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Please wait outside until I let you in, and put all your stuff at the back just like we've done about 20 times already this semester. Okay? Or this semester and last, and you will be just fine. Now your lecture exam too is 90 marks big. It is 90 multiple choice questions. Okay. It is going to be on cardiovascular disorders, urinary system, fluid balance, Okay. So let's start talking about them. First of all, okay, you need to know the difference between a myocardial infarct, ischemic attack, a congestive heart failure, and angina pectorals. You need to know what a low level inflammatory response that develops over time where the endothelium is damaged due to the aging or prolonged hypertension, where LDLs accumulate, and the endothelium is repaired with collagen is called. That might take you a long time to read. Okay? But it is a good question. Okay? You need to know now be really, really clear on these. Okay? You absolutely need to know the difference between right ventricular hypertrophy and left ventricular hypertrophy and what they cause. Because there's two questions on here, and so far, this one hasn't been done very well. Okay? Make sure you understand what right ventricular hypertrophy leads to and you understand what left ventricular hypertrophy leads to. Now the original term, congestive heart failure, that refers to left ventricular hypertrophy leading to backup in the lungs. K? You need to know what arteries or vessels are used in bypass surgery. You need to know what a mini stroke is. Okay? You need to know the difference between thrombus and ballast occlusion and arthroma. You need to know what is a restriction in blood supply generally due to factors in the blood vessels with resultant damage or dysfunction of tissue. You need to know, what are the consequences of an aging cardiovascular system. And then I I've got a matching question for you. You need to match the basic function of the proximal convoluted tubule, the glomerulus, and the peri colic duct. And then two of my favorite questions. Are you ready? Okay. You have to find out which of the following is the best explanation for why the cells of the proximal convoluted tubule contain so many microclonary. Oh, isn't that lovely? Okay. And then the other one you need to know is you need to find the best explanation for the microvilli on the apical surface of the proximal convoluted tubules. So don't get that one wrong because we've talked about microvilli about a bazillion times. Okay? This picture is gonna be on there, folks. Okay? This is the picture of the of the nephron from your textbook. Okay. You need to label things like glomerulus glomerulus afferent arteriole collecting duct nephron move. Okay. Where do you find the granular cells? Okay. The difference between the medulla and the cortex. Make sure you know all of those things. I'll read you this one. This is a good question too. Hydrostatic pressure is the primary driving force of plasma through the filtration membrane into the capsular space. All the publicly following statements reflects why hydrostatic pressure is so high in the glomerular capillaries. Select the one statement that does not explain the high pressure within the glomerular capillaries. So you need to know why glomerular capillary pressure is higher than the rest of the capillaries in the body. You need to know how or why cells or transport proteins are prevented from moving through how yeah. What drives reabsorption of organic nutrients in the proximal condylated tubule? Who drives thus? You need to know the mechanism that establishes the medullary osmotic gradient the The functional and structural unit of the kidneys is what? The g force pushing the blood and solids out of the blood across the filtration membrane is what? Okay. The macular densities cells do what? Function in angiotensin two is to do what? What is, specific gravity or density? Okay. If you talk about the specific gravity or density of urine, how is it different from water? You need to actually, this is just one question, but it should be a pretty simple one. Okay? You need to place the following and correct sequence from the formation of a drop of urine to its elimination of the body. And so you have to go through from well, I'll just read it to you. Major calyx, minor calyx, nephron, urethra, ureter, and collecting that. So you need to put those in order from start to finish. Okay? What would happen if the capsular hydrostatic pressure were increased above normal? You need to know what would happen. Reabsorption of bilevels of glucose and amino acids in the filtrate is accomplished. The 44 more. Okay. So you need to match to their definition. All of your hypo and hypers. Make sure you have some under control. Okay? And then you need to match possible causes. So there's possible causes of respiratory alkalosis, metabolic alkalosis, metabolic acidosis, and respiratory acidosis. Respiratory alkalosis, metabolic alkalosis, metabolic acidosis, and respiratory acidosis. There are possible causes for those four things. You need to match the disorder to the cause. Okay? And then you need to know, the body's motor volume is mostly tied to the level of then I have a couple of clinical correlation questions for you, but they are multiple choice this time. So something happened to Jane. You have to tell me what's happening to Jane. Okay? Now whereas sodium is mainly found in the extracellular fluid, most is found in intracellular systems are. Okay. Which of the following is not a likely source of hydrogen ions in blood plasma, so there's a few types in the tablets, so make sure you know which ones are going to produce acids and which ones aren't. And then Annie had something happen to her as well. Across capillary walls is what? Regulation of potassium balance is what? Now Dave Dave did something silly. Okay? Dave ran a marathon. Okay? And then Dave did something even more silly afterwards. I want you to tell me what happened to Dave. And in addition to that, Nancy is having a panic attack. So I want you to tell me what's happening to Nancy in terms of respiratory aesophosis and respiratory aldosterone. Okay. If thyroid and parathyroid glands were surgically removed, which of the following would go out of balance without replacement therapy? Falling arterial blood pressure holds which? An illness, Doug. Doug has severe diarrhea. Okay. And, is accompanying the loss of bicarbonate or secretions. So how is Doug gonna compensate for that for Doug? Okay. You need to know what the medical term for kidney stones is. You need to know what happens, or what could cause the passage of proteins, red blood cells, and white blood cells into the urine. You need to know how to solve prostatic enlargement, and, you need to know what the presence of white blood cells in urine is called and what is causing it. Okay? And then there's a picture of the lymphatic of the lymph node. Okay. You need to label the lymph node picture. And then you there is going to be a matching question on lymphatic structures, so you need to know what happens in the spleen, the lymph nodes, the thoracic duct, the lymph, and the pyre patches. There's a list, a small short list. Okay? So in other words, you're going to need to know what is classified as a lymphoid organ and what does not. Okay? So make sure you know what your lymphoid organs are. You need to know the pathway of lymph. So it starts in lymph capillaries. Where does it end? Make sure you know all the steps along the way. And then you need to know the functions of the spleen. What did what does the spleen do? And that is it for an example
Updated 25d ago
flashcards Flashcards (5)
Primary adrenal insufficiency = problem at level of adrenal glands Causes? Addison’s disease Pathophys? Autoimmune destruction of the adrenal glands Associated with hyperpigmentation POMC is precursor to both ACTH and MSH PAI → lack of negative feedback → high ACTH Lab findings? ACTH high Aldosterone low Destruction of zona glomerulosa Renin high Hypotension → RAAS activation Electrolytes Na+ low, K+ high CBC Eosinophils high Pathophys? Glucocorticoids → eosinophil apoptosis. Lack of glucocorticoids cause eosinophilia. Dx? Cosyntropin testing → no rise in cortisol Adrenal glands aren’t working, so no response to ACTH. Tx? prednisone/hydrocortisone/dexamethasone + fludrocortisone (mineralocorticoid) Stress-dose steroids for surgery, serious illness, etc. Secondary adrenal insufficiency = problem at level of pituitary, reduced ACTH release Causes? MC is prolonged steroid use → ACTH suppression Sheehan’s syndrome (infarction of pituitary) pregnancy Pituitary tumors (ACTH-producing tumor) Lab findings? ACTH low Anterior pituitary is being inhibited Aldosterone normal Zona glomerulosa under control of RAAS system Renin normal Electrolytes Na+ & K+ unaffected (Aldosterone levels are normal) CBC Neutrophilia due to demargination (if pt was recently taking steroids) Dx? Cosyntropin testing → rise in cortisol Adrenal gland is functional Tx? Glucocorticoids Do not need to replace mineralocorticoids since adrenals are functional and aldosterone is under RAAS control Stress-dose steroids for surgery, serious illness, etc. AI with a history of nuchal rigidity and purpuric skin lesions → Waterhouse-Friedrichson syndrome Pathophys? AI 2/2 hemorrhagic infarction of the adrenal glands in the context of Neisseria meningitidis infection Adrenal synthesis enzymes If the enzyme starts with 1 → HTN (high mineralocorticoids) and hypokalemia If the second # is 1 → virilization (high androgens) E.g. 11-beta hydroxylase deficiency → HTN & virilization E.g. 21 hydroxylase deficiency → virilization only E.g. 17-alpha hydroxylase deficiency → HTN only B12 deficiency Where does B12 come from? Animal products VS folic from plants Physiology R factor in saliva binds to B12 and protects it from acidity in the stomach. R factor protector -B12 travels to the duodenum. Parietal cells produce intrinsic factor, which travels to the duodenum. Pancreatic enzymes cleave B12 from R factor and B12 then binds IF. B12-IF complex is reabsorbed in the terminal ileum Reabsorption where? Terminal ileum Causes of B12 deficiency Extreme vegan Pernicious anemia Pancreatic enzyme deficiency Cystic Fibrosis Can’t cleave B12 from R factor Crohn’s Affects terminal ileum Lab markers Homocysteine HIGH MethlyManoicAcid HIGH Presentation? Megaloblastic anemia Subacute combined degeneration (of dorsal columns + lateral corticospinal tract) Peripheral neuropathy Dx of pernicious anemia? anti-IF Ab Folate deficiency Where does folate come from? Leafy things Causes of folate deficiency Poor diet (e.g. alcoholics, elderly) Phenytoin Lab markers Homocysteine HIGH MMA normal Presentation? Megaloblastic anemia Prophylaxis in HIV+ patients CD4 < 200 → PCP TMP-SMX, inhaled pentamidine, dapsone, atovaquone CD4 < 100 → Toxoplasm Treat: TMP-SMX CD4 < 50 → MAC Treat: Azithromycin If live in endemic area, CD4 < 250 → Coccidioides Immitis E.g. Arizona, Nevada, Texas, California Treat: Itraconazole If live in endemic area, CD4 < 150 → Histoplasma Capsulatum E.g. Kentucky, Ohio, Missouri Treat: Itraconazole Diabetes insipidus Dx? Water deprivation test Measure serum osmolality & urine osmolality Deprive pt of water Remeasure serum osmolality & urine osmolality If urine osmolality doesn’t go up → suspect DI Central DI → deficiency of ADH Pathophys? Supraoptic nucleus not making enough ADH Dx? Give desmopressin → urine osmolality increases significantly Nephrogenic DI → kidneys are not responding to ADH Dx? Give desmopressin → urine osmolality doesn’t change much Tx? Hydrochlorothiazide Unless 2/2 lithium, use amiloride or triametere Causes? Lithium SSRIs Carbamazepine Demeclocycline Tx of normovolemic hypernatremia? D5W to correct free water deficit Divine says NS, but most other resources I found said correct free water deficit Tx of hypovolemic hypernatremia? Give NS first until normal volume, then give D5W Consequence of correcting hypernatremia too rapidly? Cerebral edema Osteoarthritis Presentation? Old person with joint pain that gets worse throughout the day Risk Factr? Obesity vs decreases osteoporosis Imaging findings? Joint space narrowing Subchondral sclerosis Subchondral cysts Osteophytes Arthrocentesis findings? <2000 cells Tx? 1st line acetaminophen 2nd line NSAID (e.g. naproxen) 3rd line joint replacement surgery Returned from a business conference 1 week ago + Fever + Nonproductive cough + Abdominal pain + Hyponatremia → Legionella Dx? Urine antigen Tx? FQ or macrolide MaCroLide mnemonic = Mycoplasma, Chlamydia, Legionella What are the common causes of atypical PNA? Mycoplasma, Legionella, Chlamydia MC cause? Mycoplasma CXR findings? Interstitial infiltrates HY associations C. Psittaci → birds C. Burnetii → cows, goats, sheet Mycoplasma → college student w/ walking pneumonia Midsystolic click heard best at the apex. → mitral valve prolapse “Stenosnap & Proclick” Risk Factor? Connective tissue disease Marfarn Ehlers-Danlos ADPKD bilateral renal masses Classic demographic? Young woman psychiatric Pathophys? Myxomatous degeneration MVP vs aortic dissection: cystic medial necrosis Exam maneuvers Anything that increase amount of blood in LV → murmur softer Increase preload Increase afterload Anything that decreases amount of blood in LV → murmur louder Dx? Echo Scaly, itchy skin with yellowish crusting in the winter. → seborrheic dermatitis Tx? Topical antifungals e.g. ketoconazole or selenium sulfide shampoo Classic disease distribution? Hair → e.g. cradle cap Eyebrows Episodic/intermittent HTN + HA → pheochromocytoma Genetic disease associations MEN2A MEN2B VHL in brain (hemangioma) NF-1 growth in skin Pathophys? Catecholamine-secreting tumor Location? Adrenal medulla Posterior mediastinum Organ of Zuckerkandl (chromaffin cells along the aorta) Dx? 1st step: urine metanephrines If elevated → CT abdomen If nothing found on CT → MIBG scan Tx? Alpha blocker (e.g. phenoxybenzamine, phenotaline) THEN beta blocker Most common cause of a Lower GI Bleed in the elderly → diverticulosis Dx? Colonoscopy or barium enema Recall that you acutely do a CT scan for diverticulitis, then 6 weeks later colonoscopy to r/o cancer Ppx? Eat fiber Megaloblastic anemias Blood smear findings? Hypersegmented neutrophils MCV > 100 Classic patient demographic with folate deficiency? Alcoholics Elderly person with poor nutrition Folate synthesis inhibitors Pt with molar pregnancy → methotrexate Pulmonary issue? Pulmonary fibrosis HIV+ pt with ring-enhancing lesions → pyrimethamine-sulfadiazine Pyrimethamine inhibits DHFR AIDS pt on ppx for toxo → TMP-SMX TMP inhibits DHFR Use of leucovorin? Rescue bone marrow in setting of methotrexate toxicity Mechanism? Folinic acid analog CMV presentations Esophagitis → linear ulcers Colitis → post-transplant pt Retinitis → HIV pt with CD4 < 50 Congenital CMV → periventricular calcifications + hearing loss calcifications elsewhere → toxo Histology? Owl’s eye intranuclear inclusions Tx? Gancicyclovir Resistance? UL97 kinase mutation Tx for resistance? foscarnet CD4 < 200 + severe peripheral edema + frothy urine. → FSGS in HIV pt Variant classic in HIV+ pts? Collapsing variant Tx? Steroids + cyclophosphamide + ACE-I Indinavir AE? Kidney stones triad of fever, rash, and eosinophiluria → acute interstitial nephritis Drugs cause? Penicillins Tx? Stop the drug! Can add steroids if severe Vitamin D metabolism Liver converts Vit D to calcidiol (25OH-Vit D). Calcidiol goes to kidney. Alpha-1 hydroxylase converts calcidiol to calcitriol (1,25-OH Vit D). Common causes of Vitamin D deficiency CKD → 1-alpha hydroxyalse deficiency Liver disease → can’t make calcidiol CF → malabsorption Crohn’s → malabsorption Osteomalacia vs Rickets Osteomalacia in adults Rickets in kids Tx? Calcium + vit D Lab findings? Ca++ low Phos low Low in liver disease High in kidney disease (kidneys can’t get rid of phos) PTH high (2ary hyperpara) vs liver dx PTH low Alk phos Aspiration pneumonia Risk Factor? Alcoholism Dementia Neuromuscular problems (e.g. MG, ALS) Bugs? Anaerobes foul smelling Bacteroides FUsobacterium Peptostreptococcus Klebsiella → currant jelly sputum alcoholic Tx? Clindamycin CURB-65 criteria Purpose? Who to admit Cutoff? 2+ → hospitalize C = confusion U = uremia (BUN > 20) R = RR > 30 B = BP < 90/60 Age > 65 Drugs commonly used in PNA treatment Ceftriaxone Levofloxacin fluoroquinolone Macrolides - great for atypical PNA Pharmacological management of pulmonary arterial HTN Endothelin antagonists Bosentan ambrisentan PDE-5 inhibitors Sildenafil Tadalafil Prostacyclin analogs Iloprost Epoprostenol Treprostinil Causes? Young female → idiopathic PAH Mutation? BMPR2 55 yo F presents with a 5 week history of a rash on her forehead. PE reveals scaly macules with a sandpaper texture. → actinic keratosis Risk Factor? Sun exposure Tx? Topical 5-FU Possible dangerous sequelae? Squamous cell carcinoma Most likely disease sequelae? Resolution 1ary hyperparathyroidism 2ary hyperparathyroidism 3ary hyperparathyroidism Autonomous PTH production Causes? Adenoma Parathyroid hyperplasia PTH high Ca++ high Phos low Low Ca++ → PTH production Causes? CKD PTH high Ca++ low Phos high PTH production despite normalized of Ca++ levels Causes? CKD s/p transplant PTH high Ca++ high Phos low Tx? Parathyroidectomy (remove 3.5 glands) Cinacalcet (CSR modulator) Hypercalcemia Presentation? bones, stones, groans, psychic overtones Tx? 1st step: Normal Saline Hypercalcemia of malignancy → bisphosphonates EKG finding? Shortened QT Periumbilical pain that migrates to the right lower quadrant. → appendicitis PE findings? McBurney’s point tenderness Psoas sign (flex hip pain) Obturator sign (pain with internal rotation of hip) Rovsing’s sign (palpation of LLQ → pain in RLQ) Dx? CT scan Pregnant → US Kid → US Tx? Surgery Classic drug and viral causes of aplastic anemia. Drugs? Carbamazepine Chloramphenicol Viral? Parvovirus B19 (single stranded DNA virus) Fanconi anemia Pathophys? Problems with DNA repair Fanconi anemia vs Fanconi syndrome Fanconi anemia → cytopenias + thumb anomalies + short stature + cafe-au-lait spots Fanconi syndrome → type 2 RTA (proximal) CD4 count of 94 + MRI revealing ring enhancing lesions in the cortex → toxoplasmosis Tx? Pyrimethamine-sulfadiazine Rescue agent for pt who becomes leukopenic with treatment? leucovorin Who should get steroids? Increased ICP For PCP pneumonia: O2 sat < 92 PaO2 < 70 A-a gradient > 35 Ppx? TMP-SMX for CD4 < 100 Congenital toxo Hydrocephalus Chorioretinitis Intracranial calcifications Classic methods of