OLT 1-3 Flashcards
Function of muscle
- Motion of the body
- Movement of substances in the body
- Regulating organ volume
- Stabilising body position
- Thermogenesis
Types of muscle
Cardiac
Smooth
Skeletal
what is cardiac muscle
Cardiac muscle tissue forms most of the wall of the heart. It is striated and involuntary.
Cardiac muscle is branched
Allows conduction of electricity in multiple directions rapidly
features of cardiac muscle
nucleus, branching cell and intercalated disc
what is smooth muscle
Smooth muscle tissue is located in viscera. It is nonstriated and involuntary.
An example of smooth muscle are muscles in the respiratory tract that control broncho-constriction / dilation
what is skeletal muscle
Skeletal muscle tissue is mostly attached to bones. It is striated and voluntary.
Responsible for body movement
Skeletal muscle is covered by what three layers
◦ Epimysium, perimysium and endomysium
◦ These layers form tendons
types of myscle fibres
- Slow Oxidative fibres (Red)- contract slow, resistant to tireing
- Fast Oxidative-glycolytic fibres- also red, can generate energy in addition to mitochondria= ability to maintain exercise for longer
- Fast Glycolytic fibers (White)- most powerful and rapid contractions, cant hold onto oxygen as much
Effect of aerobic exercise on muscles
Exercise alters the size and ability of muscles
Aerobic exercise:
Greater resistance to fatigue
Muscle cells form more mitochondria (store more oxygen)
Improved digestion & elimination
Cardiac hypertrophy
Effect of resistance (isometric) exercise on muscles
Exercise alters the size and ability of muscles
Resistance (isometric) exercise:
Strong contraction against resistance
Muscle enlarges – individual cells make more contractile elements
types of Joints
◦ Nonsynovial or synovial joints
◦ Cartilage
◦ Ligament
◦ Bursa
skeletal muscle movements
flexion- bending at a joint anterior to the body extension- straightening the joint towards the body abduction- movement away from the midline adduction- movement towards the midline pronation supination circumduction rotation protraction retraction elevation depression
Examples of abnormalities of the Spine
Scoliosis
Herniated nucleus pulposus
Common Congenital or Paediatric Abnormalities of the muscoskeletal system
Congenital dislocated hip
Talipes equinovarus (clubfoot)
Spina bifida
Coxa plana (Legg-Calvé-Perthes syndrome)
joints of the shoulder
Glenohumeral joint Rotator cuff (muscles and tendon ) Subacromial bursa Acromion process Greater tubercle of the humerus
Abnormalities of the Shoulder joint
Atrophy Dislocated shoulder ◦ Hunching of the shoulder forwards Joint effusion Tear of the rotator cuff Frozen shoulder—adhesive capsulitis Subacromial bursitis
Elbow joints
◦ Medial and lateral epicondyles
Abnormalities of the Elbow
Olecranon bursitis Gouty arthritis Subcutaneous nodules Epicondylitis—tennis elbow ◦ Lateral ◦ Radiates down extensor surface
joints of the wrist
Radiocarpal joint
Midcarpal joint
Metacarpophalangeal joints
Interphalangeal joints
Abnormalities of the Wrist and Hand
- Ganglion cyst
- Colles’ fracture
- Carpal tunnel syndrome- pinched nerve
- Ankylosis- abnormal stiffening of joint
- Dupuytren’s contracture-
- Swan-neck and boutonniere deformities
- Ulnar deviation or drift
- Degenerative joint disease or osteoarthritis
- Acute rheumatoid arthritis
Hip Joints
Acetabulum and head of femur
Anterior superior iliac spine
Ischial tuberosity
Greater trochanter of femur
Landmarks of the Knee
Femur, tibia and patella Suprapatellar pouch Medial and lateral menisci Cruciate ligaments Prepatellar bursa Quadriceps muscle
Ankle and Foot joints
Tibiotalar joint
Medial and lateral
malleolus
Metatarsals
Abnormalities of the Knee
Mild synovitis Prepatellar bursitis Swelling of menisci Osgood-Schlatter disease Chondromalacia patellae
Abnormalities of the Ankle and Foot
Achilles tenosynovitis Chronic/acute gout Hallux vagus with bunion and hammer toes Callus Plantar wart Ingrown toenail
Abnormalities Affecting Multiple Joints
Inflammatory conditions ◦ Rheumatoid arthritis ◦ Ankylosing spondylitis Degenerative conditions ◦ Osteoarthritis (degenerative joint disease) ◦ Osteoporosis
what is scoliosis
Lateral curvature of the spine
how to assess for spinal abnormalities
Feel
Midline spinous processes T1 – T12
L4/5 most common site of problems
Exact site of any tenderness - bony or muscular
Move
Can patient twist around to look at you?
