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
Describe some common coagulation disorders
1. Thrombocytopenia: abnormally low platelets
either bc decr. production or incr. consumption
causes bleeding under skin/mucous membranes
2. Heparin-induced thrombocytopenia
Immune mediated drug reaction resulting in platelet aggregation
3. Platelet function alterations
may be acquired in association w various diseases, drugs (aspirin), nutrition, etc.
4. 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
5. Von Willebrand's disease: Missing Von Willebrand factor resulting in inability to activate factor X
Most commonly mucocutaneous bleeding
26
Describe the pathophysiology of disseminated intravascular coagulation (IDC)
- 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
Describe the process of anticoagulation using examples
1. 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
2. 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
3. Warfarin: vit K antagonist; inhibits the synthesis of vit K dependent clotting factors and proteins C and S.
4. Heparin: enhances activity of antithrombin III which inhibits the action of clotting factors
5. Anti-platelet agents: prevent complications associated w ACS.
E.g. platelet receptor inhibitors
28
Differentiate bw pain and nociception
- 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
Outline the key parts of the sensory pain pathway
1. Primary nociceptive neuron sends signals from nociceptors to the spinal cord (via "A delta" and C fibers)
2. Secondary nociceptive neuron sends signals from the spinal cord to the thalamus (via ascending spinothalamic tract)
3. 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
Distinguish bw the 2 types of nociceptive neurons
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
Describe referred pain
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
Identify the role of different brain regions in the perception of pain
1. Primary somatosensory cortex: type, location and intensity of pain
2. Limbic system: emotional response to pain
3. Prefrontal cortex: rationalization/understanding of pain
33
Differentiate bw pain threshold and pain tolerance
- Pain threshold: the intensity of a noxious stimuli required to generate APs in a nociceptive neuron. Similar amongst individuals but decreases w sensitization
- Pain tolerance: subjective unpleasantness of pain sensations. Highly variable amongst individuals and influenced by many factors.
34
Describe the 3 mechanisms of endogenous pain modulation
1. Non-nociceptive mechanoreceptive neurons
- Neurons activated by low threshold stimuli (e.g. touch) which act to inhibit interneurons to decr. AP frequency of secondary nociceptive neurons (in the pain pathway) which synapse at the same interneuron.
2. Descending regulation
- Neurons descending from the brainstem which release NTs that cause inhibition of nociceptive neurons. Occurs after nociception has reached the brain and decreases the intensity of the pain bc now aware of it.
3. Endogenous opioids
- 3 main classes: endorphins, enkephalins and dynorphins
- Bind to receptors in brainstem areas and dorasl root to inhibit AP firing in nociceptive neurons of pain pathway. Activate neurons of descending modulatory pathways.
35
Describe the agonist/receptor interaction of opioids
- Opioids bind to opioid receptors found in the CNS, PNS and GI tract. 3 main receptor types: μ receptors (μ1 = analgesia, μ2 = resp. despression), δ receptors (spinal analgesia) and k receptors (analgesia, dysphoria and sedation).
36
Describe the central and peripheral effects of opioids
- Central: analgesia, cough suppression, resp. suppression, sedation/sleep, euphoria, dysphoria, nausea/vomiting, hypotension and bradycardia.
- Peripheral: decr. GI motility and spasms of sphincter muscles (severe constipation), suppression of some spinal reflexes, release of histamine
37
Describe the mechanism of action of opioids
- Presynaptic inhibition: activation leads to change in resting membrane potential --> neurons involved are harder to stimulate --> inhibits opening of NT channels, so less pain signals released in spinal cord and brain
- Postsynaptic inhibition: activation hyperpolarises cell membranes, making it less likely to respond to a NT released from the presynaptic nerve.
38
Name 2 drugs used to reverse the effect of opioids
Naloxone and naltrexone, which are antagonists that non-selectively bind to opioid receptors
39
Outline the cardiovascular changes that manifest with age, the impacts of these changes on the elderly, and the implications that may result from these changes
- Decr. cardiac capacity due to decr. in myocytes and incr. myocardial fibrosis --> decr. max HR and decr. ability to adapt to cardiac stress
- Decr. blood vessel compliance --> stiffer aorta and large arteries --> incr. BP and atherosclerosis.
