1
Q
Describe the pathophysiology, including clinical manifestations, and treatment options for Parkinson’s disease
A
- progressive loss of dopaminergic neurons within the substantia nigra of the BASAL GANGLIA. –> Disrupts signals bw BG and premotor cortex –> issues w initiating, stopping and intensity of movement
- Cardinal signs: Tremor (resting); muscle rigidity and/or bradykinesia/akinesia. Also posture/gait, speech difficulty, various others
- No cure, treatment to alleviate symptoms.
1. Levodopa (L-dopa): a dopamine precursor that is converted to dopamine in the substantia nigra (effectiveness reduces over time)
2. Dopamine agonists: trigger dopamine receptors to stimulate the necessary neuronal signals
3. Anticholinergics: restore the dopamine-acetylcholine balance in the basal ganglia (important for proper signaling)
4. Deep brain stimulation: electrical stimulation of certain brain regions
5. Supportive care, e.g. physiotherapy, occupational therapy
2
Q
Describe the pathophysiology of multiple sclerosis, including disease progression types
A
- autoimmune demyelination of oligodendrocytes in the CNS (axons) and optic nerve.
- Myelination needed for AP conduction and insulating voltage
- Four main types:
1. Relapse-remitting (RRMS): periods of acute exacerbation and remission, eventually decr. ability to completely recover, causing permanent loss of neurological function (continues to relapse and remission tho)
2. Secondary progressive (SPMS): begins like RRMS, but eventually transitions to steady progression (with no periods of remission).
3. Primary progressive (PPMS): steady progression neurological dysfunction from onset of the disease without periods of remission.
4. Progressive relapsing (PRMS): steady progression with superimposed attacks of exacerbation. Rare. - The clinical manifestations are unpredictable and highly variable bc any part of the CNS can be affected.
3
Q
Describe the pathophysiology of Guillian-Barré syndrome, including common signs and symptoms
A
- Autoimmune demyelination of schwann cells in the PNS axons
- Most commonly associated with infections, functions are eventually regained
- Clinical manifestations
1. SENSORY - paresthesia, dysesthesia, diminished reflexes, pain
2. MOTOR
A) Somatic - muscle weakness, paralysis
B) Autonomic - HR and BP alterations, increased/decreased sweating, constipation, urinary retention
- Symptoms typically start peripherally w rapid onset, usually have a complete recovery
4
Q
Describe the pathophysiology of myasthenia gravis, including signs and symptoms
A
- decr. skeletal muscle stimulation due to autoimmune destruction of Ach receptors at the NMJ.
- muscle weakness and fatigue worsens upon exertion and typically improves with rest
- Signs/symptoms: limb weakness, difficulty swallowing and breathing, unstable gait, drooping eyelids
- Severe muscle weakness: quadriplegia, impaired ventilation and swallowing
- If ventilation muscles affected, risk of MG crisis
5
Q
Describe the pathophysiology of epilepsy, including the main types, key terminology and status epilepticus
A
- recurrent and unprovoked seizures (hyperactive, synchronous AP discharge)
- Main types
1. Partial (focal) seizures: involve only one part of the cerebrum.
A) Simple: remains conscious, sensory and/or muscular activity
B) Complex: loss/alteration to consciousness, sensory and/or motor experiences
2. Generalised seizures: occurs w/in most brain regions and typically result in loss of consciousness.
A) Tonic: state of increased muscle tone and rigidity w LOC (stiffness incl. resp mm)
B) Atonic: muscles go relaxed
C) Absence: brief episodes of altered consciousness characterised by staring and unresponsiveness
D) Tonic-clonic: stiffness and LOC followed by convulsions
E) Myoclonic: brief muscle twitches (usually single muscle group) - Terminology:
- prodrome: feelings, perceptions, etc. PRECEDING a seizure
- aura: feelings, thoughts, perceptions, etc. as part of a seizure.
- postictal: time after a seizure (mins to days) minutes to hours. May incl. altered consciousness and/or various other symptoms
- Status epilepticus is a serious complication of epilepsy when seizure activity of tonic-clonic seizures (mostly) is sustained for longer than 5 minutes or there are recurrent seizures without recovery of consciousness in between. Emergency bc during seizures there is an increased O2 demand and a decreased ventilation; can lead to cardiorespiratory failure very quickly (w/in minutes), as well as brain death (bc O2 deprived)
6
Q
Which of the following neuroglia are found in the CNS and which in the PNS?