Flexion, extension & lateral flexion
assess flexion, extension and lateral flexion
how to assess for pelvic abnormalities
Look Stance Shortening? Muscle wasting? Feel Tenderness – muscular e.g. strain of hamstrings Move
how to assess for abnormalities of the knees
Look
Effusion ( collection of fluid in joint)
Erythema
Deformity
Feel Heat Crepitus Patellar movement ? Ripple test
Move
McMurrays test- tests medial meniscus
Drawer test
what is the mcmurray test
examiner applies one hand at knee along medial meniscus
examiners other hand holds the foot and ankle
externally rotate the foot and apply valgus stress at the knee
slowly extend the knee
what is the anterior drawer test
examiner srasps upper calf with both hands.
fingers clasped behind the calf.
both thumbs on the tibial plateau region.
examiner pulls the tibia anteriorly in a sudden firm forward motion
assess for laxity
compare to laxity with the opposite knee
how to assess for abnormalities of the ankles
Look Swelling, deformity, erythema, bruising Feel Ottawa ankle rules Heat Move Active, passive, resisted
how to assess archilles tendon injury
“…felt like being shot…” “…heard a snap and looked around…” Minimal pain May be a palpable gap Active plantar flexion still possible Thomson Test
How to assess for abnormalities of the feet
Look Swelling, deformity, erythema, bruising Lymphangitis, wounds, Toenails Feel Ottawa ankle rules Move
how to assess for head musculoskeletal injury
Ears - ? Tophus
Eyes…?!
‘Dry eyes’ - keratoconjunctivtis
Manidible Look Symmetry Swelling / deformity Feel Tenderness – be specific – bony or soft tissue Movement
how to assess for musculoskeletal injury of the neck
Look Posture of head Deformity? Feel Tenderness – midline or soft tissue Paraspinal area, trapezius, interscapular area Move Flexion / extension Rotation Lateral flexion
how to assess for musculoskeletal injury of the shoulder
Look Normal deltoid contour? Bruising / swelling Feel Tenderness Crepitus Heat Move Flexion, extension Internal / external rotation Abduction / Adduction
how to assess for musculoskeletal injury of the elbow
Look Deformity, swelling, redness Feel Tenderness, crepitus Move Flexion / extension Supination / pronation
how to assess for musculoskeletal injury of the hand/ wrist
Look Colour change Swelling / deformity Heberdens / Bouchards nodes? Wounds / scars Feel Tenderness Parasthesia – constant / intermittent Move Loss of function Full grip Pincer grip
History taking specific to musculoskeletal system.
Presenting complaint Past history – co-morbid factors Past and current medication / drug use Family and genetic history Occupational, environmental and social history
how to assess presenting musculoskeletal complaints
Pain? – site, nature, radiation, timing, etc. Swelling / warmth Stiffness Locking Time since onset Mechanism of injury? Other symptoms…
how to assess past history in musculoskeletal assessment
Previous trauma
Previous incident of same complaint
Co-morbid factors – psoriasis, diabetes, stroke, obesity, gout…
Drug History
what family and genetic history to assess for in musculoskeletal assessment
Osteoarthritis, osteoporosis, gout, and some cases rheumatoid arthritis are hereditary.
Osteogenesis imperfecta
Marfans syndrome
Occupational, environmental and social history ( musculoskeletal assessment)
Occupational, environmental and social history
musculoskeletal assessment- principles of examination
General appearance
Cause no additional pain
Comparison of opposite sides
Examine joint proximal and distal to injury
Use standard terminology in describing positions and movement
Movements are always described from neutral position
LOOK
FEEL
MOVE
Common Musculoskeletal Disorders
- Osteoporosis
- Gout
- Arthritis – O/A R/A
structures in the long bone
cancellous bone, proximal epiphysis, articular cartilage, epiphyeal line, periosteum, compact bone, medullary cavity, diaphysis, distal epiphysis
what do OsteoBlasts do
- Form bone, but cannot divide by mitosis.