- Can lead to heart disease later on
40
Outline the respiratory changes that manifest with age, the impacts of these changes on the elderly, and the implications that may result from these changes
- Extrapulmonary changes --> decr. lung vol., compliance, and elasticity, incr. diaphragmatic fatigue --> incr. work of breathing
- Decr. alveolar surface and decr. capillary network --> V/Q mismatch --> decr. VO2 max, decr. gas exchange and decr. PaO2
41
Outline the blood and immune changes that manifest with age, the impacts of these changes on the elderly, and the implications that may result from these changes
- Altered cell functions and decr. cell count --> fragile RBCs, decr. Hb conc., decr. T cell function, decr. memory cell function, decr. production of naive T and B cells.
- Overall decr. in functionality of immune system --> incr. susceptibility to infections, blunted fever response and decr. rise in WBC in response to infection --> decr. wound healing and thermoregulation
42
Outline the skin changes that manifest with age, the impacts of these changes on the elderly, and the implications that may result from these changes
- Epidermis: decr. keratinocyte production, melanocytes and langerhans cells --> epidermal-dermal junction flattens --> incr. risk of separation; impaired protection
- Dermis: decr. collagen and elastin fibers, decr. capillaries w incr. fragility, decr. number of nerve endings --> dermal atrophies
- Decr. sweat and subcut glands w decr. function and hair follicles --> skin becomes thinner, drier and wrinkled w decr. protection and sensation
43
Outline the musculoskeletal changes that manifest with age, the impacts of these changes on the elderly, and the implications that may result from these changes
- Bone loss --> decr. density and strength of bone, more brittle.
- Decr. elasticity of cerebral vessels --> incr. vulnerability and BBB permeability
- Meninges thicken, decr. myelin, decr. dendrite density and synaptic connections --> decr. cognitive functions and memory and imbalances in the amount/distribution/breakdown of NTs.
44
Outline the neurological changes that manifest with age, the impacts of these changes on the elderly, and the implications that may result from these changes
- Progressive decr. memory/incr. memory impairment
- Incr. difficulty of info processing
- Sleep disturbances
- Decr. neuromuscular control --> decr. reaction time and reflex action, change in gait/posture, change in proprioception
- Visual changes --> hyperopia, loss of colour vision, decr. acuity
- Progressive hearing loss and vestibular function
- Diminished sense of smell
- Decr. no./sensitivity of taste buds
45
Outline the endocrine changes that manifest with age, the impacts of these changes on the elderly, and the implications that may result from these changes
- Atrophy of endocrine organs --> decr. hormone secretion
- Anterior pituitary incr. in size bc fibrosis --> decr. GH secretion, incr. FSH bc decr. negative feedback from gonadal hormones
- Fibrosis of thyroid gland
- Decr. secretion of cortisol, aldosterone and androgens from adrenal gland
- Pancreatic function altered --> incr. risk of glucose intolerance and diabetes
46
Outline the GI changes that manifest with age, the impacts of these changes on the elderly, and the implications that may result from these changes
- Decr. salivary production --> commonly dysphagia, anorexia may occur
- Stomach: decr. motility and secretions, atrophy, decr. mucosa
- Intestine: decr. motility and degeneration of villi
- Liver: decr. in size, enzyme production and lipid metabolism
- Pancreas: decr. digestive enzyme production
47
Outline the renal and fluid balance changes that manifest with age, the impacts of these changes on the elderly, and the implications that may result from these changes
- Decr. renal blood flow and nephron loss --> GFR decr. slowly, decr. reabsorption, decr. secretion/excretion, decr. urine conc.
- TBW loss occurs --> Na+ and water regulation altered; thirst may decr.
- Decr. bladder capacity and neuronal innervation
- Urinary and pelvic floor muscle weakness --> incr. likelihood of incontinence
48
Outline the reproductive changes that manifest with age, the impacts of these changes on the elderly, and the implications that may result from these changes
- Decr. testicular mass and testosterone production --> mood and temp changes
- Decr. rate of spermatogenesis and decr. sperm motility and vitality
- Prostate gland enlarges --> benign prostatic hyperplasia --> constricts urethra
- Decr. follicular estrogen production --> menopause, atrophy of sex organs, decr. bone mass, decr. protective effect on arteries. May also decr. protection of damage to brain.