Ependymal cells, Microglia, Schwann cells, Astrocytes, Satellite cells, Oligodendrocytes
A
CNS: Ependymal cells, Microglia, Astrocytes, Oligodendrocytes
PNS: Schwann cells, Satellite cells
7
Q
Which of the neuroglia produce myelin?
A
Oligodendrocytes and Schwann cells
8
Q
Which part of the brain is responsible for regulating skeletal muscle movements, particularly the initiation, intensity & ceasing of those movements?
A
Basal ganglia
9
Q
Describe the cerebral cortex and identify some of the key functional areas of the cerebral cortex and what they do.
A
- Prefrontal cortex: integrative functions, incl. many higher cognitive functions
- Primary motor cortex: decides on skeletal muscle movements in coordination w basal ganglia and cerebellum
- Primary somatosensory cortex: sends signals along upper motor neuron down spinal cord
- Somatosensory association area: determines type, location and intensity of somatic sensory stimuli (touch, temp, pain, etc.)
- Posterior association area: integrative functions, particularly higher cognitive functions associated w the senses, language and memory
- Special sense cortices: specialised area processing signals coming from the special sense organs
10
Q
Outline the homeostatic mechanisms regulating cerebral blood flow and intracranial pressure (ICP)
A
- Cerebral Blood Flow
- cerebral blood vessel diameter adjustment to maintain adequate blood flow.
- Responds to changes in blood pressure and blood gases (PaCO2 or PaO2) - ICP
- Intracranial vol made up of 80% brain tissue, 10% blood and 10% CSF
- fixed space; an increase in volume in one of the three components requires a decrease in volume of one of the other components
- normally between 5-15mmHg
11
Q
Relate consciousness and arousal (incl. which part of brainstem responsible) and outline the Glasgow Coma Scale (GCS) for measuring consciousness
A
- Consciousness is awareness of oneself and environment and ability to elicit expected responses. This involves arousal, a state of wakefulness and vigilance to immediate surroundings (reticular formation of the brainstem is responsible for maintaining arousal)
- GCS assesses an individual’s ability to open their eyes and manage verbal and motor responses, taking into account the individuals context/local factors (e.g. swelling which may prevent eye opening or hearing loss which may reduce response to commands).
- Score bw 3-15:
Eye opening
—- spontaneous (4)
—- sound (3)
—- pain (2)
—- none (1)
Verbal response
—- orientated (5)
—- confused (4)
—- words (3)
—- sounds (2)
—- none (1)
Motor response
—- obeys commands (6)
—- localized (5)
—- normal flexion (4)
—- abnormal flexion (3)
—- extension (2)
—- none (1)
12
Q
Distinguish between blunt and penetrating traumatic brain injury (TBI) and between primary and secondary injury
A
- Blunt: brain is NOT exposed to external environment
- Penetrating: broken skull/dura and neural tissue IS exposed
- Primary injury: initial tissue damage that occurs at impact. (incl. penetration, compression and shearing forces)
- Secondary injury: occurs after the primary injury and involves the inflammation, swelling/oedema and bleeding that follows the primary injury.
13
Q
Identify key factors in the evaluation and management of TBI, including use of the GCS
A
- Involves a thorough history and neurological examination. Brain imaging is used to distinguish between focal and diffuse injuries and to identify any intracranial hemorrhage/hematoma
- Glasgow Coma Scale is often used to assess the neurological impact of a TBI and provides a rough guide to the severity of the TBI:
Mild is score 13-15
Moderate is score 9-12
Severe is score 3-8 - Major component of treatment is management of ICP and CCP. Monitoring ventilation and BP is also important, as is maintaining electrolyte levels, BGL and temp
14
Q
Describe the pathophysiology of focal and diffuse TBI
A
- Focal TBI
- localized tissue damage due to blunt OR penetrating trauma. Can cause:
A) contusion injury: brain tissue damage due to the impact of the brain against the skull, associated w the compression and shearing forces. Can be:
i) coup: injury at initial impact point(s)
ii) countercoup: rebound injury
B) Hematoma: accumulation of clotted blood within the cranium. Increases ICP. - Diffuse TBI
- widespread neural damage assoc. w blunt trauma
- Ranges from concussion (mild) to severe diffuse axonal injury (DAI) w coma
- DAI occurs due to massive shearing forces and causes large numbers of damaged axons –> simultaneous AP firing –> excitotoxicity –> disruption of ATP formations –> decr. AP and coma
15
Q
Which neuroglia form the BBB? What’s the role of the BBB?
