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Pathology Pt.3 - Coggle Diagram

- - - - Benign
        
        May form a capsule
        
        Slow growth rate
        
        Non invasive (ie nil metastasis) more EXPANSIVE
        
        well-differntiated
        
        "oma"
      - Malignant
        
        Types
        
        Primary or secondary
        
        MOST import differentiating feature is METASTASIS
        
        Rapid growth rate
        
        Invasive allowing metastasis
        
        poorly differntiated (anaplasia)
        
        "scarcoma" (mesynchimal) or "carcinoma" (epithelil)
    - - Infection, inflammatory, deposits, haemotomas, congenital
  - - - Myxoma/sarcoma (connective tissue)
      - Leiomyoma/sarcoma (smooth muscle)
      - Angioma/sarcoma (Blood vessles)
      - Lipoma/sarcoma (adipose)
      - Fibroma/sarcoma (fibrous)
      - Neuroma (nervous)
      - Osteoma/sarcoma (bone)
      - Adenoma/sarcoma (glands)
  - - - ○ May arise through the accumulation of somatic mutations
      - ○ Virtually autonomous
      - ○ Highly variable gross appearance
    - - process of tumor formation
  - - - ○ Variable cell size & shape (cellular pleomorphism)
      - ○ Variable nuclear size & shape (nuclear pleomorphism)
      - ○ Increased nuclear-cytoplasmic ratio
      - ○ Hyperchromatic nuclei (increased DNA)
      - ○ Increased mitosis and abnormal mitosis
    - - ○ Loss of polarity
      - ○ Disordered maturation from basal to squamous cell
      - ○ Basal cell hyperplasia
      - ○ Dyskeratosis
      - ○ Drop shaped rete ridges
      - Desmoplasia = fibrous chnages induced by malignant cells
    - - Hyperplasia --> (dysplasia) Mild, Moderated --> Severe dysplasia as seen on histology
    - - Disseminated growth from the primary tumor
      - Seeding in body cavities, lymph spread (nodal involvement) or haemotogenous spread
    - - T
        
        Tumor Size (T0-4)
      - N
        
        Nodal involvement (N0-3)
      - M
        
        Metasis (M0-1)
  - - - Carcinogens:
        
        • Smoking, chewing tobacco, snuff dipping, areca nut use
        
        • Alcohol (synergystic with smoking)
      - Infections:
        
        • Chronic hyperplastic candidosis
        
        • Syphilitic leukoplakia
        
        • HPV infection
      - Mucosal diseases:
        
        • Lichen planus
        
        • Lupus erythematosis
        
        • Submucous fibrosis
        
        • Iron deficiency anaemia
    - - M>F, >40 years, Lower lip>> posteriolateral tongue, ant FOM
    - - Colour: red, or mixed speckled
        
        • Nb: Indurated or hard (is felt clinically)
      - Fungated margins, Raised/rolled
      - Lympahenopathy (also fely)
    - - Hx, Exam/Radiography (CT, PET scans)
      - Biopsy (incisonal vs excisional)
- - - - BMR, Cellular metabolims, Skeletal growth and Cardiovascular health
      - T4 is produced the most, T3 is the main active hormone
    - - Follicles (surrounding by follicular cells) are filled wiyth colloid, the cells secetre thyroglobulin which binds iodine and becomes T4 and T3
    - - -ve feedback loop
        
        Hypothalamic-pituitary-thyroid axis
    - - Hypothyroidism
        
        Hashimoto's thyroiditis (primary pathology)
        
        Immune-mediated
        
        Enlargement due to lymphoid infiltrate
        
        High levels of TSH, low levels of T3/4
        
        Hypopituitarism (secondary pathology)
        
        Iodine Deficiency (primary pathology)
        
        Reduced dietary intake
        
        Features
        
        Weight gain, cold intolerance, fatigue, mental sluggishness, bradcardia and hypotension
        
        nb: in childen = cretinism (short stature)
      - Hyperthyroidism
        
        Grave's Disease
        
        immune-mediated (primary pathology)
        
        autoantibodies for TSH receptor and thyroglobulin
        
        Hyperplasia of the thyroid cell (thyroid enlargement)
        
        Exopthalamous, Goitre, Pretibial Myxedema
        
        Thyroid andenoma (secondary pathology)
        
        Nb: External use of radiotherapy for thyroid cancers is important to know when amanging sugically for risk of ORN
        
        Features
        
        Weight loss, heat intolerance, tachycardia and hypertension
    - - Avoid tx patients with poorly controlled Hyperthyroidism
      - Avoiding Thyroid Storm!!
      - ORN risk for pts with external rediotherapy for adenomas
  - - - Dx: BGL (fasting) >7mM and (non-fasting) >11mM, usually indicated by elevated HbA1c
      - Inadequate Insulin Action
        
