Test 1 Flashcards
1
Q
Describe the normal pattern of primary tooth development
A
Upper: Fall out by 12yrs 2x central incisor (8-12m) 2x lateral incisor (9-13m) 2x canine (16-22m) 2x first molar (13-19m) 2x second molar (25-33m)
Lower: Fall out by 12yrs 2x central incisor (6-10m) 2x lateral incisor (10-16m) 2x canine (17-23m) 2x first molar (14-18m) 2x second molar (23-31m)
2
Q
Describe the normal pattern of secondary tooth development
A
Upper: 2x central incisor (7-8y) 2x lateral incisor (8-9y) 2x canine (11-12y) 2x first premolar (10-11y) 2x second premolar (10-12y) 2x first molar (6-7y) 2x second molar (12-13y) 2x third molar (17-21y)
Lower: 2x central incisor (6-7y) 2x lateral incisor (7-8y) 2x canine (9-10y) 2x first premolar (10-12y) 2x second premolar (11-12y) 2x first molar (6-7y) 2x second molar (11-13y) 2x third molar (17-21y)
3
Q
Identify 3 common non-tooth related changes in the oral cavity
A
- Ankyloglossia (tongue tie)
- abnormally tight/short lingual frenulum which restricts the movement of the tongue. - Cysts and sores
- Epstein pearls: benign keratin-filled cysts in the mouth of infants
- Mucocele: benign mucus-filled cystic lesion of minor salivary glands
- Ranula: mucocele of sublingual salivary glands
- Eruption cyst or haematoma: blood or fluid-filled cysts that cover the site of erupting teeth
- Apthous ulcers/canker sores: open sores due to break in the mucus membrane - Infections and growths
- Candidiasis: overgrowth of normal mouth flora
- Herpes gingivostomatitis: sores in the mouth from primary infection with Herpes Simplex 1
- Leukoplakia: white, inflammatory patches of mucus membrane. Caused by smoking.
- Hairy leukoplakia: viral infection associated w immunocompromised individuals or those w HIV
4
Q
Outline dental conditions and relate to oral hygiene and the importance of dental health screening
A
- Tooth discolouration: caused by poor oral hygiene (e.g. food/drink, tobacco, metals, fluorosis) or intrinsic factors (genetic conditions, hyperbilirubinemia, or poryphoria)
- Dental trauma: tooth avulsion, displacement or chipping. Potential recovery if presented to dentist in time.
- Dental caries (tooth decay): bacterial action in susceptible teeth, resulting in acid production which demineralises teeth. Prevented by good oral hygiene, limited dietary factors and administration of fluoride.
- Periodontal disease: inflammatory condition induced by bacteria (plaque). Gingivitis = mild inflammation of gums vs periodontitis = destructive gum disease, systematic inflammation.
Screening is important to eliminate the potential for dental caries in childhood which leads to tooth decay in adulthood and potentially gum disease.
5
Q
Outline some of the evidence around certain controversial health issues
A
Additive fluroride:
- found to decrease the likelihood of tooth decay by decr. demineralization by strengthening enamel and decr. bacterial acid production
- some associate excess fluoride exposure to dental fluorosis (cosmetic issue), skeletal issues, and/or neurotoxicity
- overall, significant conclusive evidence of protective properties of fluoride levels up to 1ppm, whereas less conclusive evidence for the proposed harmful effects. Thus safe to be added.
6
Q
Describe cancer
A
Uncontrolled and abnormal growth of cells (neoplasms).
7
Q
Outline the cellular differences bw benign and malignant tumours
A
- Benign: cells appear normal, differentiated, encapsulated, position determines impact on tissue function
- Malignant: cells poorly differentiated, spreads to nearby tissues (metastisise), not affected by normal signals to destroy damaged cells
8
Q
Describe how the identified gene classes are thought to be involved in the development of cancer: Proto-oncogenes, tumour-suppressor genes, and DNA repair genes
A
- Proto-oncogenes: code for proteins that regulate normal cell growth. Mutations cause oncogenes. Oncogenes allow unregulated cell proliferation and differentiation.
- Tumour-suppressor genes (protective): code for proteins that slow/stop cell division, initiate DNA repair, trigger apoptosis, enhance immune detection and destruction of cancer cells.
- DNA repair genes: code for proteins involved in repairing damaged DNA. Different DNA repair genes and pathways = different cancers
9
Q
Outline some of the causes of cancer
A
- Inherited or caused by genetic alterations during lifetime bc of exposure to mutagens.
- Immunity and infections: weakened immune system = less effective against foreign/abnormal cells. Chronic inflammation assists in cancer development. Viral/bacterial infections incl. Hep B/C, HPV and Epstein-Barr virus
- Carcinogenic chemicals/substances: metabolised in cells and converted to substances that damage DNA. E.g. tobacco, alcohol, asbestos, air pollutants.