A
Astrocytes
Ensures that neurons do not come into direct contact with blood or substances in blood that could be harmful to neurons. It also regulates the ECF environment around neurons
16
Q
Briefly describe autoregulation and outline why this is so important for the brain.
A
Is when organs regulate the blood flow and blood pressure within their own capillary networks.
This is important to ensure that the brain receives adequate blood flow at adequate pressure, regardless of what is happening with blood flow/pressure in the rest of the body.
17
Q
What is the circle of Willis?
A
This network of blood vessels found at the base of the brain includes numerous connecting arteries which supply the vast majority of the cerebrum.
18
Q
Order these protective layers surrounding the CNS from superficial (1) to deep (5). Arachnoid mater Dura mater Skull bones Pia mater CSF
A
Skull bones Dura mater Arachnoid mater CSF Pia mater
19
Q
What are the ‘spaces’ in the brain where CSF is produced called? And how many are there?
A
Ventricles, of which there are 4
20
Q
After circulating through the subarachnoid space, where does CSF flow into?
A
Into the dural sinus/venous blood within the dural sinus
21
Q
Outline the different classes of spinal cord injury
A
- Cord concussion: temporary loss of cord function
- Cord contusion: bruising of neural tissue w temporary loss of cord function
- Cord laceration: tearing of neural tissues (cord) w loss of function. Recovery only w minor injury
- Cord transection: severing of spinal cord causing permanent loss of function
22
Q
Describe the pathophysiology of spinal cord injury, including autonomic hyperreflexia
A
- primary injury: the actual mechanical disruption (contusion, compression, laceration or transection)
followed by - secondary injury: the subsequent inflammation, bleeding and swelling which causes functional and vascular impairment and possibly neuronal cell death
- Spinal shock occurs immediately following the primary injury (can last days-months) and involves the loss of spinal cord activity at and below the level of injury. Can have: reflex loss, skeletal muscle paralysis, decr/no sensation and decr. thermoregulation
- Complication: Autonomic hyperreflexia (or dysreflexia)
*occurs at T6 or above, after spinal shock resolves.
*excessive (reflexive) sympathetic response to sensory stimuli occurring below the lesion (e.g. distended bladder or bowel), incl. vasospasm (–> hypertension), goosebumps and pallor.
*Homeostatic responses above the lesion site to counteract the signalling happening below the injury, resulting in: sweating, skin flushing, headache, blurred vision, bradycardia
23
Q
Outline the following according to the level of spinal cord injury:
- Sensory/somatic motor control
- Ventilation**
- Autonomic control
A
- C1-C4:
- Various sensory/motor control of head/neck; quadriplegia.
- Ventilatory support required (continuous or intermittent)
- No autonomic control (renal, digestive, autonomic)
- C5-C8:
- Strong sensory/motor control of head and neck, some upper limb. Quadriplegia.
- Diaphragmatic control of ventilation, but some support may be required.
- No autonomic control (renal, digestive, autonomic)
- T1-T5:
- sensory/motor control of head, neck and upper limbs. Paraplegia.
- Can breath without assistance.
- No autonomic control (renal, digestive, autonomic)
- T6-T12:
- sensory/motor control of head, neck, upper limbs and some abdominal/back. Paraplegia.
- Can breath without assistance.
- No autonomic control (renal, digestive, autonomic)
- L1-L5:
- sensory/motor control of head, neck, upper limbs, trunk/torso, and some lower limb.
- Can breath without assistance.
- No autonomic control (renal, digestive, autonomic)
- S1-Co1:
- Typically sensory/somatic motor control of all (head-toe)
- Can breath without assistance.
- Autonomic control varies
24
Q
**Distinguish between the following nerve injuries: prolapsed disc, nerve root avulsion, burners syndrome**
A
- Prolapsed disc
- Protrusion of an intervertebral disc which compresses spinal nerve(s)
- Usually resolves on own with adequate rest and appropriate exercise/activity, can be treated w pain relief, physio, massage, osteopathy or surgery - Nerve root avulsion
- root(s) of spinal nerve torn from cord. Commonly roots in plexus affected (mostly brachial)
- Typically due to trauma
- Loss of sensation and motor control, likely permanent - Burners/stingers syndrome
- stretching/compression of nerve root(s) causing transient burning/stinging, paresthesia and muscle weakness.