        Type 1 = Insulin Deficiency
        
        Immune-mediated
        
        IDDM
        
        HLA (human leukocyte antigen) genetic suseptibility
        
        Type 2 = Insulin resistance
        
        NIDDM but they can develope dependacy after beta cell fucntion is exhausted
        
        part of Metabolic Syndrome
        
        Non-alcoholic Fatty LD, Hyperlidemia and DM
      - Acute Consequences
        
        Ketoacidosis
        
        Poor glucose uptake leads to hyperglycemia, body begins to break down fats (lipolysis) leading to an accumulation of ketone bodies. Removal of glucose and ketones in urine cuases dyhdration leading to acidemia
        
        Common in Type-1, not in Type 2
        
        Hyperglycemia (high BGL)
        
        Polyuria (freq. urination), polydipsia (thirst) and polyphagia (hunger)
      - Chronic Consequences
        
        CVS
        
        HTN, CVD and Peripheral Vascular disease (ie gangrene)
        
        Renal
        
        Chronic Renal Failure
        
        Retinopathy
        
        DM Neuropathy
        
        Neuronal degeneration
        
        AGE (advanced-Glycated End Products)
        
        contributes to poor wound healing
    - - Pancreatic islets (endo)
        
        Alpha = glucagon & beta = insulin
        
        Glucose homeostasis
        
        Nomal BGL are kept between 4-6 mM
        
        Elevation occurs with food intake, this results in insulin release from the beta cells which stimulates (glycogensis) uptake in adipose, skeletal msucle and the liver
        
        Reduced oral intake (ie at night) and lowered BGl stimulates glucagon release and (glconeogenesis) liver breaksdown glycogen to glucose
        
        Glut-4 is the main body transporter and Glut 1,3 for brain
      - Pancreatic acini (exo
        
        Digestion
  - - - Medulla = SNS, secretes NA/Adren
      - Cortex = Cortisol (Stess) and Aldosterone (RAAS)
        
        Cortisol (gluocorticoid)
        
        Functions
        
        Metabolic
        
        gluconeogenesis, lipolysis, protein degredation
        
        stress adaptation
        
        anti-inflammatory/immunosuppressive
        
        inhibits phospholipas A2/cycloogenase expression
        
        reduced IL-2 and IgG production and PMN function
    - - HPA Axis (cortisol)
        
        -ve feedback loop (CRH from Hypo, ACTH from Ant. pt)
    - - Cushing Syndrome
        
        Endogenous
        
        LT administartion of synthetic glucocorticoids
        
        Exogenous
        
        ATCH dependant
        
        Pituitray Adenomas (Cushing Disease)
        
        Non-ATCH dependant
        
        Adrenal adenoma/carcinoma
        
        Features
        
        Buffalo hump/moon face, hyperglycemia, osteroprosis, obesity
    - - Acute Adrenal Insufficency
        
        Adrenal Crisis
        
        Immediate increase in cortisol is required to respond to stress and the gland is unable to respond
        
        Features
        
        circulatory shock, severe Hypotensuion/hyponautremia, hypoglycemia, muscle cramps and weakness, confusion and possible coma
        
        Dental considerations
        
        likely need for steroid cover if on LT steroid therapy
        
        Possible risk of MRONJ is concurrent bisphosphonates
      - Chronic Adrenal Insuffiency
        
        Addison's disease
        
        90% of the adrenal cortices are dysfunctional or destroyed
        
        Features
        
        Lethargy, hypoglycemia, hypotension, suseptible to adrenal crisis
  - - - Ant Pit (80%)
        
        LH, PSH, (repoduction) TSH, (metabolism) Prolactin, (lactation) GH, (growth) ATCH (stress)
      - Post. Pit (20%)
        
        AFH (water balance), oxytoxin (lactation)
    - - -ve feedback regulation from the hypothalamus, pituitary gland and target effector cells
    - - Hormone excess, deficiencies, hypersensitivity, resistance or non-functioning tumors
- - - - Chonic reversible airway disease
        
        Inflammation odema
        
        Bronchospasm
        
        Excessive mucous
      - Symptoms
        
        wheezing, SOB, coughing
      - Types
        
        Atopic
        
        Allergic = IgE mediated (Type 1 hypersesnitivity)
        
        Sensitized mast cells dengranulate
        
        release histamine and proslagndins which cause vasocontrisction and bronchospasm
        
        Non-atopic
        
        Hyperirritability, stress, infections or drugs
        
        Same mediators of airway constriction are released and causes the same mucous. inflammation and bronchospasm
      - Treatment
        