- Radiation: UV rad. causes specific gene mutations. Ionising radiation (x-rays, radioisotopes) can cause DNA damage, gene mutations and cell death.
- Dietary factors: consumption of high amounts of red/processed meats, low fruit/veg intake, high fat diets. Obesity.
10
Q
Outline some of the generalised signs/symptoms of cancer
A
Dependent on type, location and stage but can be:
- anaemia/thrombocytopenia (decr. blood cell no.)
- pain (pressure, obstruction, stretching, inflammation, tissue destruction)
- Fatigue
- Weight loss/wasting (loss of appetite)
11
Q
Describe the various cancer treatments
A
- Surgery: removal of whole/part of tumour.
- Radiation: damages DNA and local env. + decr. tumour size
- Chemotherapy: non-selective cytotoxic drugs used to kill dividing cells
- Immunotherapy: manipulation of immune system to incr. its effectiveness against cancer cells (facilitates recognition and destruction)
- Hormone therapy: inhibits hormone production/reception for hormone-dependent cancers.
- Gene therapy: introduction of genetic material into cells to replace missing/damaged genes, prevent angiogenesis, stimulate immune response and inject chemosensitive genes into cancer cells
12
Q
Identify the types of lipoproteins
A
- Chylomicrons: transport triglycerides and cholesterol from intestines after absorption
- VLDLs: transport triglycerides from liver to adipose tissue and muscle.
- IDLs: transport (mostly) cholesterol
- LDLs: transport cholesterol
HDLs: transport cholesterol back to liver
13
Q
Outline healthy cholesterol/lipoprotein levels in blood
A
Total cholesterol <4mmol/L LDL <1.8mmol/L HDL >1mmol/L Triglycerides <2mmol/L Total cholesterol:HDL ratio <4:1 LDL:HDL <3:1
14
Q
Define atherosclerosis
A
Intra-arterial fat and fibrin deposits w/in arteries which harden over time, restricting blood flow leading to ischemic syndromes.
Leading cause of artery/heart disease.
15
Q
Outline the pathophysiology of atherosclerosis, incl. associated complications
A
- Injured endothelial wall of artery (e.g. tear) –> inflammation –> accumulation of fat and cholesterol –> fatty streak formation –> collagen production over fatty streak, forming fibrous plaque –> decr. vessel diameter.
- Risk factors: family hx, aging, smoking, hypertension, diabetes/obesity, etc.
- Complications: peripheral artery disease (decr. blood flow to limbs), aneurysm (localised dilation/outpouching of vessel), acute arterial occlusions/transient ischemic events (e.g. MI, angina, stroke, damage to affected tissue, etc.)
16
Q
Define thrombosis and embolus
A
- Thrombosis: pathological formation of blood clot (thrombus) w/in intact vessel.
- Embolus: bolus of matter circulating in bloodstream
17
Q
Outline the pathophysiology of DVT and pulmonary embolism
A
- DVT: thrombus in deep veins, typically lower limbs. Causes tenderness/pain, swelling, heat and discolouration
- Pulmonary embolism: occlusion of blood vessel by embolus which originates in systemic venous circulation or right side of heart. Most commonly due to dislodged DVT.
18
Q
Relate the stages of the cardiac cycle to an ECG trace
A
P wave = arterial depolarisation (firing of SA node)
QRS complex = ventricular depolarisation (firing of AV node)
T wave = ventricular repolarisation
19
Q
Outline the pathophysiology of coronary heart disease
A
- Narrowing/stiffness/blockage of coronary arteries (mostly due to atherosclerotic occlusion)
- Inadequate blood supply to myocardial tissue (decr. O2 = incr. lactic acid = release of inflammatory mediators = pain)
- Leads to angina and/or MI
20
Q
Describe angina and distinguish bw stable and unstable
A
- Chest pain caused by myocardial ischemia (usually transient). Occurs when O2 demands outweigh supply due to progressive narrowing of arteries and decr. vasodilation ability
- Stable: predictable (i.e. occuring w incr. physical exertion or stress) and resolved by normal response
- Unstable: less predictable response, plaque rupture or outer erosion; strong indicator of impeding MI. Characterised by angina occurring at rest, new onset angina, and/or angina of incr. severity/length/freq.