- Secrete collagen & other organic compounds
- needed to build osseous tissue.
what are osteocytes
• Prinicipal cells of bone tissue
No longer build bone
what do osteoclasts do
• Settle on surface of matrix and responsible for resorbtion
what is bone remodelling
- Bone is active and undergoes continual renewal
- Osteoclasts responsible for bone resorbtion
- Osteoblasts responsible for laying down new bone
- Need to be in balance so that bone is continually renewed or remodelled
- Parathyroid hormone, Calcitonin, Calcium levels and Vitamin D play a part in bone remodelling
- Balance alters with age and osteoclasts outnumber osteoblasts as we age
- Bones become more brittle
- Imbalances result in increased loss of bone mass ( osteoporosis)
- Inadequate mineralisation due to vitamin D deficiency (rickets, osteomalacia).
- Excessive bone destruction and repair resulting in structural weaknesses (Paget’s Disease)
what is Osteoporosis
• Defined as ‘porous bones’
• Loss of bone mass
• Imbalance between octeoclasts and osteoblasts.
• Manifests silently
• May present as a fracture (Hip)
• Bone becomes like fine china plate and minimal stress can cause a fracture
- dowagers hump may be seen
osteoporosis risk factors
• Risk factors: age, > females, males, post menopausal, sedentary lifestyle and calcium deficiency.
• Affects 15% of women and 3% men in Australia
• Pathogenesis is unclear
Hormonal factors play a part
osteoporosis diagnosis
• Bone Mineral Density Scan (BMD) • Dual-energy x-ray absorptiometry (DEXA) • Lab tests • Alk phos Osteocalcin (Gla protein)
what is osteoarthiritis
Non-inflammatory degenerative disease
Most commonly occurring form of arthritis
Leading cause of pain and disability in older adults
Begins with main load bearing joints – hips, knees – R.A. begins with smaller joints
how does osteoarthiritis occur
- Inflammation of the joints often secondary to physical damage (loss of hyaline cartilage, as bones rub and damage= inflammation)
- Reduced joint space & osteophyte formation
- Damaged joint tries to heal itself
- Creating osteophytes or spurs
- Cartilage contains more water, less collagen
- Cartilage becomes weak, rough, eroded
- No longer protects the surface of the bone
osteoarthiritis manifestations
- Gradual onset – progresses slowly
- Localised joint pain
- Pain may be associated with paresthesia
- < ROM of joints
- Enlarged joints
Osteoarthritis - diagnosis
- Subjective history
• X-rays of affected joints
• MRI
• Synovial fluid
what is rheumatoid arthiritis
- Chronic systemic autoimmune disorder
- Antibodies against IgG fragments
- Inflammation in the joint
- Abnormal healing responses lay down granulation tissue (pannus)
rheumatoid arthiritis cause
- Cause not yet established… possibly
- Behavioural – smoking
- Environmental
- Genetic
- Combination
- Defined as a systemic inflammatory disease
- Main effect is the destruction of articular cartilage and underlying bone
- Systemic effects include malaise, anorexia weight loss.
Nursing care in Rheumatoid
Arthritis
- Nursing care centres on the chronic nature of the disease
- Onset usually slow/gradual
- Patients can suffer acute exacerbation
- Medications
- Improve functional ability
- Involve the patient and family
- Encourage self care
what is gout
- Inflammatory response
- Caused by reduced excretion of uric acid
- Resulting in high levels of uric acid in the blood (hyperuriceamia)
- Causes deposits of urates in connective tissue
gout clinical manifestation
- Acute onset
- Usually involves 1st metatarso-phalangeal joint
- Attacks can be sporadic
- Long term
- Gouty arthritis
- Tophi- white deposits of uric acid you can see around joints
how is gout diagnosed
• Blood test o Uric Acid > o WCC > o ESR > (Acute attack) • 24hr Urine Specimen • Fluid aspirate from inflamed joint
how is gout treated
- Medications
- Nutrition
- Lose weight if >
- Fluid intake of >2L/day ( to help excrete uric acid)
- Rest
what is osteomylitis and who is at risk
- Infection of the bone
- Bacteria infection
- Older adults at > risk - < immune function
osteomylitis manifestations
- Cardiovascular
- GI
- Musculoskeletal
- Integumentary
osteomylitis diagnosis
- Bone scans
- MRI
- Bloods
- WBC
- ESR
- Biopsy
osteomylitis treatment
- Medications
- Antibiotic Therapy
- Surgery
- Debridement
- Muscle flaps
- ? amputation
Complications of Musculoskeletal injuries
Compartment Syndrome
• Necrosis
• Infection
what is Compartment Syndrome
Swelling inside the muscular compartment leading to decreased perfusion which in turn can lead to necrosis and muscle death.