49
Outline factors that influence the conc. of alcohol in the blood
- Dose, rate and conc. of ethanol consumed
- Presence of food in the GI system
- Body type and weight
- Age and sex
- Metabolic and genetic variations
50
Outline the metabolism of alcohol in the body
- Metabolised/oxidised in the liver by alcohol dehydrogenase and cytochrome P450
- Produces acetaldehyde (toxic) which is further metabolised into acetic acid (non-toxic)
- Also produces reactive oxygen species (ROS); an excess of which causes oxidative stress in body tissues
51
Outline the effects of intoxication
- Acute physiological and psychological state induced by ethanol (occurs when BAL > metabolic capacity)
- Effects incl.: vasodilation, irritation of GI tract, decr. oxytocin and testosterone levels, inhibition of ADH, CNS depression
52
Outline the effects of heavy or chronic alcohol abuse on the skin/ integumentary system
Facial puffiness
Spider veins
Palmar erythema
53
Outline the effects of heavy or chronic alcohol abuse on the musculoskeletal system
Osteoporosis
Osteonecrosis
Gout
Muscle wasting
54
Outline the effects of heavy or chronic alcohol abuse on the endocrine system
Elevated ACTH
Incr. SNS activity
Hypothyroidism
55
Outline the effects of heavy or chronic alcohol abuse on the CVS
Cardiac arrhythmias/dysrhythmias
Cardiomyopathy
Hypertension
Incr. stroke risk
56
Outline the effects of heavy or chronic alcohol abuse on the resp. system
Incr. risk lung infections (pneumonia, TB)
Acute resp. distress syndrome
Obstructive sleep apnoea
57
Outline the effects of heavy or chronic alcohol abuse on the immune system
Suppressed immunity
| Incr. risk of infections
58
Outline the effects of heavy or chronic alcohol abuse on the NS
Loss of consciousness
Coma (potentially --> resp. depression and death)
Peripheral neuropathy
Cerebellar damage (decr. coordination)
Brain damage (e.g. alcoholic dementia, convulsions)
59
Outline the effects of heavy or chronic alcohol abuse on the GI system
```
Salivary gland hyperplasia
Esophagitis/esophageal varicies
Gastritis
Mallory-Weiss tear
Liver complications: fatty liver, alcohol hepatitis, cirrhosis, portal hypertension
Pancreatitis
```
60
Outline the effects of heavy or chronic alcohol abuse on nutrition and metabolism
Malnutrition
Nutrient deficiencies (e.g. vit B2 and B6)
Hypertriglyceridemia
Lactic acidosis and ketoacidosis
61
Outline the carcinogenic effects of heavy or chronic alcohol abuse on body systems
Incr. risk of various cancers incl. oral/GI, liver, and breast
62
Outline the effects of heavy or chronic alcohol abuse on the reproductive system
- Testicular atrophy and decr. testosterone (decr. libido, impotence and ejaculatory problems, growth of breast tissue in males and infertility)
- Decr. female fertility and alterations to menstrual cycle
- Incr. risk of STIs
- Teratogenic (may lead to Fetal alcohol spectrum disorders/fetal alcohol syndrome)
63
Discuss the modes of action of antacids and their potential interactions
- Target the chemo-trigger zone (CTZ) to completely inhibit or decrease vomiting
- Most work by inhibiting blood-borne drugs (e.g. opioids and chemotherapeutics) from binding to receptors in the CTZ. Either:
- -> block binding site of chemoreceptors from emetics to prevent emesis
- -> Bind to chemoreceptors to send signals to other parts of the vomiting centre to inhibit emesis
- -> Lower the amount of dopamine in the brain, which affects ow much interacts w receptors in the CTZ
64
Identify the main groups of antiemetics and list one drug from each group
- Histamine antagonists (e.g. Cyclizine Promethazine)
- Muscarinic antagonists (e.g. Hyoscine)
- Serotonin receptor antagonists (e.g. Ondansetron)
- Phenothiazines (e.g. Dopamine)
- Butyrophenones (e.g. Droperidol)
- Maxalon domperidone (e.g. Maxalon)
65
Describe pharmacological approaches to managing GERD and peptic ulcer disease
- H2 (histamine) receptor antagonists: decr. basal and food-stimulated acid secretion by ~90% and promotes healing of peptic ulcers.
- Proton Pump Inhibitors (PPI): irreversibly inhibit H+/K+ ATPase which is the final step in acid secretory pathway.
