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
complications of Oesophageal varices
Infection (e.g. bacterial peritonitis)
Bleeding/haemorrhage
Hepatic encephalopathy
Oesophageal stricture (post banding or sclerotherapy)
treatment of Oesophageal varices
Pharmacological – beta blockers (e.g. propranolol) to ↓ portal HTN & bleeding risk; Blood transfusion; vasoactive medications (vasopressin). Antibiotics (e.g. ceftriaxone) if bleeding present.
Surgical: variceal banding; sclerotherapy, Balloon Tamponade (last resort)
- Bleed first then varices
• Pharmacological:
Medication to reduce portal hypertension and prevent bleeding
• Endoscopic:
Variceal Banding – Elastic Band used to tie the point of bleeding
Sclerotherapy – Drug injected into bleeding site
• Balloon Tamponade:
Emergency Proceedure
Sengstaken tube/Minnesota Tube
pathophysiology of pancreatitis
Pathophysiology: Inflammatory disorder (inflammation of the pancreas) - can be acute (short term) or chronic (persistent/ongoing inflammation)
Causes: alcoholism & smoking- most common- (acute /chronic), blocked biliary tract (acute) to strictures and pancreatic cysts (chronic)
--- Rare Tends to affect people >50 Causes • Alcoholism • Biliary tract obstruction • Peptic Ulcers • Trauma • Hyperlipidaemia • Medications
clinical manifestations of pancreatitis
Upper abdominal pain (radiating towards the back)
Nausea & vomiting
Fever
Tachycardia
Steatorrhoea (fatty stools) – chronic..
..monitoring withdrawal symptoms..
complications of pancreatitis
Complications: Pancreatic cancer Infection Kidney failure Type 2 diabetes- cos effect on pancreas and beta cells
treatment of pancreatitis
Treatment: Analgesia (e.g. Opioids) NBM IV Fluids Medications to manage alcohol withdrawal symptoms (e.g. diazepam)
often made nil by mouth
Treatment
o Analgesia
Opioids
NBM (nil by mouth)
NG Suction (subjective data ascertain risk of vomiting meaning NG tube required)
IV Fluids (if actively vomiting or has been NBM for a while)
Medications eg. Antispasmotic, buscam, antimetics, antibiotics
pathophysiology of diverticulitis
Pathophysiology:
Development of diverticula (pockets/pouches) in the colon. Become inflamed & infected.
3 areas associated with the development of this condition.
1. structural abnormalities of the colonic wall
2. disordered intestinal motility
3. Low fibre diet (fibre deficiencies)
clinical manifestations of diverticulitis
Clinical manifestations:
Intermittent or constant abdominal pain (lower left quadrant)
Fever
N & V
Constipation (most common) diarrhoea (less common)- some patients chop and change, but often one or other
low fibre diet
diverticulitis complications
Complications:
Abscess, Fistula , Bowel obstruction, Bleeding, sepsis,
Rare: pylephlebitis (inflamed thrombosis of portal vein) – complication secondary to intra-abdominal infection.
diverticulitis treatment
Treatment:
Pharmacological: double/triple antibiotic therapy (metronidazole, tazosin, ciprofloxacin, cephazolin), IVT, analgesia (opioids)
Surgical: sever/life threatening
Bowel resection (e.g. sigmoidectomy) ? Colostomy Open or laparoscopic
Other: dietary changes (e.g. ↑fibre)
often encourage patient to keep a diet diary ( as there are some foods that exacebate symptoms for patients)
Peritonitis
(inflammation of the peritoneum) pathophysiology
Pathophysiology:
Inflammation of the peritoneum (serous membrane that lines abdominal organs)
Physiological response to a severe bacterial infection either via the bloodstream or as the result of the rupture of an abdominal organ.