SITES OF COMPARTMENT SYNDROME
most common is the lower leg
anterior compartment
lateral compartment
deep posterior compartment.
Increase in volume in compartment caused by
bleeding, infiltration of intravenous fluid or post-traumatic or ischaemic swelling.
the two compartments of the forearm,
the three compartments of the thigh
abdomen after laparotomy for major trauma
abdomen difficult or impossible to close.
open wound if the skin laceration is insufficient to decompress the oedema or if there is haemorrhage.
Elsewhere: the feet of patients with diabetes and the lower limbs after malignant hyperthermia.
steps of compartment syndrome
• 1. Pressure rise in compartment
• 2. Decrease in perfusion & oxygenation
• 3. Interstitial pressure overcomes intravascular pressure of capillaries ( don’t get blood supply!!!)
• 4. Vessel walls collapse, causing impedance of blood flow
• 5. Local tissue ischaemia
• 6. Oedema (leading to pressure rise in compartment )
(Irreversible necrosis of muscle and nerve tissue within the compartment will begin occurring in less than 12 hours if no action is taken.)
main signs of compartment syndrome
- PAIN: That is persistent, progressive and unremitting, is out of proportion to the injury, exacerbated by touch, stretching & elevation.
- PALLOR: The limbs may be a pale or dusky colour.
- PULSELESSNESS: By the time a limb has become pulseless it is an orthopaedic emergency. The pulse may be absent or diminished.
- PARAESTHESIA: As the nerves become ischaemic, paraesthesia may occur within the affected compartments.
- PARESIS: Report feelings of weakness in limb or it’s extremities
how is necrosis a complication of muscoskeletal injury
Usually secondary to compartment syndrome
Can be related to initial mechanism of injury. Blood supply is interrupted and the tissues die leading to necrosis.
Neurovascular injuries:
Permanent deficit due to initial trauma
Intra-operative damage to nerves and blood supply.
how is infection a complication of muscoskeletal injury
- Open fracture - opportunistic infection to occur in the bone
- Osteomyelitis
- Osteomyelitis in compromised patients where there is disruption to skin integrity
treatment for musculoskeletal injury pain
Appropriate pain relief should be administered as soon as possible Splinting Appropriate route for injury Heat/cold Elevation Compression Muscle relaxants Traction
4 main structures of the musculoskeletal system
- Bones
- Muscles
- Tendons
- Ligaments
4 types of musculoskeletal injury
Strain
Sprain
Dislocation
Fracture
sprain vs strain
Sprain - partial or complete tearing of LIGAMENTS and tissues at the joint.
Strain - An extreme stretching or tearing of MUSCLE &/OR TENDON.
dislocation?
Dislocation - displacement or separation of a bone from its normal position at the joint.
fracture?
Fracture - a break or disruption in bone
Open - the skin is pierced by broken bone fragments
Closed - the broken bones do not penetrate the skin
Recognizing Musculoskeletal Injury
General Injuries
Pain? – site, nature, radiation, timing, etc. Swelling / warmth Stiffness Locking Time since onset Mechanism of injury? Other symptoms…
Recognition of Suspected Serious musculoskeletal Injury
- Significant deformity
- Moderate or severe swelling and discoloration
- Inability to move or use the affected part
- Bone fragments protruding from the wound
- Bones grating or a pop or snap heard by the victim
- Loss of circulation in an extremity.
signs and symptoms of sprains and strains
- Signs and Symptoms include
* Swelling, pain, redness, inability to bear weight on affected joint.
treatment of sprains and strains
R
I
C
E
Rest
Ice
Compression
Elevation
signs of fractures
- Immediate localised pain
- Decreased Function
- Inability to weight bear or use affected part
- Muscle spasm
- Swelling, guarding, ecchymosis
- Self splinting
fracture classifications
Transverse Oblique Spiral Comminuted Segmental Butterfly Impacted
describe the bone healing process
Hematoma forms and fibrin network fills it
Cells grow along fibrin meshwork to form new tissue
Calcium salts deposited in new tissue
New tissue remodeled into normal shape
fracture management treatment options
Closed Reduction
Non Surgical
Manual Realignment
Plaster casting
describe cast splintage
Can be made of plaster or synthetic material
A backslab is used initially
Adequate padding over bony prominences
The joint above and below the # should be immobilised
Limb kept elevated
Regular neurovascular observations
cast care advice
Encourage patient movement of fingers and toes
Elevate the limb to help reduce pain and swelling.