        Mild/Mod/Severe
        
        delivery of medications escaltes with severity
        
        Abotive vs prophylactic
        
        ideally getting them to preventor tx only
        
        Dental Consideration
        
        Avoid preciptitating factors (stress)
        
        Defer elective care in unstable disease
        
        Caution using NO, NSAIDs
        
        Caution with LT steriod txs (inhaled vs oral)
    - - Emphysema
        
        Pernament enlargement/destruction of the bronchioles
        
        A deficiency of Alpha-1 antitrypsin (which protects the lungs from elastases) leads to this airways destruction
        
        Features
        
        Destruction/collapse of the airways, barrel chested weightloss,
        
        PINK PUFFERS
        
        Outcome
        
        hyperinflated lungs, pursed lips due to airways restitcion
      - Bronchitis
        
        Outcome
        
        Pulmonary HTN = cor pulmonale (R sided HF)
        
        Features
        
        mucous production, cough, wight gain and cyanosis
        
        BLUE BLOATERS
        
        Dx: Chronic cough for at least 3 consecutive months in 2 consecutive years
      - Management
        
        Smoking cessation
        
        SA/LA brochodilates
        
        Inhaled corticosteroids
        
        ?risk or immunocompromised
        
        Low flow oxygen
        
        ie hypoxia is a respiratory driver, the high flow would shut down the respiratory drive and lead to a respiratory arrest
  - - - Interstitial lung disease or Stiffness (fibrosis) of the lungs causing restriction in breathing ability
        
        resulting in pulmonary HTN --> R sided HF --> IHD
- - - - Hepatocytes are zoned (1-3) as per their proximity to portal vein
        
        Zone 1 = close to portal vein, richly supplied with oxygenated blood and nutrients and toxins
        
        Zone 3 = Closes to Central vein, hypoxic blood, and toxins
    - - Formed by hepatocytes in the bile ducts (bilirubin and cholesterol) which is transported to the duodenum
      - Emulify and aid in the digestion of fats
      - Bilirubin
        
        initally uncongugated (albumin-bound) then becomes congugated (water soluble) in the liver and is secreted into the GIT via the bile duct
  - - - Ie gluconeogenesis or storage
    - - Factors bleeding
    - - Bile salts and bilirubin
    - - Iron and copper, Vitamin A, B
      - Fat digestion
  - - - Inflammation
        
        alcohol or non-lcoholic-fatty disease
      - Infection
        
        viral hepatitis
      - Maligancy
        
        hepatocellular carcinoma
      - Autoimmune
    - - Regeneration
        
        needs an intact ECM (minimal damage)
      - Degeneration
        
        Accumulation of products w/ fatty changes
      - Fibrosis and Cirrhosis
    - - Jaundice
        
        yellowing of skin/mucosa
        
        Due to accumulation of bilrubin in the blood
        
        Causes
        
        Prehepatic
        
        excess production of bilirubin from lysis of RBCs
        
        excess bilrubin is (albumin bound) not excreted by the urine
        
        Intrahepatic
        
        accumulation within the live
        
        Seen in viral hepatitis, drug or alcohol induced injury
        
        Post-hepatic
        
        obstruction of the extra-hepatic bile ducts
        
        conjugated bile is not excterted (ie due to gall stones or tumors)
      - Cirrhosis
        
        Features
        
        Fibrosis (bridging fibrous septae)
        
        Parenchymal nodules
        
        Pathophysiology
        
        persistent hepatocyte death
        
        hepatocyte hyperplasia and nodule formation
        
        chronic inflammtion and fibrosis
        
        Consequences
        
        Portal HTN
        
        increased hepatic pressure = causes splenic backflow (Splenomegaly)
        
        congestion can lead to Ascites (of flow of fluid into the abdominal space)
        
        Hepatocellular failure
        
        = results in thrombocytopenia (failed prod. clotting factors)
        
        Hepatocellular Carcinoma
      - Hepatic Failure
        
        Acute
        
        rapid deteriotaion of liver function (within 8 weeks)
        
        results in hepatic encephalopathy
        
        usually due to viral hepatitis and paracetamol toxicity
        
        Chronic
        
        slow decompensation (over >6 months)
        
        results hepatic encephalopathy, ascites
        
        usually due to Hep B and C, NAFLD and ALD)
      - Alcohol Liver Disease (ALD)
        
        Types/Morph
        
        Alcohlic Steatosis (fatty change)
        