Life threatening - emergency
clinical manifestations of peritonitis
Clinical manifestations: Feeling of bloating of fullness in abdomen Fever, anorexia, N & V, Oliguria / anuria Diarrhoea, fatigue, confusion, Presence of a paralytic ileus
peritonitis complications
Complications:
Life threatening –sepsis, multi-organ failure, shock, hepatic encephalopathy.
peritonitis treatment
Treatment:
Multidisciplinary
NBM (nil by mouth), NGT, Antibiotics (ceftriaxone/ cephazolin & metronidazole). IVT, analgesia (opioids), iDC (to monitor urine output- min req 30ml per hour average/ 0.5 ml per kilo per hour) , A-E. Surgery-resection (to remove infected tissue)
malnutrition pathophysiology
■ Pathophysiology
Inadequate nutrient intake, impaired nutrient absorption or loss of nutrients (short or long-term) that results in an imbalance between intake and the body’s protein and energy requirements = loss of tissue and functionality.
glycogenesis/breakdown of fats/ketones/ ? metabolic acidosis
malnutrition clinical manifestations
Fatigue, anorexia, muscle weakness & cramping, altered cognitive functioning –confusion/poor concentration, depressive symptoms, impaired healing, impaired thermoregulation etc.
Pale oral mucosa, poor skin turgor, emaciated, brittle hair, pressure ulcers/chronic wounds, stunting (children)
malnutrition management
Treat underlying cause, nutrient replacement
Dietician referral
oral, parenteral (e.g. NGT, PEG) or enteral nutrition (IV): temporary high cal food supplement.
Development of healthy diet plan (e.g. small/frequent meals)
Psychological /psychiatric assessment and support
Speech therapist referral - assess for dysphagia - ? Need for NGT or PEG tube
OT referral – assess home needs (meals on wheels, kitchen/eating aids etc.).
Family involvement –as appropriate
malnutrition complications
↓muscle & tissue mass; ↓mobility; convulsions
↑ risk of Diabetes, cardiovascular disease, kidney disease, infertility, stroke, pneumonia and other respiratory complications.
Gastrointestinal: Age related changes
■ ↓ saliva production (1/3)
■ Gingiva retraction
■ Reduced oesophageal function (↓ propulsion, weaker gag reflex).
■ Gastric mucosa atrophies, ↓acid production, (atrophic gastritis due to ↓ digestion of proteins (e.g. intrinsic factor). Elderly at ↑risk of developing:
Pernicious anaemia
Gastric cancer
■ Atrophy of walls of small and large intestine. ↓motility
Small intestine: ↓production of digestive enzymes
Large intestine: formation of pockets (diverticuli)
■ No. of pancreatic secretory cells ↓ = ↓ digestion of fats.
■ Impact of long-standing/underying conditions:
diabetes can = ↓ gastric emptying (approx. 50%)
Helicobacter Pylori can cause gastric atrophy rather than aging (approx. 60%).
What is the GI tract
‘….a long tube running from the mouth to the anus, which is divided into different organs: mouth, pharynx, oesophagus, stomach, small intestine and large intestine’
What is the Upper GI tract
‘Mouth , the oesophagus and the stomach’
What is the sphincter
• Specialised ring of circular muscle
When contracted food cannot progress.
• Sphincters located at at accessory organ ports
Sphincters need to relax to allow accessory organ secretions to enter the GI tract
• Sphincters allowing secretions into GI tract allow for digestive processes
what happens in the mouth
Mix food and saliva to begin digestive process
causes stimulation of chemoreceptors and olfactory nerves- encourage desire to eat and encourage uptake of nutrients
1.5 liters of saliva a day
what does the pharynx do
Nasopharynx/oropharynx/laryngopharynx
Pharynx Leads to the oesophagus
what is the oesophagus
- Hollow muscular tube
- Approx. 25cm long
- Sphincter at each end. Upper prevents air entering, lower prevents regurgitation from stomach
- Upper third contains striated/ voluntary Muscle- innervated by motor neurons
- Lower two thirds contain smooth muscle- innervated by parasympathetic nervous system
- Peristaltic action for swallowing
what is the stomatch
- Muscular organ
- Stores/mixes food for correct absorption
- Continues digestion- expels chyme into small intestime after
- Major anatomical considerations
sphincters of the stomatch
Oesophageal sphincter- allows food to be passed through stomach once it dilates
Pyloric sphincter- relaxes and food is propelled through the gastro-duodenal junction into the duonenum