transmission? handling cat litter Lupus nephritis Associated autoantibody? anti-dsDNA Classic “immunologic” description? “Full house” pattern Tx? Steroids + cyclophosphamide Osteoporosis Screening population? women > 65 Screening modality? DEXA scan Dx? T-score < -2.5 Risk Factor? Postmenopauseal Low BMI Smoking Alcohol Preventive strategies? Weight bearing exercise Smoking cessation Reduce alcohol consumption Tx? 1st line: bisphosphonates + Ca/Vit D supplementation Raloxifene (SERM) Agonist in bone Blocker Antagonist in breast Classic locations of osteoporotic fractures Vertebral compression fracture Hip fracture Name the PNA Red currant jelly sputum. → Klebsiella Rust colored sputum. → Strep pneumo PNA in an alcoholic. → Klebsiella Post viral PNA with a cavitary CXR lesion. → Staph aureus PNA in a patient that has chronically been on a ventilator. → Pseudomonas MC cause of Community Acquired Pneumonia. → Strep pneumo Pharmacological management of MRSA. Vancomycin Clindamycin Linezolid Ceftaroline (5th gen cephalosporin) Tigecycline, tertracycline Pharmacological management of Pseudomonas. Ceftazidime (only 3rd gen cephalosporin) Cefepime (4th gen cephalosporin) Pip-tazo Fluoroquinolones Carbapenems Aztreonam Aminoglycosides JVD and exercise intolerance in a patient with a recent history of an URI. → dilated cardiomyopathy 2/2 viral myocarditis MC cause? Coxsackie B VS Coxsackie A: Hand foot mouth dx Drug causes myocarditis Clozapine Anthracyclines Prevention? Dexrazoxane (iron chelator) Trastuzumab reversible tx for breast cancer Classic cause in a patient with recent history of travel to S. America? Chagas T. Cruzi Potential sequelae? Achalasia Dilated cardiomyopathy Megacolon (2/2 degeneration of myenteric plexus) Massive skin sloughing (45% BSA) in a patient that was recently started on a gout medication? TEN Dx? <10% BSA → SJS >30% BSA → TEN Tx? STOP the drug IVF Topical abx to prevention infection Tetany and a prolonged QT interval in a patient with recent surgical treatment of follicular thyroid carcinoma. → hypocalcemia due to removal of parathyroids Recurrent viral infections + QT prolongation + tetany → DiGeorge syndrome Pathophys? Failure of development of 3rd/4th pharyngeal pouches Trousseau and Chvostek signs. Trousseau → inflation of BP cuff causes carpopedal spasm Chvostek → taping on cheek causes facial muscle spasm Hypocalcemia that is refractory to repletion → consider hypomagnesemia Electrolyte/drug causes of prolonged QT intervals Electrolytes? Hypocalcemia Hypomagnesemia Hypokalemia Drugs? Macrolides FloroQunlones Haloperidol Ondensatron Methadone Hypoalbuminemia and Ca balance Hypoalbumenia → decrease in total body Ca++, no change in ionized Ca++ Drop of 1 in albumin → add 0.8 to Ca++ Abdominal pain radiating to the back → acute pancreatitis Causes? #1 = Gallstones #2 = Alcohol Hypertriglyceridemia Hypercalcemia Scorpion sting Handlebar injuries Lab markers? Lipase - most sensitive Amylase Physical exam signs in pancreatitis. Cullen’s sign = periumbilical ecchymosis Grey Turner sign = flank ecchymosis Tx? NPO + IVF + pain control Meperidine is a good agent because it doesn’t cause sphincter of Oddi spasms Management of gallstone pancreatitis Dx? US then ERCP Tx? DELAYED cholecystectomy What if the patient becomes severely hypoxic with a CXR revealing a “white out” lung? ARDS noncardiogenic pulm edema PCWP? <18 mmHg NORMAL 20 yo M with red urine in the morning + hepatic vein thrombosis + CBC findings of hemolytic anemia. → paroxysmal nocturnal hemoglobinuria Pathophys? Defect in GPI anchors, which attach CD55 and CD59 to cell (they prevent complement from destroying RBC) Sleep → hypoventilation → mild respiratory acidosis → activation of complement cascade Gene mutation? PIGA Dx? Flow cytometry Tx? Eculizumab (terminal complement inhibitor) Vaccine required? pnemococal Neisseria meningitidis Chronic diarrhea and malabsorption in a HIV+ patient + detection of acid fast oocysts in stool. → cryptosporidium parvum Acid-fast organisms Cryptosporidium TB MAC Nocardia Dx? Stool O&P Tx? Nitazoxanide Route of transmission? Contaminated water Muddy brown casts on urinalysis in a patient with recent CT contrast administration (or Gentamicin administration for a life threatening gram -ve infection) → Acute Tubular Necrosis Woman with morning joint stiffness > 1 hr → Rhematoid Arthritis. Antibodies? Rheum Factor (IgM against IgG) anti-CCP - more specific HLA? DR4 Pathophys? IgM constant region activates complement → inflammation → formation of pannus (hypertrophied synovium) → damage to cartilage and bone Caplan syndrome = RA + pneumoconiosis Felty syndrome = RA + neutropenia + splenomegaly (“RANS”) Classic hand/finger findings/distribution? MCP & PIP joints of hands (DIP joints spared) Imaging findings? Symmetric joint space narrowing Tx? Methotrexate (DMARDs) If no response → TNF alpha inhibitor (e.g. infliximab) Required testing prior to starting methotrexate? PFTs Required testing prior to starting infliximab? TB Hep B/Hep C Differentiating Strep pharyngitis from Infectious Mononucleosis LND distribution Anterior cervical → Strep Posterior cervical → Mono Disease onset Acute → Strep Over weeks → Mono Organ involvement Splenomegaly → Mono Pt with sore throat takes amoxicillin and gets rash → mono NOT allergic rxn! CENTOR criteria C = absence of Cough E = tonsillar Exudates N = nodes/anterior cervical lymphadenopathy T = temp (fever) OR <15 → +1 >=45 → -1 Using CENTOR score 0/1 → don’t test, don’t treat 2/3 → rapid antigen test Positive → treat Negative → throat culture 4/5 → treat empirically Tx of Strep pharyngitis? Amoxillcin If PCN allergic → azithromycin Potential sequelae of Strep pharyngitis RF - preventable with abx PSGN Endocarditis MC cause of endocarditis? IVDU Bug? Staph aureus Valve? tricuspid Prosthetic valve endocarditis Bug? Staph epidermidis Endocarditis after dental procedure? Viridans group streptococci Strep viridans, Strep mitis, Strep mutans, Strep sanguineous Patient with malar rash and echo showing vegetations on both sides of the mitral valve → Libman-Sacks endocarditis Presentation? Fever + night sweats + new murmur Splinter hemorrhages Roth spots (retinal hemorrhages) Painless Janeway lesions + painful Osler nodes (immune phenomenon) Dx? 1st step: blood cultures TEE Tx? Abx that include Staph aureus coverage (e.g. vancomycin) for WEEKS Bugs implicated in culture negative endocarditis HACEK H = haemophilus A = actinobacillus C = cardiobacterium E = eikenella K = kingella Coxiella burnetii Blood cultures in a patient with endocarditis reveal S. Bovis (or S. Gallolyticus bacteremia). NBS? Colonoscopy Who needs antibiotic prophylaxis? Hx endocarditis Prosthetic valve Unrepaired cyanotic congenital dz Heart transplant with valve dysfunction Erythematous salmon colored patch with silvery scale on the elbows and knees. → psoriasis Tx? Topical steroids If this patient presents with joint pain (especially in the fingers)? Psoriatic arthritis Imaging? Pencil-and-cup deformity Tx? NSAIDs T of 104 + tachycardia + new onset Afib in a patient with a history of Graves disease. → thyroid storm Lab findings? TSH low T3/T4 high Tx? 1st step: propranolol 2nd step: PTU Then: Prednisone Potassium iodide (Lugul’s solution) Wolff-Chaikoff effect → large amounts of iodine inhibit thyroid hormone synthesis Biopsy revealing tennis racket shaped structures in cells of immune origin. → Langerhans cell histiocytosis Electron microscopy? Birbeck granules (tennis rackets) Marker? S100 Small bowel obstruction in a HIV patient with purple macules on the face, arms, and lower extremities. → Kaposi’s sarcoma Bug? HHV8 Tx? HAART Pathophys of vascular lesions? Overexpression of VEGF Fever + rash + eosinophiluria 10 days after a patient started an antistaphylococcal penicillin. → acute interstitial nephritis Tx? STOP drug + steroids SLE SOAP BRAIN MD S = serositis O = oral ulcers A = arthritis P = photosensitivity B = blood disorders (cytopenias) R = renal A = ANA/anti-dsDNA I = immunologic N = neurologic findings M = malar rash D = discoid rash Type 2 vs 3 HSRs in lupus Type 2 → cytopenias Type 3 → all other manifestations Lupus Ab? ANA anti-dsDNA anti-Smith Lupus nephritis → full house pattern on IF Antiphospholipid antibody syndrome → recurrent pregnancy losses Pathophys? Thrombosis of the uteroplacental arteries. MC cause of death in lupus patients? What I’ve read recently: CV disease Per Divine: Treated → infection Untreated → renal dz Also 40x risk MI Endocarditis in lupus pt? Libman-Sacks endocarditis Neonatal 3rd degree heart block → neonatal lupus Maternal autoimmune dz? Sjogren’s SLE Ab? anti-SSA/anti-Ro anti-SSB/anti-La Tx? Steroids Cyclophosphamide Hydroxychloroquine → good for skin lesions Pulmonary abscesses Bugs? Staph Anaerobes Klebsiella RF? Alcoholism Elderly Post-viral pneumonia MC location of aspiration pneumonia? Superior segment of RLL Chest pain worsened by deep inspiration and relieved by sitting up in a patient with a recent MI or elevated creatinine or URI or RA/SLE. → pericarditis EKG findings? Diffuse ST elevations + PR depression PE finding? Friction rub (“scratchy sound on auscultation”) A few days after MI → fibrinous pericarditis Weeks after MI → Dressler’s Tx? NSAIDS Consider adding on colchicine Cardiac tamponade Beck’s triad = hypotension + JVD + muffled heart sounds EKG findings? Electrical alternans Type of shock? Obstructive cardiogenic (Amboss) CO low SVR high PCWP high Tx? Pericardiocentesis or pericardial Pearly lesion with telangiectasias on the ear in a farmer. → Basal Cell Carcinoma MC type skin cancer Location? Upper lip Dx? Biopsy Tx? Mohs surgery Cold intolerance in a 35 yo white F → hypothyroidism MC cause? Hashimoto’s Histology? lymphoid follicles w/ active germinal centers Lab findings? TSH high T3/T4 low Ab? anti-TPO Anti-thyroglobulin HLA? DR3/DR5 Tx? Levothyroxine Future complication? thyroid lymphoma Massive hematemesis in a patient with a history of chronic liver disease. → ruptured varices Pathophys? L gastric vein has anastomosis with azygos veins. Increased portal pressure → backward flow from L gastric veins to azygous vein (which empties into SVC). Acute tx? IVF + octreotide + ceftriaxone/cipro + EGD w/ ligation/banding Do NOT give a beta blocker for acute tx Prophalaxsis? Beta blocker + spironolactone Other manifestations of elevated portal pressures Caput medusa Internal hemorrhoids Tx for cirrhotic coagulopathies? FFP If uremia → give desmopressin Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH Hemophilia A Pathophys? deficiency of factor 8 Inheritance? XLR Coag labs? Bleeding time normal PTT HIGH b/c clotting problem PT normal Hemophilia B Pathophys? deficiency of factor 9 Inheritance? XLR Coag labs? Bleeding time normal PTT HIGH PT normal Hemophilia C Pathophys? deficiency of factor 11 Inheritance? AR Coag labs? Bleeding time normal PTT HIGH PT normal Bernard Soulier Syndrome Pathophys? Deficiency of GpIb Coag labs? Bleeding time HIGH PTT normal PT normal Glanzmann Thrombasthenia Pathophys? Deficiency of GpIIbIIIa Coag labs? Bleeding time HIGH PTT normal PT normal Von Willebrand’s disease Pathophys? Deficiency of vWF Inheritance? AD Coag labs? Bleeding time HIGH PTT HIGH vWF is a protecting group for factor 8 PT normal ITP Pathophys? Ab against GpIIbIIIa Classic pt? Pt with SLE Tx? Observation Steroids IVIG Splenectomy TTP Pathophys? Deficiency in ADAMTS13 enzyme → cannot cleave vWF multimers → activation of platelets → thrombosis → thrombocytopenia Presentation? microangiopathic hemolytic anemia + thrombocytopenia + renal failure + fever + neurologic problems Tx? Plasma exchange transfusion****** HUS Bugs? Shigella or E. coli O157:H7 Presentation? Fever+ microangiopathic hemolytic anemia + thrombocytopenia + renal failure + neurologic Platelet deficiency vs coagulation factor bleeds Platelet deficiency → mucosal bleeds, petechiae, heavy menses Coag factor deficiency bleeds → hemarthrosis Why do patients with CKD develop coagulopathy? Uremia → platelet dysfunction Tx? Desmopressin Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH Exercising caution with transfusion in patients with Bernard Soulier syndrome Do NOT give transfusion that includes platelets They can have an anaphylactic rxn to GpIb (since they don’t have GpIb) Oropharyngeal candidiasis. RF? HIV Chronic ICS use TNF inhibitor Micro finding? Germ tubes at 37 C Tx oral candidiasis? Nystatin swish-and-swallow Tx invasive candidiasis? Amphotericin B Prevention of Amphotericin B toxicity? Liposomal formulation Pleural effusions Light’s criteria (must meet all 3 to be considered transudative!) LDH < 2/3 ULN LOW Pleural LDH/serum LDH < 0.6 LOW Pleural protein/serum protein < 0.5 LOW Causes of transudative effusion CHF Cirrhosis Nephrotic syndrome Note: Per UW 2021: Mechanism of transudate effusion? Decreased pulmonary artery oncotic pressure, e.g. hypoalbuminemia in nephrotic syndrome Increased pulmonary capillary hydrostatic pressure, e.g. volume overload in heart failure Causes of exudative effusion Malignancy Cancer Parapneumonic effusion Tb Note: Per UW 2021: Mechanism of exudate effusion? Inflammatory increased in vascular permeability of membrane (increased flow of interstitial edema into pleural space) Unique cause of both transudative & exudative effusions? PE Classic Pleural Effusion findings? Decreased breath sounds Dullness to percussion Decreased tactile fremitus Tx? Chest tube Chylothorax = lymph in the pleural space Pathophys? Obstruction of thoracic duct or injury to the thoracic duct Pleural fluid findings? High Triglycerides Holosystolic murmur heard best at the apex with radiation to the axilla in a patient with a recent MI. → mitral regurg 2/2 papillary muscle rupture Dx? Echo Why widely split S2? Aortic valve is closing earlier (LV is emptying into both aorta & LA) Maneuvers that increase intensity Increase preload (putting more blood in that can be regurgitated) Increase afterload Decubitus ulcers RF? Elderly Paraplegic Fecal/urinary incontinence Poor nutrition Staging Stage 1 = non-blanchable erythema Tx? Repositioning q2hrs Stage 2 = loss of epidermis + partial loss of dermis Tx? Occlusive dressing superficial Stage 3 = involves entire dermis, extending to subQ fat Does NOT extend past fascia Tx? Surgical debridement Stage 4 = muscle/tendon/bose exposed Tx? Surgical debridement General tx strategies? Repositioning + good nutritional support Marjolin’s ulcer = non-healing wound that is actually squamous cell carcinoma T1DM Pathophys? Autoimmune destruction of pancreas Ab? anti-GAD 65 (glutamic acid decarboxylase) anti-IA2 (islet tyrosine phosphatase 2) Islet cell autoantibodies Insulin autoantibodies Dx? A1c > 6.5% (twice) Fasting BG >= 126 (twice) Oral glucose tolerance test >= 200 (twice) Sxs of DM + random glucose > 200 Tx? Long-acting insulin + mealtime insulin Long-acting Glargine Detemir Rapid-acting Lispro Aspart Glulisine 3 HY complications Nephropathy Retinopathy & cataracts Neuropathy Chronic DM care A1c q3 months Foot exam annually Eye exam annually Microalbumin:Cr ratio annually Nephroprotection in DM? ACE-I GI bleed algorithm 1st step: ABCs + 2 large-bore IVs + IVFs 2nd step: NG lavage Clear fluid → go deeper Blood → UGIB → upper endoscopy Bilious fluid → have ruled out UGIB → proceed to colonoscopy See source → intervene as needed See nothing → CT angiography for large bleed Tagged RBC scan for smaller bleed Antiplatelet Pharmacology Aspirin Mechanism? Irreversibly inhibits COX-1 and COX-2 Clopidogrel/ticlopidine = P2Y12 (ADP receptor) blockers Mechanism? Inhibit platelet activation Abciximab/eptifibatide/tirofiban = GpIIbIIIa receptor blockers Mechanism? Inhibit platelet aggregation Ristocetin cofactor assay Issues with adhesion step → abnormal result Abnormal ristocetin cofactor assays: Von Willebrand disease Bernard Soulier disease Normal ristocetin cofactor assay: Glanzmann Thrombasthenia Von Willebrand disease effects on PTT? Increased Pathophys? vWF is a protecting group for Factor 8. Treatment of VWD? Desmopressin Mechanism? Increases release of vWF from Weibel-Palade bodies of endothelial cells Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH HSV1 vs HSV2. Oral herpes → HSV1 Genital herpes → HSV2 Dx? PCR (most up-to-date) Tzanck smear (outdated, not very sensitive, nonspecific) → intranuclear inclusions Brain area affected by HSV encephalitis? Temporal lobes CSF findings in HSV encephalitis? RBCs******* Tx herpes encephalitis? Acyclovir AE? Crystal nephropathy Can’t see, can’t pee, can’t climb a tree. → reactive arthritis HLA? B27 Classic bug? Chlamydia Tx? steroids Need abx? Only if ongoing infection Can’t see, can’t pee, can’t hear a bee → Alport syndrome Inheritance? X-linked dominant Tx of NG & CT NG → treat empirically for both → ceftriaxone + azithro/doxy CT → azithro/doxy Hypovolemic Septic Neurogenic Cardiogenic CO low PCWP low SVR high*** CO high PCWP normal SVR low Tx? norepi CO low SVR low CO low PCWP high*** SVR high*** Tx anaphylactic shock? epinephrine Melanomas ABCDE A = asymmetry B = irregular borders C = color variation D = diameter > 6 mm E = evolving Dx? Full-thickness biopsy Excisional for small lesions Punch for larger lesions Most important prognostic factor → Breslow depth DM pharmacology Lactic acidosis → metformin Decreases hepatic gluconeogenesis → metformin Hold before CT w/ contrast → metformin Weight gain → sulfonylureas & TZDs (-glitizones) Diarrhea → acarbose & migliton Inhibits disaccharidases (can’t reabsorb disaccharides) Recurrent UTIs → SGLT-2 inhibitors Weight loss → GLP-1 agonists (e.g. liraglutide, exenatide) & DPP4 inhibitors (-gliptins) Contraindicated in pt with HF → TZDs PPAR-gamma receptor found in kidney → water retention Contraindication in pt with MTC → GLP-1 agonists Biggest risk of hypoglycemia? Sulfonylureas RF esophageal adenocarcinoma Barrett’s esophagus RF esophageal squamous cell carcinoma Smoking Drinking Achalasia Location esophageal adenocarcinoma? Lower 1/3 Location esophageal squamous cell carcinoma? Upper 2/3 MC US? Adenocarcinoma MC worldwide? Squamous cell carcinoma Presentation? Dysphagia to solids → dysphagia to liquids Dx? EGD Staging? CT scan or esophageal US Factor V Leiden Pathophys? Resistance to protein C Dx? Activated Protein C resistance assay Patient needs super large doses of heparin to record any changes in PTT → AT-III deficiency Recall that heparin is a AT-III activator 35 yo with a hypercoagulable disorder that does not correct with mixing studies. → antiphospholipid antibody disorder Anaphylaxis in a patient with a long history of Hemophilia A → Ab against factor 8 that cause type 1 HSR with