Human disease USEFUL
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| 🇬🇧 | 🇬🇧 |
| What does the double bond in the corticosteroids do | Increases the drug potency |
| How long anti-inflammatory drugs take affect via transactivation and transrepression pathway | 6-8 hours |
| An adrenal-cortex hormone (trade names Hydrocortone or Cortef) that is active in carbohydrate and protein metabolism | Hydrocortisone and cortisone |
| Long acting >36 hours glucocorticoids are | Dexamethasone |
| Glucocorticoid uses outside of dentistry | Allergies- (Allergic rhinitis) and (Dermatitis/eczema) |
| Uses of glucocorticoids in dentistry | Oral ulceration- denture induced trauma (not used for hepetic ulcers) |
| Chronic glucocorticoid use is similar to | Cushing's disease |
| Rapid stopping of glucocorticoids can lead to | Addisons disease |
| RISKS with chronic GC | Infection risk |
| Anti immunomodulators examples-- | MAb- adalimumab and cetrolizumab |
| Paraneoplastic syndrome can cause | Cushings- lungs produce ACTH like compound |
| Define cachexia | TNF produced causes fat mobilisaiton and loss of apetite |
| Where does leukemia originate | Bone marrow red blood cells |
| Where does lymphoma originate | Lymphocytes |
| NSAID examples | Ibuprofen Diclofenac Naproxen Piroxicam Aspirin Paracetamol Celecoxi |
| COX-1 is found in | Most cells |
| COX-2 is found in | Inflammatory cells |
| COX-1&2 Irreversible drug | Aspirin |
| COX-1&2 reversbile drug | Ibuprofen |
| Weak COX inhibitor in the presence of peroxides | Paracetamol is a |
| NSAID effects | Analgesia-absence of the sense of pain without loss of consciousness |
| Uses In dentistry of NSAIDs | Temporary relief of mild/moderate detnal pain or inflammation 1-7 days |
| Effective NSAID for dentistry | Ibuprofen |
| Analgesic but not anti-inflammatory | Paracetamol |
| Contraindication for NSAIDs | Empty stomach ibuprofen |
| Aspirin actions | Analgesic |
| Why is aspirin irreversible | COX is blocked permanently as no nucleus |
| Paracetamol effects | Analgesic and antipyretic but poor anti-inflammatory |
| Lipoxygenase inhibitor example | Zileuton |
| Mural thrombi | Not fully occluded |
| Occluding thrombi | Fully occluded |
| Ischaemia | Reduced blood supply to a tissue or organ |
| Infarction | Death of tissue due to ischaemia |
| MI types | Transmural most common |
| Posterior myocardial infarction is due to | Thrombosis of right coronary artery |
| Gangrene is | Tissue necrosis plus added bacterial infection |
| Metaplasia | Replacement of one cell type for another |
| Dysplasia | Disordered cell growth due to an accumulation of non lethal mutuations |
| Tumour | Mass or swelling |
| Neoplasm | Abnormal mass of tissue, the growth of which exceeds as is uncoordinated with that of the normal tissues and persists in the same excessive manner after cessation of stiumuli which evoked the change |
| Benign | Neoplasm which is localised and cannot spread |
| Malignant | A neoplasm which can invade and destroy adjacent structures and spread to distant sites |
| Metastatis | Spread of cancer to a distal site |
| Driver mutations | Push cells to malignant phenotype |
| Passenger mutations | Are inconsequential |
| Classification of neoplasms | Behaviour- benign or malignant |
| Bone pain may prelude | Metastatic deposits |
| Paraneoplastic | Where T-cells invade host tissues |
| Hemicholinium- no clin. uses mechanism | Competitive inhibitor of the choline carrier |
| Vesamicol works by | Preventing storage of ACh (via vesicular ACh transporter) |
| Bottulin toxin prevents | Exocytosis |
| Bottulin used to treat | Salivary dlrooling |
| Neostigmine and physostigmine are- | Cholinesterase inhibitors |
| Suxamenthonium works by | Agonising nicotinic receptors over two sub parts of the receptor which desensitises the receptors cauisng paralsysis |
| What are butylcholinesterases | Non specific cholinesterases |
| Complication with suxamenthonium | Is broken down by butrycholinesterases some individuals genetically lack this systemic enzyme meaning suxamenthoniuma has a paralysising effect |
| What are galantamine and rivastigimine | Nicotinic allosteric potentiating ligands |
| Decarmethonium is selective for | Nicotinic skeletal muscle |
| Antimuscarinics work via | Inhibition of parasympathetic nervous system |
| What is atropine used to treat | Bradycardia |
| Pirenzepine is used to | Decrease gut motility and secretions |
| Why is atropine given presurgery | Decreases secretions therefore decreasing AChEI side effects |
| What is tropicamide used for | Pupil dilation |
| Oxybutynin is used for | Urinary incontinence |
| What is hyoscine used for | Motion sickness |
| What is vasculitis | Inflammation of the blood vessel wall |
| What is an aneurysm | Bulge in a blood vessel that is weaker than the blood vessel |
| What is angina | Lack of O2 to the heart but no necrosis of heart tissue |
| What is critical stenosis | At least in 75% reduction in vessel size which cant be compensated for by vasodilation |
| What does hypertension lead to | Hypertrophy |
| What is sarcoidosis | Where inflammatory cells clump together to make a clump of cells forming a granuloma |
| What is stenosis | Failure of the valve to open completely |
| What is valve incompetence | Failure to close fully blood flows in reverse |
| Those at risk of infective endocarditis may need what when carrying out a dental/surgical procedure | Prophylactic antibiotics |
| 3 main congenital heart diseases | Left to right shunt |
| Heart rate problems | Arrthmia |
| Stroke volume problem | Heart failure |
| Volume problems | Renal impairment- diuretics |
| Blood composition issues | Anaemia, immune, anticoagulants |
| High TPR is caused by | Hypertension |
| Poor flow leads to | Angina |
| What controls rate of heart beat | SAN action potentials |
| Stroke volume is determined by | Ventricular sympathetic activity and EDV |
| Issues with SAN signal generation include | Alternate pacemkaers (ectopic) |
| Class II antirhymics are | Beta blockers e.g. propanol (Beta 1 and 2) atenolol B1 |
| What can be used to treat sinus bradycardia and how does the drug work | Atropine works by blocking chollinergic PNS receptors |
| How do class 1 antirhymics works | Extend the refractory period by locking fast sodium channels |
| Examples of class 1 antirhymics are | Lidocaine and quinidine |
| Class III antirhymics work by | Slowing down repolarisation |
| Class IV antiarrhythmics work by | Slowing down conduction through the AVN |
| Nifedipine and verapamil work by | Blocking L-type calcium channel conduction |
| The calcium block also effects | Cardiomyocytes |