functional areas of the stomatch
• Functional areas- these areas have glands producing different enzymes to aid with digestion
Fundus (top of stomach)
Antrum (bottom of stomach)
how much can the stomatch expand
At rest- 50ml of fluid and is small but can expand to maintain 4L
Upper Gastrointestinal: Age related changes
• Teeth >root cavities Enamel harder/brittle.. lead to increased root canities >loss of bone supporting teeth • Gums Gingiva retracts.. can lead to less bone supporting teeth or oral cavities.. can lead to pts needing dentures • Saliva tooth loss/fractures of teeth/dentures • Gums > periodontal disease • Saliva < ability to break down starches > swallowing time • Oesophageal Motility Discomfort > risk of aspiration • Stomach > gastric irritation
what does the lower GI tract consist of
Small intestine
Large intestine
o Ancillary organs
what do the Ancillary organs do
Secrete substances that are required for digestion of chyme and therefore maintain a healthy GI tract
Connected to but does not form part of the GI tract:
liver, pancreas, gallbladder
what does the liver do
Liver prouces bile= necessessary for the digestion and absorption of fat. Liver mainly processes nutrients absorbed from the small intestines, bile from liver secreted into the small intestine also plays an impotant role in digesting fat… Enzymes are secreted by the pancreas into the SI, there they continue breaking down food that has left the stomach
what does the pancreas do
Pancreas produces enzymes= responsible for digestion of carbohydrates, proteins and some fats
These enymes are an alkaline fluid that neutralises the chyma
what does the gallbladder do
Gall Bladder stores bile when not being used. primary function is to store and concentrate bile yellow/ brown digestive enz prod by liver. The gallbladder is bart of the billary tract
what does bile do
Bile helps the digestive process by breaking up fats, it alsodrains waste products from the liver and duodenum- part of the small intestine
Secretions enter duodenum through ducts and different enzymes are released at different times at different places depending on the specific need of the GI tract at that specific time
small intestine size
Small diameter- 2.5 cm
5m long
describe small intestine
3 structures
Duodenum
Jejenum
Ileum
- All very similar
- Illeal cecal valve controls flow of digestive material from the illium to the large intestine
- Movements of the small intestine aid digestion and absorption, chyme stimulates movement, mixes scretions from the ancillary organs, peristalsis moves food to the lage intestines
large intestine size
- Large diameter 7cm
- Short 1.5m long
describe large intestine
- Cecum, appendix and colon divided into ascending transverse, descending and sigmoid colon, As well as rectum and anal canal are essential for understanding anatomy and physiology
- Cecum receives chyme
- 2 sphincters control how the chyme is moved through the large intestine. The illeocaecal valve allows chyme to move from the small to the large intestine and the O’bierne sphincter which controls movement from the colon to the rectum
how does the anus and rectum work
- Complex
- Multiple components
- Aids defecation
- Movement of faeces into sigmoid colon and rectum stimulate defecation/ rectal reflex
- Controlled by anal sphincter which relaxes and creates urge to defecate.. which is controlled by the autonomic nervous system
- Defecation reflex can be over ridden by the contraction of the external anal sphincter
parts of anal/ rectal canal
Anal canal Sphincters Anal columns Anorectal junction Anal valve Anal crypt Rectum Valves of Houston Peritoneal reflection
Oesophageal Disorders
- Dysphagia • Gasto-oesophageal Reflux Disease (GORD) (Heartburn) • Oesophageal Moniliasis (Infection) • Hiatus Hernia • Carcinoma • Oesophageal Perforation • Oesophageal Bleeding
what is a hiatus hernia
• Hernation of a portion of the stomach through the oesophageal hiatus in the diaphragm • Disrupts the lower sphincter function • Impairs oesophageal Clearance • More common in women Most frequent in middle age onwards
Hiatus hernia symptoms
• None • Gastric Reflux • Heartburn • Pain common after eating • Pain on bending • Pain when lying down Bleeding – Anaemia
hiatus hernia treatment
• Lifestyle changes Losing weight Small meals Avoid bending from waist Sleeping well supported Smoking cessation Medication (see GORD) Surgery
