have a specific direction in which their muscle fibers run. External runs downwards; same direction as your fingers if you put your hands in your pant pockets. Internal runs approximately perpendicular and upwards to external. Transversus abdominis runs horizontally, like the name implies.
Found between the epidermis and abdominal muscles is two layers:
Gross Anatomy Lab
In dissection lab, we opened up the neck to identify the muscles, bones, vessels, nerves and glands in the area. Some of the noted structures included:
Exam today; no lecture.
Gross Anatomy I
Today we discussed anatomical structures found in the anterior body wall and peritoneal cavity. The muscles of the anterior body wall consist of three major layers, from external to internal: external oblique muscle, internal oblique muscle, and transversus abdominis muscle. Each have a specific direction in which their muscle fibers run. External runs downwards; same direction as your fingers if you put your hands in your pant pockets. Internal runs approximately perpendicular and upwards to external. Transversus abdominis runs horizontally, like the name implies.
Found between the epidermis and abdominal muscles is two layers:
- fatty layer (Camper's)
- fascia layer (Scarpa's)
- descending aorta
- superior epigastric arteries (from subclavian -> internal thoracic)
- musculophrenic arteries (from subclavian -> internal thoracic)
- superficial circumflex iliac artery
- deep circumflex artery
- inferior epigastric artery
- ductus (vas) deferens
- testicular artery
- pampiniform plexus of veins
- genitofemoral nerve
Gross Anatomy Lab
In dissection lab, we opened up the neck to identify the muscles, bones, vessels, nerves and glands in the area. Some of the noted structures included:
- sternocleidomastoid muscle (cut back to access the hyoid-related muscles)
- thyroid gland
- hyoid bone
- sternothyroid muscle
- sternohyoid muscle
- thyrohyoid muscle
- thoracic duct (hard to find)
- carotid sheath, containing: common carotid artery, internal jugular vein, and vagus nerve
- cartilages, including: thyroid cartilage (Adam's apple!), cricoid cartilage.
- trachea and esophagus