transfusion Hx of hemophilia, diagnosed 5 years ago. Before you would give them factor 8 concentrate and PTT would normalize. Now they’re requirizing larger doses of factor 8 to normalize PTT. → inhibitor formation (antibodies against clotting factors) Skin necrosis with Warfarin → protein C/S deficiency Prothrombin G20210 mutation → overproduction of factor II Rash in dermatomal distribution → VZV infection Contraindications to VZV vaccination? Pregnant woman Kid < 1 year Severe immunosuppression (e.g. HIV with CD4 < 200) Tx? Acyclovir If resistant, foscarnet Tzanck smear findings? Intranuclear inclusions Shingles vaccination guidelines? Adults over 60 #1 cause of ESRD in the US → DM nephropathy Histology? Kimmelsteil-Wilson nodules #2 cause of ESRD in the US → hypertensive nephropathy Pt with BP 240/150. How fast should you lower BP? 25% in first 24 hrs Drugs for hypertensive emergencies? Nicardipine Clevidipine Nitroprusside AE? Cyanide poisoning Tx? Amyl nitrate + thiosulfate OR hydroxocobalamin Labelol Renal protective medications in patients with DKD or hypertensive nephropathy? ACE-I Anemia + Cranial Nerve deficits + Thick bones + Carbonic Anhydrase 2 deficiency + Increased TRAP + Increased Alkaline Phosphatase. → osteopetrosis Pathophys? Carbonic anhydrase is defective → osteoclasts cannot produce acid to resorb bone Tx? IFN-gamma Osteoclasts are a specialized macrophage IFN-gamma is an activator of macrophages Clinical diagnostic criteria for Chronic Bronchitis Diagnostic criteria? 2 years 3 months/year of chronic cough PFT findings FEV1 low FEV1/FVC ratio low RV high TLC high Which PFT market can differentiate CB from emphysema? DLCO DLCO normal → CB DLCO low → emphysema ****** Tx acute exacerbation? Abx + bronchodilators + corticosteroids (“ABCs”) Prevention? Stop smoking! Afib #1 RF? Mitral stenosis #1 RF MS? Rheumatic fever #1 RF CAD and AAA: smoking #1 RF stroke and aortic dissection: HTN MC arrhythmia in hyperthyroidism → Afib MC site of ectopic foci in Afib → pulmonary veins EKG findings? “Irregularly irregular” + no P waves Location of emboli formation? LA appendage Who should be cardioverted back to sinus rhythm? New onset (<48 hrs) Afib Anticoagulated for 3 weeks + TEE negative for clot Afib that’s refractory to medical therapy Afib & HDUS Q on T phenomenon? Depolarization during T wave (repolarization) can cause QT prolongation → Torsades → death Prevention? SYNCHRONIZED cardioversion Tx? Rate control Beta blockers ND-CCB (e.g. verapamil, diltiazem) Rhythmic control Amiodarone Reducing stroke risk in Afib? Anticoagulation for CHA2DS2VASc score >= 2 Anticoagulation options Valvular cause (e.g. MS) → warfarin Any other cause → warfarin or NOAC (apixiban) Reversal of AC Warfarin → Vit K, four-factor PCC Heparin → protamine sulfate Dabigatran → idarucizumab Crusty, scaly, ulcerating lesion with heaped up borders → squamous cell carcinoma Classic location? Below Lower lip Precursor lesion? Actinic keratosis What if it arises in a scar or chronic wound? Marjolin ulcer Hypothermia + hypercapnia + non pitting edema + hyponatremia + HR of 35 + hypotension in a patient with a history of papillary thyroid cancer → myxedema coma Tx? Levothyroxine + steroids Lab findings? TSH high T3/T4 low LDL high Acute onset “dermatologic” breakout in a patient with a recent history of weight loss and epigastric pain. → Leser–Trélat sign associated with visceral malignancy pancreatic cancer Lymph node associations Supraclavicular → Virchow’s node Periumbilical → Sister Mary Joseph What are mets to the ovaries called? Kruckenberg tumor Classic bug associated with gastric cancer? H. pylori (MALToma) Classic histological finding in the diffuse type of gastric cancer? Signet ring cells RBCs without central pallor + elevated MCHC + anemia. → hereditary spherocytosis Inheritance? AD Pathophys? Deficiency of spectrin, ankyrin, or band 3.2 Intravascular or extravascular hemolysis? Extravascular (RBCs bound by IgG, attacked by splenic macrophages) Dx? Osmotic fragility test Eosin-5-maleimide Acidified glycerol lysis test Tx? Splenectomy Post-splenectomy preventative care? Strep pneumo Hinflue vaccine Neisseria Septic shock Hemodynamic parameters CO high SVR low PCWP normal MvO2 high Tx? IVF + norepi + broad-spectrum abx (cover MRSA + Pseudomonas) E.g. vanc + pip-tazo E.g
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CT4-LECTURE 1- JAN 2025 OBJECTIVES Developmental Anatomy (Embryology): • Outline the stages of human growth and development, focusing on dental anatomy and root morphology. • Correlate developmental processes with hard and soft tissue formation in the oral cavity. Microscopic Anatomy: • Classify cells (cytology) and tissues (histology) based on their structure and specialization. • Evaluate the role of microscopic structures in maintaining oral health. GROSS Anatomy • Identify anatomical landmarks of the oral head and neck, including the TMJ, circulatory system, glands, and nervous system. • Describe the structures visible to the naked eye and their clinical relevance. Physiology: • Explain the functions of body systems and their integration in oral health. • Analyze the physiological processes affecting the oral cavity. 1/16/2025 3 Mitosis Meiosis One cell division Two cell division Produces two daughter cells Produces Four daughter cells Produces diploid cells Produces haploid cells Daughter cells are genetically identical Daughter cells are non- identical Produces body cells Produces sex cells • Mitosis and meiosis are both types of cell division. • Mitosis is how new body cells are produced, whereas meiosis is used to produce gametes (i.e. sperm and egg cells). first week Spermatozoa + Oocyte = Zygote (12-24hrs.) Cell division via mitosis = Cleavage 1st solid ball called Morulla Inside Morulla secretion of fluids becomes blastocyte (5days) Blastocyte has 2 regeions Trophoblast(peripheral cells) & Embryoblast layer(inner mass) CLINICAL CONSIDERATIONS FOR PREIMPLANTATION PERIOD •If any disturbances occur in meiosis during fertilization, major congenital malformations result from the chromosomal abnormality in around 10% of cases. •A syndrome is a group of specific signs and symptoms. PREIMPLANTATION PERIOD • After a week of cleavage, the blastocyst consists of a layer of peripheral cells, the trophoblast layer, and a small inner mass of embryonic cells or embryoblast layer. • The trophoblast layer later gives rise to important prenatal support tissue while the embryoblast layer later gives rise to the embryo. SECOND WEEK • A bilaminar embryonic disc • The superior epiblast layer is composed of high columnar cells. • The inferior hypoblast layer is composed of small cuboidal cells. THIRD WEEK • Primitive streak (rod shaped thickening) forms a bilateral symmetry within the bilaminar embryonic disc. • Some cells from the epiblast layer move or migrate toward the hypoblast layer only in the area of the primitive streak and become • Mesoderm, an embryonic connective tissue, and embryonic endoderm. END OF THIRD WEEK • With three layers present, the bilaminar disc has thickened into a trilaminar embryonic disc. • The epiblast layer is now considered ectoderm. • 3 germ layers • Ectoderm-becomes skin, nervous system, and neural crest cells. • Mesoderm-Becomes muscles, bones, blood, and connective tissues. • Endoderm-Forms internal organs like the digestive and respiratory systems. 1/16/2025 10 Neural Crest Cells & Mesenchymal Transition(dental tissue) • Neural crest cells are derived from the ectoderm during neurulation (around weeks 3-4). • NCC migrate and undergo epithelial-to-mesenchymal transition (EMT), becoming highly migratory mesenchymal cells. • They contribute to the formation of facial bones, cartilage, peripheral nerves, and parts of the heart. 1/16/2025 11 Embryonic Period: Physiological Process(changes in structure &function) • INDUCE, PROLIFERATE, DIFFERENTIATE AND MORPH, DON’T WAIT! MATURE AND GROW, IT’S YOUR FATE!" 1. Induction The process where one group of cells influences another to differentiate into a specific tissue or organ. 2. Proliferation Rapid cell division, increasing the number of cells. 3. Differentiation(Cyto, Histo, Morpho) Cells specialize to perform specific functions. 4. Morphogenesis The development of the overall shape and structure of tissues and organs. 5. Maturation The final stage where tissues and organs reach their fully functional form. 1/16/2025 12 Facial Development  The facial development that starts in the fourth week of the embryonic period will be completed later in the twelfth week within the fetal period.  At the fourth week, the developing brain, face, and heart are noted. 1/16/2025 13 • All three embryonic layers are involved in facial development: the ectoderm, mesoderm, and endoderm. • The upper part of the face is derived from the frontonasal process, the midface from the maxillary processes, and the lower from the mandibular processes. Early development of the face is also dominated by the proliferation and migration of ectomesenchyme, derived from neural crest cells (NCCs). Facial Development 1/16/2025 14 Stomodeum and Oral Cavity Formation With this disintegration of the membrane, the primitive mouth is increased in depth and enlarges in width across the surface of the midface. Nose and Paranasal Sinus Formation Apparatus Formation  First branchial/ pharyngeal arch also known as the mandibular arch and its associated tissue, includes Meckel cartilage.  