- Brachial or cervical roots
- Recovery in minutes
25
Briefly describe the following syndromes that can occur with incomplete injuries:
1. Central cord syndrome
2. Brown-Séquard syndrome
3. Anterior cord syndrome
4. Posterior cord syndrome
1. Central cord syndrome
- motor impairment of upper limbs, with bladder dysfunction and varying sensory loss
2. Brown-Séquard syndrome
- Loss of motor function, light touch, proprioception and vibration sensation ipsilateral to the injury, and loss of pain and temperature sensation contralateral to the injury.
3. Anterior cord syndrome
- Loss of bilateral motor functions and pain & temperature sensations.
4. Posterior cord syndrome
- Loss of bilateral light touch sensation and proprioception.
26
Distinguish between sprains and strains
- Sprain: overstretched or torn ligament
| - Strain: overstretched or torn tendon
27
Describe the three grades of severity for sprains and strains
- Grade I: only a few fibers torn. Some localized inflammation including tenderness/pain, swelling and possibly bruising.
- Grade II: partial tear, with significant inflammation and pain.
- Grade III: complete tear right through the ligament/tendon/muscle(all collagen fibers torn). Intense pain and obvious signs of inflammation.
Sprain: joint immobility
Strain: loss of muscle/mobility
28
Outline the healing process for sprains and strains
1. Inflammation: after initial injury, fiber necrosis and bleeding may occur resulting in inflammation and exudate filling the space between the torn fibers.
2. Granulation: granulation tissue is laid down and holds the injured tissues together, re-vascularization will begin.
3. Remodeling: in ligaments and tendons, the initially disorganized granulation tissue will be remodeled in the final stage of tissue healing so that fibers are properly oriented. In muscles, the granulation tissue will be replaced by new muscle fibers.
29
Distinguish between the following types of fractures: open, closed, complete, incomplete, comminuted, displaced
1. Open: Bone penetrates the skin
2. Closed: Skin remains intact, bone does not penetrate
3. Complete: Bone broken all the way through
4. Incomplete: Break does not go all the way through the bone
5. Comminuted: Bone is broken into more than three pieces
6. Displaced: Broken bone ends are mis-aligned
30
Identify common signs/symptoms of bone fracture
```
tenderness and/or pain
unnatural alignment/deformity
swelling
muscle spasm
impaired sensation
decreased mobility/limb function
```
31
Describe the four stages of fracture healing
1. Haematoma: clotted blood accumulates, forming a hematoma.
2. soft callus formation: fibrous connective tissue and fibrocartilage fill the gap and connect the bones. New blood vessel formation.
3. Bony/hard callus formation: bone tissue replaces soft callous tissue
4. Remodelling: reshaping to gain original shape/size (bulge goes away)
32
Outline complications related to fracture
1. Delayed union or malunion of the bone fragments: bone fragments misaligned or take longer to align due to improper immobilisation or reduction
2. Non-union: bone fragments don't reunite, leaving a gap filled w soft tissue, instead of bone tissue
3. Hypovolemic shock: bones are highly vascular and there can be significant blood loss when bone is damaged
4. Fat embolism syndrome: fat globules enter circulation from broken long bones
5. Bone necrosis: disruption to blood supply/poor circulation can lead to bone cell necrosis
6. Infection: microbe invasion of fracture area; greater risk with open fractures
33
Describe osteoporosis
Decrease in bone density bc osteoclast activity > osteoblast activity.