- Antacids: chemically neutralize gastric acid. May promote healing of duodenal ulcers but not really gastric ulcers
- Helicobacter Pylori treatment: elimination of the bacteria present w gastric ulcers to produce long-term remission of ulcers. Reinfection can occur.
66
Understand the nursing considerations in the management of diarrhoea
- Main risk is dehydration (esp. infants and elderly)
- Oral dehydration drinks to replace lost salts and minerals
- IV replacement in severe cases
- If caused by infection, anti-diarrhoeal medications may prolong the infection
67
Describe laxatives and their modes of action
- Used to stimulate bowel movement to relieve temporary constipation.
- Contain chemicals that help incr. stool mobility, bulk and frequency
- 3 types:
1. Bulking agents: incr. H2O content of stool
2. Lubricant laxatives: make stools slippery
3. Emollient laxatives: soften stool
68
Describe the process of dental caries (tooth decay)
Stages of progression:
1. Initial lesions: chalky white spots on tooth due to demineralization of enamel
2. Enamel decay: erosion of enamel, where natural remineralization cannot replace lost enamel (yellow-brown discolouration)
3. Dentine decay: breakdown of dentine by bacteria and acids; cavitation occurs
4. Pulp involvement: decay reaches pulp of tooth; bacterial infection kills blood vessels and nerves
5. Abscess formation: risk of infection to surrounding structures (i.e. bone)
69
Outline the signs and symptoms common to GI disorders
- Anorexia
- nausea
- vomiting
- abdominal pain
- GI bleeding (haematemesis, blood in stool, occult/hidden bleeding)
70
Describe the pathophysiology of GERD incl. signs and symptoms
- Decr. muscle tone: decr. sphincter contraction, decr. oesophageal peristalsis, delayed gastric emptying.
- Chronic condition of reflux causing acidic gastric contents to irritate/damage oesophageal mucosa; persistent oesophagitis
- Signs/symptoms: heartburn, dysphagia, chronic cough, upper abdominal pain
71
Describe oesophageal varices and pyloric stenosis and their complications
- Oesophageal varices: enlarged, swollen veins of the oesophagus; commonly occurs secondary to liver disease (bc of blood back up to nearby veins causing distension); risk of rupture and bleeding (potentially fatal)
- Pyloric stenosis: birth defect of thickened pyloric sphincter/pyloric musculature; narrowed opening prevents food from moving into the duodenum; results in forceful, projectile vomiting --> dehydration and electrolyte imbalance, persistent hunger and weight loss, decr. stools w incr. mucous.
72
Distinguish bw acute and chronic gastritis
- Gastritis = inflammation of the gastric mucosa
- Acute = damage to the surface epithelium, usually heals spontaneously w/in a few days, caused by irritants (e.g. alcohol and smoking)
- Chronic = progressive disease resulting in thinning and degeneration of stomach wall; caused by autoimmune disease or H. pylori infection; progresses to atrophic state
73
Describe the pathophysiology and implications of peptic ulcer disease
- Peptic ulcers: break/ulceration in stomach mucosa or duodenum which exposes layers of GI tract wall to gastric and digestive enzymes
- Complications: perforation of ulcer --> bleeding (cause of mortality), duodenal obstruction
74
Describe some types of hernia and the implications of hernia
Hernia = abnormal protrusion of organ through defect or natural opening in membrane or cavity wall
- Hiatal hernia: stomach herniates through diaphragm into the thoracic cavity. 2 types:
1. Sliding hiatal hernia: stomach slides into thoracic cavity
2. Para-oesophageal hiatal hernia: stomach herniates alongside oesophagus
- Inguinal hernia: intestines bulge through inguinal canal
- Umbilical hernia: intestines protrude through abdominal wall at/near umbilicus
Complications: acute bowel obstruction and/or strangulation of hernia --> avascular tissue necrosis --> perforation --> peritonitis, septicaemia
75
Outline the causes of intestinal obstruction and the associated signs/symptoms
- Occurs in any condition that prevents the normal flow of contents through the intestine
- Mechanical: adhesions, intussusception, volvulus, hernia
- Functional (failure of motility): abdominal surgery complication, intra-abdominal infections, chemical/electrolyte imbalances, intestinal ischemia
Symptoms: abdominal pain/cramping, nausea/vomiting, abdominal distension (bloating), constipation (or diarrhoea if some gets past)
76
Compare and contrast UC and Crohn's disease
Compare
- Similar signs/symptoms: abdominal pain/cramping, bleeding, diarrhoea, vomiting, weight loss/fatigue/anaemia, fever when active.