Supplied by Trigeminal nerves Apparatus Formation  Second branchial/pharyngeal arch, which is also known as the hyoid arch, is cartilage like that of the mandibular arch, Reichert cartilage. Apparatus Formation  Third branchial/ pharyngeal arch  Has an unnamed cartilage associa ted with it. This cartilage will be responsible for forming parts of the hyoid bone. Apparatus Formation  Both the fourth and the sixth branchial /pharyngeal arch also have unnamed cartilage associated with them, they fuse and form most of the laryngeal cartilages. 1/16/2025 20 TOOTH DEVELOPMENT: INITIATION STAGE Stages of Tooth Development: I Bought Candy Bars After Midnight." I → Initiation Bought → Bud Candy → Cap Bars → Bell After → Apposition Midnight → Maturation 1/16/2025 23 1. Initiation Stage (Week 6-7): • Dental placodes form as localized thickenings of oral ectoderm. • Interaction with neural crest cells induces the formation of the tooth germ. 2. Bud Stage (Week 8): • The enamel organ invaginates into the underlying mesenchyme, creating a tooth bud. 3. Cap Stage (Week 9-10): • The enamel organ forms a cap-like structure over the dental papilla. 4. Bell Stage (Week 11-12): • Cells differentiate into ameloblasts (enamel-forming cells) and odontoblasts (dentin-forming cells). 5. Apposition and Maturation: • Enamel, dentin, and cementum are laid down and mineralized. 1/16/2025 25 • Dental Epithelium → Enamel Organ Enamel organ arises from the dental epithelium and forms ameloblasts, the cells responsible for producing enamel, the hardest substance in the body. Dental Mesenchyme → Dental Papilla Dental papilla forms from the mesenchyme and gives rise to: • Dentin -Odontoblasts: Cells that produce dentin (the layer beneath enamel). • Pulp: The soft, living core of the tooth, containing nerves and blood vessels. • Root Dentin: The dentin in the root of the tooth. Dental Follicle • Surrounds the developing tooth and forms: • Cementum: A calcified tissue covering the root of the tooth, anchoring it to the jaw. • Periodontal Ligament: Connective tissue fibers that hold the tooth in its socket and absorb chewing forces. Teeth w e a r c a n b e t r e a t e d A t t r i t i o n Abrasion Abfraction E r o s i o n Hunter-Schreger bands (HSB). • Hunter-Schreger bands (HSB): • Dark and light bands due to curvature or bends of the rods. • increasing the enamel’s strength. • Near the cusps or incisal ridges, where the enamel is the thickest Celiac Disease ˜ Dental enamel problems stemming from celiac disease involve permanent dentition and include tooth discoloration—white, yellow, or brown spots on the teeth—poor enamel formation, pitting or banding of teeth, and mottled or translucent-looking teeth. ˜ The imperfections are symmetrical and often appear on the incisors and molars. ˜ Tooth defects that result from celiac disease may resemble those caused by too much fluoride or a maternal or early childhood illness 1/16/2025 29 ROOT DEVELOPMENT  The process of root development takes place long after the crown is completely shaped, and the tooth is starting to erupt into the oral cavity.  The structure responsible for root development is the cervical loop.  The cervical loop is the most cervical part of the enamel organ, a bilayer rim that consists of only inner enamel epithelium (IEE) and outer enamel epithelium (OEE). ROOT DEVELOPMENT  To form the root region, the cervical loop begins to grow deeper into the surrounding ectomesenchyme of the dental sac, elongating and moving away from the newly completed crown area to enclose more of the dental papilla tissue, forming the Hertwig epithelial root sheath (HERS). Thus, HERS will determine if the root will be curved or straight, short or long as well as single or multiple. 1/16/2025 33 • Cervical Loop Formation ▪ The cervical loop, located at the junction of the enamel organ and the crown, elongates to form Hertwig’s Epithelial Root Sheath (HERS). ▪ HERS determines the shape, length, and number of roots. • Root Dentin Formation ▪ Inner cells of HERS induce adjacent dental papilla cells to differentiate into odontoblasts, which form root dentin. ▪ Once dentin is deposited, HERS disintegrates. • Epithelial Rests of Malassez ▪ After HERS disintegrates, remnants form clusters called epithelial rests of Malassez in the periodontal ligament. ▪ These remnants can sometimes form cysts later in life. PRIMARY DENTITION PROPERTIES  The actual dates are not as important as the eruption sequence, because there can be a great deal of variation in the actual dates of eruption.  However, the sequence tends to be uniform. Enamel Histology • Enamel tufts: Hypomineralized, Located at the dentino-enamel junction and filled with organic material. Forms between groups of enamel rods at the dentino-enamel junction. • Enamel lamellae are partially mineralized vertical sheets of enamel matrix that extend from the DEJ near the tooth’s cervix to the outer occlusal surface. Transverse section of enamel showing enamel tufts (white arrow) and enamel lamella (black arrow). Dentin Matrix Formation DENTINOGENESIS LPROCESS o$ CREATING DENTIN PRIMARY TEETH _ 14th WEEK of FETAL DEVELOPMENT PERMANENT TEETH L 3 MONTHS AFTER -PROCESS HAPPENS SLOWLY PERFORMED by ODONTOBLASTS —OUTSIDE INWARDS - BEGINS with MANTLE DENTIN ODONTOBLASTS -PREDENTIN -SOFT ORGANIC MATRIX -PROTEINS FIBROBLASTS -KORFF'S FIBERS -THICK COLLAGEN FIBERS -FRAMEWORK of DENTINOGENESIS 1/16/2025 39 Principal Fibers Protect, Gingival Fibers Guard." •Principal → Protection and anchorage of the tooth. •Gingival → Guard and stabilize gingiva. 1/16/2025 40 Principle Fibers "All Hungry Octopuses Appreciate Ice cream!" •All → Alveolar Crest •Hungry → Horizontal •Octopuses → Oblique •Appreciate → Apical •Ice cream → Interradicular 1/16/2025 41 Gingival Fiber : "Dentists Always Care Deeply for Teeth!" •Dentogingival •Alveologingival •Circular •Dentoperiosteal •Transseptal 1/16/2025 42 Primary (Deciduous) Teeth Eruption "Children Like Fruit Candy More" •C → Central Incisors •L → Lateral Incisors •F → First Molars •C → Canines •M → Second Molars CELL ORGANELLES SKIN ANATOMY COME, LET'S GET SOME BREAD" C ORNEUM (OUTER), L UCIDUM, G RANULOSUM, S PINOSUM, B ASALE. • Corneum - tough and protective. • Lucidum - clear layer (found only in thick skin like palms/soles). • Granulosum - cells with granules for keratinization. • Spinosum - "spiny" cells, providing strength and flexibility. • Basale - base layer where cell division happens. 1/16/2025 45 1/16/2025 46 Tooth Designation ∙ Commonly used in orthodontics, is the Palmer Notation Method, also known as the Military Tooth Numbering System. ∙ In this system, the teeth are designated from each other with a right-angle symbol indicating the quadrants and arch, with the tooth number placed inside. 1/16/2025 47 Mixed Dentition Period ∙ The mixed dentition period follows the primary dentition period. ∙ This period occurs between approximately 6 and 12 years of age. ∙ Both primary and permanent teeth are present during this transitional stage. ∙ The final dentition period is the permanent dentition period. ∙ This period begins with shedding of the last primary tooth. 1/16/2025 48 General Dental Terms •Each dental arch can be further divided into two quadrants, with four quadrants in the entire oral cavity. • The correct sequence of words when describing an individual tooth using a D-A-Q-T System is based on the tooth within its quadrant: D for dentition, A for arch, Q for quadrant, and T for tooth type. • Sextants: three parts according to the relationship to the midline: right posterior sextant, anterior sextant, and left posterior sextant. 1/16/2025 49 Root Axis Line (RAL) ∙ Root axis line (RAL), which is an imaginary line representing the long axis of a tooth, drawn in a way to bisect the root (and thus the crown) in the cervical area into two halves. 1/16/2025 50 Restorations: Biologic Width ∙ Biologic width is the distance established by the junctional epithelium and lamina propria attachment to the root surface of a tooth. ∙ This distance is important to consider when fabricating dental restorations, because they must respect the natural architecture of the gingival attachment if harmful consequences are to be avoided. ∙ Assessment for biologic width can be made clinically by measuring the distance between the bone and the restoration margin using a periodontal probe. 1/16/2025 51 PRIMARY DENTITION 1/16/2025 52 1/16/2025 53 Eruption 1/16/2025 54 1/16/2025 55 1/16/2025 56 Differences-(Enamel depth/pulp) 1/16/2025 57 Differences: Roots 1/16/2025 58 Importance of Primary teeth - PRIMATE Space 1/16/2025 59 Leeway Space 1/16/2025 Primary Occlusion 60 •Majority of children have Mesial step between distal of Primary 2nd molars. Mandibular 2nd molars are situated mesially than maxillary. •A smaller but still large group of children exhibit a flush terminal plane. The distal surfaces of the primary 2nd molars are even with each other. •A still smaller minority have a distal step. The mandibular 2nd molars are situated more distally than their maxillary counterparts. Thus, they form a distal step. 1/16/2025 Anatomy of Primary teeth 61 Incisors: resemble the outline of permanent counterpart except Primary do not have mamelons on the incisal ridge and there are no pits on the lingual surface. 