DO NOT use anything to scratch under the cast.
NEVER allow the patient to cut or trim the cast
Avoid allowing the cast becoming wet.
types of fracuture management options
Surgical Intervention
Internal fixation
External Fixation
fracture management- surgical intervention
- ORIF (Open Reduction, Internal Fixation)
- Indications for internal
- fixation are:
- Failure of closed reduction
- Unstable #’s
- Pathological #’s
- Fractures that generally unite poorly
- Multiple fractures
- Methods:
- Screws & Plates
- Steel Wires
- Intra-Medullary nails
describe external fixation for fracture treatment
Transfixing screws are passed through the bone and are attached to an external frame.
Indications for external fixation include:
# ‘s associated with severe soft tissue injury
Severe multiple injuries
Pelvic # ‘s
Infected #’ ‘s
function of the oral cavity
is the first part of the digestive tract. It is adapted to receive food by ingestion, break it into small particles by mastication, and mix it with saliva. The lips, cheeks, and palate form the boundaries.
function of the tongue
Your tongue helps out, pushing the food around while you chew with your teeth. When you’re ready to swallow, the tongue pushes a tiny bit of mushed-up food called a bolus (say: BO-luss) toward the back of your throat and into the opening of your esophagus, the second part of the digestive tract
function of the pharynx
Also called the throat, your pharynx is the part of the digestive tract that gets the food from your mouth. Branching off the pharynx is the esophagus, which carries food to your stomach, and your trachea or windpipe, which carries air to your lungs.
function of the Salivary glands (parotid, sublingual, submandibular)-
Parotid- These glands secrete a protein-rich fluid which is a suspension of alpha-amylase enzyme
parotid glands produce a serous, watery secretion. submaxillary (mandibular) glands produce a mixed serous and mucous secretion. sublingual glands secrete a saliva that is predominantly mucous in character.
function of the oesophagus
- The esophagus is a muscular tube that goes from your pharynx (throat) to your stomach. Food is pushed through your esophagus and into your stomach with a series of muscle contractions.
function of the intestines
Small- Your small intestine also breaks down food using enzymes made in your pancreas and bile from your liver. The small intestine is the “work horse”’ of digestion – while food is there, nutrients are absorbed through the walls and into your bloodstream.
Large- The large intestine is much broader than the small intestine and takes a much straighter path through your belly, or abdomen. The purpose of the large intestine is to absorb water and salts from the material that has not been digested as food, and get rid of any waste products left over.
what are accessory organs
An organ that helps with digestion but is not part of the digestive tract. The accessory digestive organs are the tongue, salivary glands, pancreas, liver, appendix and gallbladder.
pathophysiology of nausea and vomiting
Stimuli (environmental, psychological, physiological)
Peripheral → Autonomic Nervous System
↓parasympathetic and ↑sympathetic activity (vagus [pneumogastric] nerve or vestibular nerve)
Central: CNS -Medulla oblongata → vomiting centre & CTZ (chemoreceptor trigger zone- triggered by chemicals, contains dopamine and serotonin receptors- CTZ stimulates muscarinic receptors of vomiting centre, when muscarinic receptors of VC are stimulated this causes emetic reflex)
Hormones – serotonin (5-HT) and dopamine (D2)
how does motion sickness work
Motion causes stimulation of the labyrinth of inner ear (balance & movement perception) → vestibular nerve → CTZ → histamine release → release of serotonin and dopamine → Vomiting centre = N & V.
role of diaphragm in nausea and vomiting
Motor response/act of vomiting – stimulation of phrenic nerve = contraction of abdominal muscles, parasternal intercostal muscles, and costal part of the diaphragm during vomiting = ↑ abdominal pressure and aid expulsion of gastric contents.
causes of nausea and vomiting
Medications (e.g. opioids, chemotherapy, some antibiotics etc.) –including interactions & adverse reactions.