        Elevated LFTs
        
        Lipid accumulation
        
        Alcoholic Cirrhosis
        
        Varices + ascites
        
        Alcoholic Hepatitis
        
        Jaundice + Hepatomegaly
        
        Can be reverible (abstence) if alcoholic cirrhosis has not occured
      - Non-alcoholic Fatty Liver Disease (NAFLD)
        
        Causes
        
        sedenatry and high-fat diet
        
        Steatosis --> steathohepatitis --> cirrhosis --> primary liver cancer
      - Malignant Tumors
        
        Liver and lungs common site for metastatic spread
        
        Hepatocellular (primary tumor)
        
        risk factors
        
        alcoholism
        
        liver cirrhosis
        
        HBV infetionc
        
        Features
        
        Oral Manifestations
        
        Coagulopathies
        
        reduced production of clotting factors
        
        Risk assesment (local or systemic factors for HA management?)
        
        Drug Metabolism altered
        
        PCT, Codiene, Metronidazole AVOIDED
        
        lignocaine is SAFE
        
        Jaundice of mucosa, xerostaomia, possible OLP
        
        Slient heptaomegaly
        
        rapid increase in size of liver and ascites
- - - - Activation
        
        Caused by: Normotension, Laminar flow, Growth factors, Cytokines Hypoxia/acidosis
        
        Results in: Growth fcators vasoactive mediators, adhesion molecules, anticoagulants
      - Dysfunction
        
        Results in: Turblent flow, HTN, Cytokines, Complement, bacterial products, lipid products, AGE, hypoxia, Smoking
        
        Caused by: Chemokines pro-coagulant, molecules, adhesion ect...
      - Vessel structure = Tunica intima, media, adventicia
    - - Risk factors
        
        Consitutional/Non-modifiable
        
        Genetics, age, sex
        
        Modifiable ((x2) fold)
        
        Hyperlipdemia
        
        HTN
        
        DM
        
        Smoking
        
        Lifestyle/obesity
      - Pathogenesis
        
        Chronic response to endothelial injury
        
        Inducing endothelial dysfunction
        
        Increased permeability, and WBC adhesion and emigration
        
        Recuitment to intima and Mo activation
        
        Mo engulf lipids and create foam cells resulting in fatty streaks (reversible)
        
        Smooth muscles proliferate and stablise a fibrofatty atheroma (irrversible)
        
        Atheroma
        
        Fibrous cap (w/ foam cells) necrotic centre, over the tunica media
        
        Caues narrowing, or occlusion of the artery and weaking of the vessel wall
        
        Inflammation
        
        promotes thinning of the cartilageous cap, causes fissuring, surface of the plaque is stripped, erosion exposing the basement membrane endothelium
        
        can cause destabilizing of the plaque and distant thrombosis
      - Major Targets
        
        Large vessels (Aortic, illiac, or carotid)
        
        Medium vessles (coronary, renal, popiteal)
      - Outcomes
        
        MI, stroke, Aortic aneurysm, peripheral vascular disease
    - - Types
        
        Congenital
        
        Collagen disorders
        
        Aquired
        
        Athersclerosis
        
        Underlying elastic tissue becomes weak due to the sclerotic plaque
        
        HTN
        
        High BP causes trauma and weakens the lumen
      - True aneurysms
        
        Saccular (one side)
        
        Fusiform (both sides)
      - False Aneurysms
        
        Extravastion of blood
        
        Communication w/ a haemotoma from the vessel lumen which looks like a dilated vessel wall
        
        Dissection
        
        Tear in the intima causes a dissection within the intima
  - - - Four chambers, valves which allow for uni directional flow, compromising of cardiac muscle, specialised cells connected by Gap junctions, SA/AV noses special cells which are rthymic pacemaker cells.
      - Nb: Differences in ventricle size
        RV 0.3-0.5cm, LV 1.3-1.5 cm
    - - 1) Failure of the pump
        
        Reduced tissue perfusion
      - 2) Obstruction to flow
        
        Valve prevention or vessel
        
        need to overwork to pump passed (becomes hypertophic/dilated)
      - 3) Regurgitate flow
        
        Backward flow
      - 4) Shunted flow
        
        Defects cause diverted flow
        
        Congenital or aquired defects of heart or vessels
      - 5) Disorders of cardiac conduction
        
        SA or AV nodes cause non uniform contractions of the heart, poor CO
      - 6) Rupture of the heart or a major vessel
        
        Generally due to trauma
    - - Congenital Heart Abnormalties
        
        Prersent from birth = only the less severe anomalies will allow the baby to come to full term
        
        Normal shunts = Foramen ovale, ductus arterious/venousus, this closes when we take our first breath
        