1/16/2025 Primary Canines 62 Canines- resemble the outline of their permanent counterparts. The maxillary canine has a sharp cusp and appears especially wide and short. Maxillary Central and Lateral Incisors Central Incisors: • Larger overall; they are the widest teeth mesiodistally in the anterior maxillary arch. • Crown is more symmetrical and fan (mesiodistally wider compared to incisocervical length). • Lingual fossa is less pronounced. • Cingulum is well-developed and centered. • Root is shorter and more conical, with a blunt apex. • Rarely exhibit significant variation. Lateral Incisors: • Smaller and narrower mesiodistally than the central incisors. • Crown is less symmetrical and more rounded. • Lingual fossa is deeper, with more pronounced marginal ridges. • Cingulum is narrower and often slightly off-center to the distal. • Root is longer and thinner, with a more pointed apex. • Frequently display developmental variations (e.g., peg-shaped lateral incisors, congenitally missing). 1/16/2025 66 1/16/2025 67 1/16/2025 68 1/16/2025 69 CLASSIC TRAITS ➢ From the occlusal view, molar crowns taper from the buccal to the lingual EXCEPT for maxillary 1st molars. ➢ From the occlusal view, molar crowns taper distally; this allows more of the occlusal surface to be visible from the distal aspect than the mesial. ➢Maxillary molars have 3 roots: MB, DB, and lingual (palatal). The lingual root is usually the longest and the DB is the shortest. ➢ Mandibular molars have 2 roots: a long mesial root and a slightly shorter distal root. ➢ The root furcation on mandibular molars is close to the cervical line, making the root trunk shorter than on the maxillary molars. MAJOR AND MINOR CUSPS ➢In general, each cusp is formed from its own lobe. ➢Major cusps are large and well developed. ➢Minor cusps are less developed and have smaller proportions. They are less functional than the major cusps and may not always be present. ➢Supplementary cusp is very small and completely afunctional. They are rarely present. 1/16/2025 72 ➢First molars are the most highly developed and largest of the molars and more likely to have major, minor and supplementary cusps. ➢Both the 1st and 2nd maxillary molars have 4 major cusps but only 2 are visible from the buccal view. ➢The longest of the 4 major cusps are the ML, followed by the MB, DB, and the shortest DL (if present). 1/16/2025 73 • Molars (general: crowns larger, squarer, bear more cusps than any other tooth class, have multiple roots, 3rd molars sometimes mistaken for premolars) • Generally speaking, the maxilla molars go from largest to smallest (1st molar to 3rd molar) in size and morphology. The crowns generally have 4 cusps. • The 1st molar has three roots (two buccal and one lingual, which when seen from the buccal position the lingual root comes into view in the middle of the two buccal roots). The occlusal surface is described as a rhomboid in shape with 4 distinctive cusps. • Oblique ridge max molars only and transverse ridge one on max 2 on mandibular. • The 2nd molar has three roots but the two buccal roots are nearly parallel with each other and is described as heart shape in the occlusal view. • The 3rd molar has three roots present but the two buccal roots are often fused, and the outline of the occlusal surface is also described as a heart shape. The 3rd molar also shows greater developmental variation than either the 1st or • 3rd molars are often the tooth that is congenitally missing. All roots of the molars angle distally with respect to the major crown axes (White & Folkens 2005: 152). 1/16/2025 74 1/16/2025 75 Joint Movement ˜ Two basic types of movement of the mandible are performed by the TMJ and its associated muscles of mastication: ˜ a gliding movement and ˜ a rotational movement. 1/16/2025 76 • The muscles of mastication include the • Temporalis, • And Masseter, • Pterygoid muscles, medial and lateral. • These muscles are involved in mastication using these two movements. 1/16/2025 77 1/16/2025 78 TMD: Acute Episode • Trismus or the inability to normally open the mouth. • When the patient tries to close and elevate the mandible, the condylar heads cannot move posteriorly because both the bony relationships prevent this, and the muscles have become spastic. 1/16/2025 79 Overjet • Overjet is measured in millimeters with the tip of a periodontal probe, once a patient is in CO. • The probe is placed at 90°or at a right angle to the labial surface of a mandibular incisor at the base of the incisal ridge of a maxillary incisor. 1/16/2025 80 • Overbite is measured in millimeters with the tip of a periodontal probe after a patient is placed in CO. • The probe is placed on the incisal edge of the maxillary incisor at 90º or at a right angle to the mandibular incisor. • When the reverse is the case and the mandibular arch and its incisors extends beyond the maxillary arch and its incisors, it is causes an underbite. 1/16/2025 81 Lymph Nodes • The lymph flows (arrows) into the lymph node through many afferent vessels. (A is first comes in) • On one side of the node is a depression, or hilus, where the lymph through fewer vessels, or even a single efferent vessel. (E is Exit) • Primary or Secondary. • Region drains into primary nodes. • Primary nodes, in turn, drain into secondary nodes (or central nodes). Lymphatics: General Drainage pattern of body Right jugular trunk Left jugular trunk Enters venous system near junction of left subclavian vein and left internal jugular Thoracic duct Left side of head, neck, thorax, entire abdomen, pelvis, lower extremities Enters venous system near junction of right subclavian vein and right internal jugular Right side of head, neck, thorax *Lymphatic vessels are small and directly drain tissues and connect lymph nodes. *Lymphatic ducts are much larger, receive lymph from many lymphatic vessels, and drain into the venous system. 1/16/2025 83 Superficial Lymph Nodes of the Head (five categories) 1. Facial; lie along facial vein. 2 Superficial Parotid; superficial to parotid gland. 3. Anterior Auricular; anterior to external auditory meatus. 4. Posterior Auricular; posterior to external auditory meatus. 5. Occipital; lie in the occipital region. *Tissue drainage: buccal mucosa, skin of zygomatic and infraorbital regions, scalp, external ear, lacrimal gland Deep Lymph Nodes of Head (two categories) 1. Deep Parotid; lie deep in the parotid gland, superficial to the masseter muscle 2. Retropharyngeal; posterior to the pharynx at the level of the atlas (first cervical vertebrae). *Tissue drainage: parotid gland, paranasal sinuses, hard and soft palate, middle ear Superficial Cervical Lymph Nodes (4 categories) 1. Submental; inferior to the chin in the submental space. 2. Submandibular; along the inferior border of the mandible, superficial to the submandibular salivary gland 3. External Jugular; along the external jugular vein, superficial to the sternocleidomastoid muscle. 4. Anterior Jugular; along the anterior jugular vein, anterior to the sternocleidomastoid muscle. Tissue drainage: 1.Submental and submandibular; teeth and related tissues, apex and body of tongue, anterior hard palate, floor of mouth, lips, chin, sub- mandibular and sublingual glands, cheeks. 2. External and anterior jugular; superficial tissues in the anterior and posterior triangles. Deep Cervical Lymph Nodes (2 categories) 1. Superior Deep Cervical; lie along internal jugular vein, superior to the omohyoid muscle. *Jugulo-digastric- becomes enlarged when a palatine tonsil or the pharynx is involved in infection. 2. Inferior Deep Cervical; lie along internal jugular vein, inferior to the omohyoid muscle. *Jugulo-omohyoid-drains the submental region and base of the tongue. Additional Deep Cervical Nodes 1. Accessory; lie along accessory nerve 2. Subclavicular; lie along clavicle. *Tissue drainage: mostly secondary nodes 1/16/2025 88 Sequence of lymph nodes draining various tissues Most of face, scalp, ear, orbit, sinuses, nasal cavities Most maxillary and mandibular teeth and associated tissues, apex and body of tongue, floor of mouth, sublingual and submandibular glands, lips Maxillary third molars and associated tissues, base of tongue, pharynx, tonsils Tissue Primary nodes Secondary nodes Submental and submandibular nodes Facial, anterior auricular, retroauricular, occipital superficial and deep parotid, and retropharyngeal nodes Submandibular, deep cervical nodes Retropharyngeal, deep cervical nodes Neck and cervical viscera Superficial and deep cervical nodes Right jugular trunk Right subclavian vein Left jugular trunk Left subclavian vein Thoracic duct Endocrine-secrete substance into blood, examples-adrenal gland pituitary gland, thyroid gland Exocrine-secretes substance through a duct leading outside the body (digestive tract, skin). Examples- sweat glands, salivary glands, mucous glands, pancreas Where are the salivary ducts located intraorally? Parotid (Stensen) duct opening > Parotid Papilla. Submandibular (Wharton) duct opening Sublingual Caruncle. Plica Sublingualis Sublingual Caruncle Parotid Papilla Sublingual duct opening - Via Duct of Bartholin → Sublingual Caruncle. OR Via smaller Ducts of Rivinus > Plica Sublingualis. Thyroid and Parathyroid glands (endocrine) Thyroid: 1.Located inferior to the larynx along the sides of the trachea. 