21
Q
Define arrhythmias and outline the 3 life-threatening arrhythmias
A
- Alterations of cardiac conduction causing alteread heart beat rhythm
1. Ventricular tachycardia: abnormal and rapid discharge of electrical signals in ventricles.
2. Ventricular fibrillation: ventricles quiver instead of contracting
3. Asystole: cessation of electrical and mechanical action of heart
22
Q
Describe the impact of cardiac hypertrophy
A
Incr. mass of cardiac muscle cells results in
- an increased energy requirement bc of incr. myocytes,
- decr. ventricular space or ventricular dilation
causes decr. SV and CO leading to heart failure
23
Q
Outline the pathophysiology of heart failure and the aim of treatment
A
- Inadequate perfusion of tissue due to cardiac dysfunction/inability to generate adequate CO (decr. contractility/incr. preload/afterload). Risk factors incl. MI, cardiac hypertrophy, heart valve incompetence, hypertension.
- Left side failure: pulmonary hypertension and oedema –> impaired gas exchange
- Right side failure: systemic venous hypertension –> peripheral oedema –> hepatic congestion
24
Q
Outline the steps of haemostasis
A
- Vasoconstriction
- Platelet aggregation (platelets stick to exposed collagen fibers –> release prostaglandin –> release serotonin)
- Coagulation: phase I is clotting cascade to create prothrombin activator –> phase II prothrombin activator converts prothrombin to thrombin –> phase III thrombin converts fibrinogen to fibrin to facilitate clot formation
- Requires Ca2+ a d platelet clotting factors
25
Q
Describe some common coagulation disorders
A
- Thrombocytopenia: abnormally low platelets
either bc decr. production or incr. consumption
causes bleeding under skin/mucous membranes - Heparin-induced thrombocytopenia
Immune mediated drug reaction resulting in platelet aggregation - Platelet function alterations
may be acquired in association w various diseases, drugs (aspirin), nutrition, etc. - Factor VIII deficiency (haemophilia A) and factor IX deficiency (haemophilia B): both factors work together to activate clotting factor X
causes prolonged bleeding, easy bruising, bleeding in joints - Von Willebrand’s disease: Missing Von Willebrand factor resulting in inability to activate factor X
Most commonly mucocutaneous bleeding
26
Q
Describe the pathophysiology of disseminated intravascular coagulation (IDC)
A
- Widespread coagulation and haemorrhage due to enhanced clotting and clot breakdown; positive feedback loop; high mortality rate
- Severe endothelial damage causes overactive coagulation response leading to clot formation in undamaged vasculature, leading to new tissue damage bc of all the tiny blood clots in vasculature; Uses up all clotting factor stores. Simultaneously, clot degradation is occurring causing additional haemorrhage.
27
Q
Describe the process of anticoagulation using examples
A
- Endogenous anticoagulation
- Protein C (and cofactor protein S) inhibit some coagulation factors
- Antithrombin III: inhibits thrombin and other coagulating enzymes
- Tissue factor pathway inhibitor: inhibits tissue factor in extrinsic pathway
- Prostacyclin: promotes vasodilation and inhibits platelet activation - Plasminogen activators (anticoagulants)
- tissue plasminogen activator (tPA) and urokinase: catalyzes plasminogen –> plasmin to breakdown fibrin
- recombinant tPA (rtPA): more active on fibrin-bound plasminogen
- Streptokinase: bacterial produced protein that activates plasminogen - Warfarin: vit K antagonist; inhibits the synthesis of vit K dependent clotting factors and proteins C and S.
- Heparin: enhances activity of antithrombin III which inhibits the action of clotting factors
- Anti-platelet agents: prevent complications associated w ACS.
E.g. platelet receptor inhibitors
28
Q
Differentiate bw pain and nociception
A
- Pain is an unpleasant feeling associated w actual or potential tissue damage which is SUBJECTIVE and accompanies nociception
- Nociception is a real sensory process initiating signals that trigger pain. Produced by nociceptors triggered by noxious stimuli and inflammatory chemicals
29
Q
Outline the key parts of the sensory pain pathway
A
- Primary nociceptive neuron sends signals from nociceptors to the spinal cord (via “A delta” and C fibers)
- Secondary nociceptive neuron sends signals from the spinal cord to the thalamus (via ascending spinothalamic tract)
- Tertiary nociceptive neurons send signals from the thalamus to other brain regions (primary somatosensory cortex, limbic system and prefrontal cortex)
Note: for face/head, signals travel via trigeminal pathway
30
Q
Distinguish bw the 2 types of nociceptive neurons
A
Primary:
- A delta fibers: large diameter and myelinated –> quick transmission resulting in sharp, localised pain sensation
- C fibers: smaller diameter and unmyelinated –> slow transmission resulting in dull, aching types of pain sensation.
31
Q
Describe referred pain
A
Feeling pain in a location other than where it originates, usually generalised area.
Caused by visceral nociceptor fibers converging on the same interneurons as somatic nociceptors.
32
Q
Identify the role of different brain regions in the perception of pain
A
- Primary somatosensory cortex: type, location and intensity of pain
- Limbic system: emotional response to pain
- Prefrontal cortex: rationalization/understanding of pain