        Right --> Left Shunt
        
        Ex. Tetralogy of Fallot
        
        Pulmonary stenosis
        
        Ventricular septal defect (VSD)
        
        mixing of blood causes deoxyegenation blood to enter systemic circulation
        
        S&S: Cyanosis + Clubbing of fingers and tones
        
        Ex. Transposition of Circulation = usually results in death prematurely
        
        Ex. Trunctus Arteriosis - mixed blood is supplied to both pulm/systemic cicrulation
        
        Left --> Right Shunt
        
        Ex. Atrial Septial defect
        
        EX. Ventricular Septal Defect
        
        Ex. Patent ductus arteriosus
        
        Early surgical intervention required
        
        = pulmonary HTN and cause right to left shunts, and need to be corrected immediately
        
        Obstruction
        
        Coartorcation of the aorta
        
        Aortic stenosis (AS)
        
        Pulmonary stenosis (PS)
        
        Which ever chamber is pumping against the obstruction becomes hypertrophic
      - Ischaemic HD
        
        Changes to myocardial oxygen demand and altered blood supply
        
        Normally by coronary atherosclerosis
        
        Acute IHD
        
        Angina Pectoris
        
        Stable
        
        Transient, 30-40s, exacerbated by stress/exercise, relived by stress or GTN spray
        
        Chronically enlarging atherosclerotic plaque
        
        Unstable
        
        Precipitated by low level of activities or rest, not always relieved by GTN, 90% occlusion of Coronary artery
        
        Unstable plauqe causes fissuing and possbile thrombus formationleading to an MI
        
        Variant
        
        Vasospasm of the coronary arteries
        
        Pyramidal angina
        
        MI
        
        Ischemic necrosis due to acute ischemia
        
        area of risk = where the occlused vessled supples
        
        Transmural
        
        Full thickness ischaemia
        
        ST elevation infarct
        
        Subendocardial
        
        inner third/half ischameia
        
        Non-ST elevation ischaemia
        
        Troponin = release when myocardial cells are damaged
        
        Complications
        
        • 1. Contractile dysfunction
        
        • 2. Arrhythmias
        
        • 3. Myocardial rupture --> cardiac tamponade (bleed in the heart)
        
        • 4. Pericarditis
        
        • 5. Mural thrombus (possible embolization)
        
        • 6. Ventricular aneurysms (scar tissue forms aneurysms)
        
        • 7. Papillary muscle dysfunction (valve deformations)
        
        Progressive late heart failure
        
        Sudden Cardiac death
        
        Complete loss of CO = asystole
        
        Usually a result of ventricular fibriliation
        
        Chronic IHD (CHF)
        
        Pump failure due to ischeamic myocardial damage
        
        nb: Compensatory mechanisms
        
        SNS activation
        
        Frank-starling mechanism = SV and EDV increased (greated contraction is need for ejection to be successful)
        
        L side Hypertrophy = increased preload and SV
        
        if there is no increase in capillary size, leads to decomensation of the heart
        
        RAAS system activated
        
        via renal hyperperfusion = worsens pulmonary hypoperfusion
        
        ANP released
        
        Relased when there is a stretch at the R atrium, this causes diuresis to stop the RAAS system but is not enough to stop it!
        
        Left side failure
        
        Systolic = inability to for heart contract
        
        Diastolic = inability for heart to expand and fill
        
        = stasis of blood on the left side, leads to congestion in the pulmonary vessels and hypoperfusion into critical vessels
        
        Right Sided failure
        
        Pulmonary HTN
        
        Leads to L ventricular failure
        
        Peripheral odema, Systemic venous congestion
        
        Liver cirrhosis, secondary to liver enlargement
      - Cardiac Valve Disease
        
        Rheumatic fever
        
        Acute immuo-mutli system disease
        
        Follows after Group A strep pharngitis (strep throat)
        
        Active Phase
        
        Jones Criteria
        
        Pan, myo or endo - carditis
        
        Subcutaneous nodes
        
        Polyarthritis of major joints
        
        Abs Strep antigens cross react with self-antigens
        
        Aschoff Bodies
        
        nodules seen in the myocardial walls in rh fever
        
        Rh Heart Disease
        
        Leads to vegittations, aschoff bodies and fibrionus pericarditis
        
        leading to fibrotic valve disease
        
        Suseptible to IE
        
        Infective endocarditis
        
        Acute IE
        
        infection by a previously healthy valve by a highly virulent organism
        
        Ex. Staph aureus
        
        Subacute IE
        
        infection by a previously deformed valve by a lower virulent organism
        
        haemolytic-streptococci
        
        Dx:
        
        Blood culture and Echocardiogram
        
        Also: fever, vascular emboli
        
        Requires Ab propylaxis for dental tx