2. Has 2 lobes, connected by an isthmus. 3. Secrets thyroxin which influences metabolic rate Parathyroid: 1. Four small glands located on the posterior aspect of the thyroid gland. 2. Secrete parathyroid hormone, which regulates calcium and phosphate levels. Thymus 1. Located in the thorax and anterior region of the base of the neck, deep to the sternum and sternohyoid and sternothyroid muscles. 2. Involved in the maturation of T-cell lymphocytes 3. Shrinks in size with age Teeth and Periodontium Commonly Involved in Clinical Presentations of Abscesses and Fistulae 1. Abscess in maxillary vestibule or palate, 2. Penetration of nasal floor 3. Abscess in nasolabial skin region 4. Penetration into maxillary sinus 5. Abscess in buccal skin region 6. Abscess in mandibular vestibule 7. Abscess in submental skin region 8. Abscess in sublingual region → Any maxillary tooth (except maxillary canines for palate) • Maxillary central incisors → Maxillary canine → Maxillary molars • Maxillary or mandibular molars → Any mandibular tooth • Mandibular incisors → Mandibular molars with short roots superior to mylohyoid Teeth/Periodontium and Spaces Possibly Involved With Various Clinical Presentations of Cellulitus Location Space Involved Teeth/Periodontium Involved Infraorbital region Zygomatic region Buccal region Buccal space Maxillary premolars, and maxillary and mandibular molars Submental region Submental space Anterior mandibular teeth Submandibular region (unilateral) Submandibular space Posterior mandibular teeth Submandibular region (bilateral) Submental, sublingual Submandibular spaces Spread of mandibular dental infection Lateral cervical region Parapharyngeal space Spread of mandibular dental infection 4 major routes 1. Spread to the paranasal sinuses 2. Spread by the vascular system 3. Spread by the Lymphatic system 4. Spread by spaces Bacteria can spread through the blood from infected dental tissues to other areas. (1) An infected thrombus (blood clot) can travel as an embolus and spread infection. (2) Transient bacteremia (presence of bacteria in the blood) can occur during dental treatment. For example, a needle advanced too far during an attempt at PSA block can penetrate the pterygoid venous plexus after being inserted through infected tissue (needle track contamination). (3) The pterygoid venous plexus drains the dental tissues and communicates with the cavernous sinus via the inferior ophthalmic vein. (4) Infections in dental tissues can initiate an inflammatory response, which can result in thrombus formation, blood stasis, and increased extravascular pressure. (5) Veins in the head do not have valves, so backflow of blood carrying pathogens into the cavernous sinus can occur. Cranial Nerve Names & Function Names: "Only One Of The Two Athletes Felt Very Good, Victorious, And Healthy" Function: "Some Say Marry Money, But My Brother Says Big Brains Matter Most" 1. Only (Some) = Olfactory (S) 2. One (Say) = Optic (S) 3. Of (Marry) = Oculomotor (M) 4. The (Money) = Trochlear (M) 5. Two (But) = Trigeminal (B) 6. Athletes (My) = Abducens (M) 7. Felt (Brother) = Facial (B) 8. Very (Says) = Vestibulocochlear (S) 9. Good (Big) = Glossopharyngeal (B) 10. Victorious (Brains) = Vagus (B) 11. And (Matter) = Accessory (M) 12. Healthy (Most) = Hypoglossal (M) Blood Branching of Carotid Arteries from Aorta Common Carotid Arteries To upper limb Subclavian artery Subclavian artery Brachiocephalic trunk Aortic arch From heart To thorax, abdomen, legs Blood Flow LAB RAT LEFT ATRIUM=BICUSPID RIGHT ATRIUM= TRICUSPID Right ABC'S THE AORTIC ARCH GIVES RISE TO -BRACIOCHEPHALIC TRUNK COMMON COROTID ARTERY SUBCLAVIAN ARTERY Left: carotid & subclavian LUNG BAGHT PULMONARY ARTERY PILNONARY WEIN TRICUSPID VALVE L E F T LUNG S U P. VENA CAVA AORTIC ARCH LEFT PULMONARY ARTERY RIGHT ATRIUM PALMONART PULMONARY ARTERY LEFT ATRIUM PULMONARY VINN PELNONARY WEIN LEFT VENTRICLE RIGHT VENTRICLE B L O O D FLOW THROUGH THE HEART MITRAL VALVE I N 2 MINUTES INF. VENA CAVA Foramina, Canals, etc. Traversed by Various Blood Vessels Vertebral artery- transverse foramina in cervical vertebrae, foramen magnum Internal carotid artery-carotid canal, foramen lacerum, groove for the internal carotid artery Maxillary artery-terminates in pterygoid fossa Posterior superior alveolar artery-posterior superior alveolar foramina Infraorbital artery-inferior orbital fissure, infraorbital groove, infraorbital canal, infraorbital foramen Sphenopalatine artery-sphenopalatine foramen, incisive canal, incisive foramen Descending palatine artery-divides into greater and lesser palatine arteries which traverse same named foramina Inferior alveolar artery-mandibular foramen, mandibular canal Mental artery-mental foramen Mylohyoid artery-mylohyoid groove Ophthalmic artery-optic canal Anterior and posterior ethmoid arteries-anterior and posterior ethmoid foramina Middle menningeal artery-foramen spinosum Internal jugular-jugular foramen EXTERNAL CAROTID ARTERY LINGUAL- → SUPRAHYOID → DORSAL LINGUAL → SUBLINGUAL → DEEP LINGUAL - TONGUE - SOFT PALATE - SUBLINGUAL SALIVARY GLAND - MUSCLES ATTACHED to HYOID ARTERIAL SUPPLY: FACIAL- - MAXILLARY (3 PARTS) → ASCENDING MANDIBULAR PART: PALATINE → INFERIOR ALVEOLAR → TONSILAR - LOWER TEETH - CHEEK → SUBMENTAL - MYLOHYOID → GLANDULAR BRANCHES MUSCULAR PART: → SUPERIOR LABIAL → MASSETERIC → - MASSETER → INFERIOR LABIAL → DEEP TEMPORAL → - TEMPORALIS PTERYGOPALATINE PART: - SOFT PALATE - PALATINE TONSIL - ROOT of TONGUE - SUBMANDIBULAR & SUBLINGUAL SALIVARY GLANDS - LIPS → DESCENDING - HARD PALATE PALATINE - SOFT PALATE → POSTERIOR SUPERIOR ALVEOLAR - PALATINE TONSIL - UPPER PREMOLAR & M O L A R S → INFRAORBITAL → - UPPER TEETH It gives off six branches before it divides into two terminating branches. They are in ascending order: • superior thyroid, • ascending pharyngeal, • lingual, • facial, • occipital, and • posterior auricular. The two terminating branches are the • maxillary and • superficial temporal arteries. Lingual artery supplies the tongue, Floor of the mouth and suprahyoid muscles. FACIAL ARTERY 1) The facial artery runs anteriorly and superiorly near the labial commissure and along the lateral side of the naris of the nose. 2) The facial artery terminates at the medial canthus of the eye. 3) Supplies the face in the oral, buccal, zygomatic, nasal, infraorbital, and orbital regions. o Cervical – Ascending Palatine, submental and tonsillar o Facial branches – Glandular (submandibular), Angular, Superior Labial & Inferior labial *Face, palate, tonsils, submandibular, stylohyoid, digastric muscles Maxillary artery Acessory middle meningeal artery Masseteric artery Middle meningeal artery Deep temporal arteries Pharyngeal artery - Artery of pterygoid canal Sphenopalatine artery Infraorbital artery Anterior superior alveolar artery Deep auricular artery Anterior tympanic artery Inferior alveolar artery Mylohyoid artery Posterior superior alveolar artery Greater palatine artery Lesser palatine arteries Buccal artery Lingual branch Incisive branches Mental artery • 1st Mandibular part • 5 branches → Retromandibular foramen • 2nd Pterygoid part • 5 branches → Infratemporal foramen • 3rd Pterygopalatine part • 6 branches → Pterygopalatine foramen Epicranial Surprise Orbicularis oculi Closing eyelid and squinting Corrugator supercilii Frowning Orbicularis oris Closing and pursing lips as well as pouting and grimacing Buccinator Compresses the cheeks during chewing Risorius Stretching lips Levator labii superiori s Raising upper lip Levator labii superiori s alaeque nasi Raising upper lip and dilating nares with sneer Zygomaticus major Smiling Zygomaticus minor Raising upper lip to assist in smiling Levator anguli oris Smiling Depressor anguli oris Frowning Depressor labii inferi oris Lowering lower lip Mentalis Raising chin protruding lower lip Platysma Raising neck skin and grimacing Class I Malocclusion •The MB cusp of the maxillary first molar occludes with the MB groove of the mandibular first molar. Facial profile as described by many clinicians with the older term mesognathic. Class II Malocclusion Class II malocclusion (distoclusion) MB cusp of the maxillary first molar occluding (by more than the width of a premolar) mesial to the MB groove of the mandibular first molar. • The older term for describing the facial profile in Class II, division I, is retrognathic. Class II Malocclusion Division I Division II • Based on the • Position of the anterior teeth. • Shape of the palate • Resulting facial profile. Class II Malocclusion Division I maxillary incisors protrude facially from the mandibular incisors causing a severe over bite (or deep bite). Upper incisors are tilted outwards, creating significant overjet. Division II Protrusive maxillary incisors, the maxillary central incisors are either upright or retruded. Upper incisors are labially inclined. Class III Malocclusion The MB cusp of the maxillary first molar occludes (by more than the width of a premolar) distal to the MB groove of the mandibular first molar. • The older term that describes the facial profile with a Class III malocclusion is prognathic.
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