- compact bone becomes porous and thinner and there is decreased integrity of cancellous bone
34
Identify the risk factors for osteoporosis
1. Ageing
2. Calcium and/or vitamin D deficiency
3. Family history
4. Certain endocrine or metabolic factors (e.g. obesity, Cushing's syndrome, hyperparathyroidism)
5. Lifestyle factors (e.g. sedentary lifestyle, smoking, excessive alcohol consumption)
6. Certain drugs (e.g. corticosteroids, heparin)
7. Gender
35
Distinguish between the different types of arthritis based on pathophysiololgy, including signs & symptoms
1. Rheumatoid arthritis:
- autoimmune condition causing inflammation of joint tissue, particularly synovial membrane and articular cartilage
- multiple joints bilaterally
- Leads to decr. (potentially permanent) joint function and mobility, pain
2. Ankylosing spondylitis:
- autoimmune condition causing inflammation of entheses of the vertebral column
- bones become fixed together (fibrosis --> ossification), causing stiffening and fusion of vertebral column (bamboo spine)
- Back pain, restricted/painful movement, reduced flexion/extension/rotation
- Decreased lordosis and increased kyphosis
3. Gout
- formation and deposition of sharp uric acid crystals within joints
- Occurs due to hyperuricemia (breakdown product of purine)
4. Psoriatic arthritis:
- arthritis in individuals who have psoriasis
5. Infectious arthritis
- joint inflammation occurring due to invasion of joint tissues by microbes
6. Osteoarthritis:
- degenerative damage to joint tissue due to wear and tear and inflammation
- breakdown of the articular cartilage in joints leading to inflammation, joint damage and osteophyte formation
- Causes joint stiffness and pain, decr. ROM
36
Outline some of the treatment options for arthritis
- anti-inflammatory drugs
- physical therapy
- hydrotherapy
- application of heat/cold
- pain management
- lifestyle modifications, e.g. diet, exercise
- surgery, e.g. joint replacement
37
Describe folliculitis, furuncles and carbuncles. What do they all have in common?
- Folliculitis: inflammation of the hair follicle due to invasion by bacteria; forms small pustules and erythema/discolouration
- Furuncles (boils): bacterial infection of follicles that spreads to the surrounding dermis; causes pustular nodules which can lead to necrosis, which may ultimately leave a scar
- Carbuncles: large collection of bacterial infected hair follicles and dermis. Affects the deeper tissues of the dermis and the subcutaneous tissue resulting in red/darkened, painful and swollen nodules that drain pus through multiple openings on the surface of the skin
All infectious conditions
38
***Describe the pathophysiology of cellulitis, including signs and symptoms
- bacterial infection of the dermis and subcutaneous tissue
- Signs/symptoms: erythema, swelling, warmth and pain, possibly blister formation
- can lead to sepsis
39
Outline treatment options and preventative advise for cellulitis
- Treatment: typically treated with antibiotics, if in leg elevate it
- Prevention: keep skin wounds clean and covered, treat fungal infections and other skin conditions to heal breaks in the skin
- Examine feet daily, use a moisturiser, avoid injury by wearing proper shoes
- Maintain adequate circulation and skin integrity
40
Describe dermatitis (eczema), acne vulgaris and psoriasis. What do they all have in common?
1. dermatitis (eczema)
- pruritus, erythema/discolouration
- Various forms depending on causative factors (irritant vs allergic contact dermatitis, etc.)
- can lead to: vescicles (serous fluid), scales (dry and flakey), and fissures (cracks)
2. Acne vulgaris
- inflammation of sebaceous glands
- results in papules, cysts (arise from dermis, semi-solid fluid), pustules
3. Psoriasis
- hyperproliferation of keratinocytes w incr. vasculature indermis
- immune-regulated chronic condition, comes and goes, can have triggers and/or be genetic
- leads to plaques and erythema
Non-infectious, inflammatory
41
Outline the three types of skin cancer
1. Basal cell carcinoma
- arises within the basal cells of the epidermis, most commonly in sun-exposed areas
- slow growing and rarely metastasizes
- highly variable in presentation
2. Squamous cell carcinoma
- arises within keratinocytes in the outer layers of the epidermis, can also arise from other sites lined with squamous epithelium (e.g. mouth, vagina)
- most commonly in sun-exposed areas
- slow-growing, but invasive (penetrates deeper layers); greater likelihood of metastasizing compared to basal cell carcinoma
- also high variation in presentation
3. Melanoma
- malignant tumours arising from melanocytes
- rapid growth and progression, high rate of metastasis
- Doesn't necessarily occur in sun-exposed areas
- changes over time in size, colour and shape; often have: irregular border, discolouration, diameter >6mm, and itching, bleeding, inflammation, oozing, crusting
42
Describe pressure injury and outline the six stages
- localized skin injury due to sustained pressure.
- compression --> reduced blood flow --> ischemia --> tissue necrosis and ulceration.
- Six stages:
1. Skin remains intact with localized area of erythema or discolouration that is non-blanchable.
2. Partial thickness injury that exposes the dermis; may appear blister-like.
3. Full thickness loss of skin that exposes the hypodermis; ulcer typically has rolled edges.
4. Full thickness loss of skin that exposes further underlying tissues such as fascia, tendon/muscle, ligament, bone, etc.