Anaesthesia
Pain, anxiety, unpleasant sight/smell/taste
Symptoms associated with an underlying GI condition (e.g. bacterial/viral infection, bowel obstruction, constipation, GORD, gastroenteritis, diverticulitis, peritonitis etc.)
treatment of nausea and vomiting
dopamine (D2) and serotonin (5HT) antagonists (A substance that acts against and blocks an action) (e.g. metoclopramide, ondansetron)
examples of 5HT3 (serotonin) receptor antagonist antiemetic medications
ondansetron, dolasetron, tropisetron
indications of 5HT3 (serotonin) receptor antagonists
N and V, GORD, hyperacidiy, peptic ulcer disease, gastric and duodenal ulcers, hypermotility, erosive osophagitis
MOA of 5HT3 (serotonin) receptor antagonists
blocks seretonin 5HT3 receptos in the CTZ and vomit center, which are located in the medulla obongata. also blocks seretonin receptors peripherally (vagus nerve). this reduces communication with the vomit center and the chemoreceptor triggerzone (CTZ) therefore inhibiting the initiation of the vomiting reflex.
adverse effects of 5HT3 (serotonin) receptor antagonists
headache, warm/ flushing sensation, constipation, xerostoma (dry mouth from decreased saliva production), irritation at injection site dizziness
contraindications of 5HT3 (serotonin) receptor antagonists
- giving it with apomorphine ( lowers BP, LOC)
- Not to be given concurrently with other serotonergic drugs as may cause seretonin syndrome
- patients with congenital QT syndrome and patients with electrolyte abnormities, CHF, bradyarrhythmia
Pathophysiology of GORD
– periodic relaxation of lower oesophageal sphincter = mucosa exposed to acid enzymes & become damaged = abnormal spaces in mucosal epithelium = overstimulation of nerve endings and peripheral sensation.
• Symptoms of Mucosal Damage (Oesophagitis)
• Exposure to acidic stomach contents
• Very Common
• Due to relaxation of the gastro-oesophageal sphincter
Causes of GORD, what excabates it
Exacerbated by other gastrointestinal disorders (e.g. Hiatus hernia, central obesity, impaired gastric emptying). H-Pylori, medications that cause dyspepsia (indigestion)
Other causes include– stress, high fat & spicy foods, NSAIDS, alcohol & caffeine.
Clinical manifestations of GORD
Clinical manifestations – heartburn, regurgitation, belching, nausea, feeling bloated, angina type chest pain, cough, hoarse/sore throat, wheeze.
--- • Pain Epigastrium Chest Throat Jaw Arms • Dysphagia • Sweating •
Treatment of GORD
Treatment /Management-:
Pharmacological: Proton Pump Inhibitors (PPI’s) – e.g. omeprazole, pantoprazole etc.
Non-pharmacological: diet –avoiding alcohol, caffeine, high fat & spicy foods ; stress minimisation and management
• None- self limiting
• Medication:
Acid blocking medications (H2 -receptor agonists eg Ranitadine)
Stomach acid production inhibitors (Proton Pump Inhibitors eg Omeprozole)
• Diet
• Smoking cessation
Weight loss
Complications of GORD
Complications: oesophagitis, oesophageal strictures, Barrett’s oesophagus (pre-cancerous changes to epithelium), gastro-oesophageal ulcers & bleeding, aspiration, sinusitis, adult onset of asthma.
examples of Proton pump inhibitor medications (PPIs)
omeprazole, pantoprazole, esomeprazole
indications of PPIs
GORD, Hyperacidity, peptic ulcer disease, gastric and duodenal ulcers, hypermotility, erosive osophagitis
PPI MOA
Inhibits gastric acid secretion by inhibiting the K+/ H+ pump ( potassium pump) located on the apical membrane of the gastric pariental cells, inhibiting secretion of H+ acid into stomatch
PPI adverse effects
headache, constipation/ diarrhoea, abdominal discomfort, flatulence, fever
PPI contraindications
patients taking cilostazol ( as its an antiplatelet/ vasodilator)
ppts with acute intestial nephritis
if given with clopidrogel
entric coated- must not be dissolved, halved or crushed
what are Oesophageal varices
(dilation of distal oesophageal veins that connect portal & systemic circulations)
Pathophysiology of oesophageal varices
Pathophysiology:
Oesophageal varicose veins
→ direct result of liver dysfunction secondary to a clot or scarring
= ↓blood flow to the liver → Blood flow therefore redirects to smaller vessels (e.g. such as those located in the lower aspect of the oesophagus)→ raised oesophageal venous pressure/portal HTN
Clinical manifestations of Oesophageal varices
Clinical manifestations:
Pain, Nausea, Haematemesis, +++ blood loss, Hypovolaemia, collapse, death (30-50% - 1st bleed)
--- • Pain • Nausea • Haematemesis (blood in vomit) • MASSIVE blood loss • Hypovolaemia • Collapse • DEATH