- Both typically diagnosed via colonoscopy and treated w drug therapy
Contrast
- UC is inflammation of the MUCOSA of colon vs C which is ALL LAYERS of GI tract WALL anywhere in tract.
- Ulceration occurs w repeated inflammation in UC vs occurs leading to formation of fissures, fistulae, strictures and/or adhesions
- Damage/result: in UC mucosal destruction ensues w possible formation of anal fissures, abscesses or haemorrhoids whereas in C enteric NS damaged leading to bowel dysfunction
77
Describe the BMI and its use in evaluating body weight
- BMI = weight/height^2
- Gives an idea of someone's body weight classification
<18.5 = underweight
18.5 - 24.9 = normal weight
25.0 - 29.9 = overweight
30.0 - 34.9 = class I obesity
35.0 - 39.9 = class II obesity
>40.0 = class III obesity
doesn't take into account body composition
78
Outline the causes and risk factors for obesity
Causes:
- Genetics: leptin gene mutations (no/deficient leptin, leptin receptor deficiency) or Prader-Will syndrome
- Metabolic: Cushing's syndrome, polycystic ovarian syndrome (PCOS) or hypothyroidism
Risk factors:
- Diet: energy consumed > expenditure and nutrient balance of food consumed
- Physical inactivity: labour-saving devices in daily life, sedentary recreational activities, incr. technology, decr. in labour intensive work, transportation methods
- Stress: physical and physiological impacts (e.g. incr. cortisol levels, effects on metabolism, sleep), also psychological impacts (e.g. emotional eating, alteration of eating patterns)
79
Describe the pathophysiology of obesity
- Adipose tissue has endocrine functions, as it releases at least 20 adipocytokines that act as hormones; these are involved in the regulation of food intake, lipid storage, metabolism, insulin sensitivity, female reproduction, aspects of immunity and vascular activity
- Adipocytokine regulation is disrupted w excess adipose cell mass; interact w other peripheral regulating signals and neuropeptides in hypothalamus; excess leptin levels can lead to resistance
- Incr. visceral fat associated w various metabolic alterations
80
Outline the health risks/complications associated w obesity
- Cardiovascular: development of coronary artery disease, incr. likelihood of thrombosis, hypertension, cardiac changes
- Resp: obstructive sleep apnoea, asthma, complications w general anaesthetic
- Neurological: dementia and Alzheimer's disease, stroke, depression
- Renal: renal failure, urinary incontinence, kidney stones
- GI: gastroesophageal reflux, gallstones, non-alcoholic fatty liver disease, pancreatitis
- Endocrine: type 2 diabetes
- Reproductive: erectile dysfunction and male infertility, decr. female fertility, PCOS, pregnancy complications
- Musculoskeletal: decr. mobility, lower back pain, osteoarthritis, gout
- Cancer: incr. risk for development and/or poorer prognosis of certain types of cancer, treatment complications
- Psychosocial implications: social stigmatisations/discrimination, depression, incr. likelihood of risky behaviours (e.g. substance abuse, risky sexual behaviour, etc.)
81
Outline some of the treatment/management strategies for obesity
- Assessment: risks for complications, compounding factors (e.g. smoking, cholesterol), motivation/support, possible reasons for weight gain, goal setting
- Diet: decr. overall dietary intake, decr. sat. fat intake, limit sugars/simple carbs, incr. fruit and veg, some incr. in wholegrains/nuts/legumes
- Physical activity: freq., moderate intensity activity most days >30mins
- Behaviour therapy: help set realistic goals, self-monitor eating habits and activity, stress management, identify challenges and develop tools to overcome
- Pharmacotherapy: introduced only after diet, exercise and behaviour therapy have failed/been insufficient; various meds available to be used in conjunction w diet and exercise
- Surgery: usually only BMI>40; considered only after diet/exercise treatments have been in place. Either gastric banding (decr. size of stomach pouch) or gastric bypass (separation of stomach w bypass to duodenum)
607 Pathophysiology
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