Unstageable: Full thickness loss of skin in which the extent of damage is unable to be confirmed due to dead tissue obscuring some of the injury.
Deep tissue injury: Injury in tissues deep to the skin which appears as a persistent, non-blanchable, deep red, maroon or purple discolouration or blood-filled blister (skin may or may not be intact).
43
*****Distinguish between arterial and venous ulcers
1. Venous ulcers:
- Venous insufficiency, e.g. varicose veins, DVT, venous hypertension
- Commonly located between the ankle and knee
- Shallow with irregular shape
- Exudate; moist, oozing
- Granulation tissue and fibrin present
- Assoc. w swelling, itching, skin hardening, dermatitis
- Discomfort alleviated w elevation
2. Arterial ulcers:
- Arterial insufficiency e.g. atherosclerosis, diabetes, arterial thromboembolism
- Commonly located on the toes, feet or shin
- Small, deep, round and well demarcated (punched out)
- Drier, less oozing
- Pale, necrotic
- Associated w: decr./no pedal pulses, intermittent claudication (cramp-like pain in limbs w mobilization), cool limbs, pallor (pale skin), lack of hair in region
- Discomfort alleviated w lowering of affected limb
44
Briefly describe the different possible mechanisms of neurotransmitter dysfunction
- Depression results from functionally deficient monoaminergic (noradrenaline and/or serotonin) transmissions in the CNS
-
45
describe the mechanism of action and side effects of tricyclic antidepressants, selective serotonin reuptake inhibitors and antipsychotics
1. TCAs:
- inhibit the reuptake of noradrenaline from synapse into monoaminergic nerve terminals, which incr. availability
- Dry mouth, blurred vision, urinary retention, constipation, sedation, postural hypotension. Also lower seizure threshold in people predisposed to epilepsy
2. SSRIs
- block reuptake of serotonin from synapse into presynaptic serotonergic nerve terminals, which incr. availability
- Mostly GI; Nausea, anorexia, insomnia
3. Antipsychotics
- Block (antagonists) D2 type receptors in postsynaptic receptors, incr. amount in the synaptic terminal
- Atypical antipsychotics also bind to other dopamine subtypes and serotonin receptors
- Atypical have fewer extrapyramidal effects, no tardive dyskinesia, negative symptom efficacy
46
outline the advantages and disadvantages of selective serotonin reuptake inhibitors
Advantages:
- Lack of anticholinergic and CV effects
- Less problem w weight gain
- Acute toxicity less than MAOIs or TCAs, so less risk of death by overdose
- No food reactions
Disadvantages:
- Nausea, anorexia, tremor, insomnia are common
- Can result in serotonin syndrome (hyperthermia, muscle rigidity, CV collapse) when combined w MAOIs
- Washout period required
- May cause syndrome of inappropriate ADH secretion particularly in elderly patients --> hyponatremia
47
describe neuroleptic induced motor disturbances
- Occur bc antipsychotics block dopamine receptors in the basal ganglia which may produce extrapyramidal (motor control) effects
- 3 main types of disturbances:
1. Acute reversible parkinson-like symptoms of tremor and rigidity
2. Dystonic reactions involving facial grimacing and muscle spasticity. Severe form is oculogyric crisis (eyes, jaw and tongue spasm --> choking)
3, Tardive dyskinesia: mainly involuntary movements of the face and limbs, usually not reversible
48
describe how NSAID's provide pain relief by inhibiting COX enzymes
COX-2
- enzyme that produces prostanoid mediators of inflammation
- Converts arachidonic acid into inflammatory prostaglandins
- therefore, inhibition blocks prostaglandin production and consequently reduces inflammation, pain, and fever
49
name the main classes of NSAID's
```
Aspirin
Paracetamol
Ibuprofen
Diclofenac
Indomethacin
Naproxen
```
50
describe why different classes of NSAID's would be chosen for treatment
1. Paracetamol:
- analgesic and antipyretic w little or no anti-inflammatory effects
- Well absorbed in GI tract, small vol. of distribution, 20-50% bound to plasma proteins
- t1/2 2-4 hours
2. Diclofenac (Voltaren)
- analgesic, antipyretic and anti-inflammatory effects
- well absorbed (oral)
- >99% bound to plasma proteins
- t1/2 0.5-2hrs
- Crosses placenta and expressed in breast milk
So: varying effects/targets, different metabolism and excretion depending on the person (e.g. kidney disease, pregnant, etc.)
607 Pathophysiology
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