causes of oesophageal bleeding
- Oesophagitis- where stomatch acid has been exposed to esophagus causing inflammation. Prolonged exposure can cause erosion which can cause bleeding, if vessels become eroded can cause larger bleeds
- Mallory Weiss Tear- small tear in the esophagus often caused by increased pressure in the esophagus caused by wrething and vomiting. Normally not a big problem unless you have clotting disorder caused by congenital disorder or alcoholism
- Varices
- Neoplasia/ growths in the oesophagus
- Drugs: NSAIDS/ Aspirin / Alcohol
what are varices
- Varicose veins that occur in GI tract
- Account for 5-10% of all medical admissions
- Mortality 30-50% on presentation of 1st bleed
- Varices formed as direct result of liver dysfunction (as indicated with alcohol abuse) which resulting in raised oesophageal venous pressure causing the varicose veins
oesophageal varices nursing interventions
• LOOK at your Patient • ABCDE • Blood Transfusion • Support • Monitor Observe patient Closely
why do we vomit/ get nauseaus
• Defence mechanism
– removes toxic or harmful substances from body
– memory of previous encounters leads to avoidance
• Medical interventions (e.g. surgery, chemotherapy, radiotherapy, drugs) can interfere with normal mechanisms
Causes of N and V
• Forceful expulsion of gastric contents from the mouth • Caused by – powerful sustained contraction of abdominal muscles – descent of diaphragm – opening of gastric cardia • Involves co-ordination of – abdominal muscles – gastrointestinal muscles – respiratory muscles • Controlled by the Vomiting Centre
Types of nausea and vomiting
- Post-operative nausea and vomiting (PONV)
- Opioid-induced nausea and vomiting
- Chemotherapy- and radiotherapy-induced nausea and vomiting
- Nausea and vomiting in early pregnancy
- Motion sickness and vestibular disorders
• PONV - patient risk factors
• Incidence 20-37 % • Risk factors o Patient factors o Procedural factors o Anaesthetic factors o Post-operative factors
- Gender (female patients especially)
- Age (peak 11-14 years)
- Obesity
- Migraine
- Pre-operative eating patterns
- Prior history of PONV or motion sickness
- Anxiety
- Gastroparesis (problem with muscles and nerves of the stomatch)
• Consequences of PONV
• Practical consequences o Patient discomfort o Soiling • Medical complications o Wound dehiscence o Aspiration of vomit o Electrolyte imbalance and dehydration o Delayed oral therapy • Economic burden o Medical personnel time o Unplanned admission/delayed discharge o Bed blocking
what is gastritis
inflammatory disorder of the gastric mucosa’ (Craft and Gordon 2015 p 779)
Acute or Chronic
Acute erodes the surface epuithelium resulting in superficial damage
Chronic often affects the elderly, causes thinning and degeneration of the stomach wall
Acute gastritis commonly caused by ingestion of irritant e.g. NSAIDS or alcohol
causes of gastritis
Acute gastritis commonly caused by ingestion of irritant e.g. NSAIDS or alcohol Chronic Gastritis caused by: Pernicious anaemia Autoimmune disorders Alcohol abuse Peptic ulceration Certain cancer Chronic contains the antramoni and occurs 4 times more often than bundle gastritis Antral- bottom, bundle top of stomatch
gastritis symptoms
PAIN ( localised over stomatch) Bloating Nausea Vomiting Anorexia Indigestion
gastritis treatment
• Acute Episode: Antiemetic IV Fluids if Vomiting +++ Mouth Care Analgesics • Medication: Antacid H2 blocker • If Helicobactor pylori found – antibiotic therapy • Dietary Advice
what is a peptic ulcer
Occurs in Stomach and Duodenum
Caused by damage to areas exposed to acid and pepsin containing secretions
Smoking and Stress increase acid production
Alcohol and coffee cause gastric erosion
Helicobactor Pylori (1982) significant cause of peptic ulcer disease
symptoms of peptic ulcer
Pain (Burning) Epigastrium Usually pain is localised
Dyspepsia
Duodenal Ulcer= usually pain 3-4 hours post meal
Gastric ulcer= pain 30-60min post meal
Belching
peptic ulcer diagnosis
Moved from Hospital care to Primary Care
Recognition of Helicobacter pylori 1982
H Pylori major factor in causing damage
H Pylori present in 90% of all patients with DU
Present in 75-80% patients with gastric ulcers
Diagnosis made from blood, biopsy or breath test
Endoscopy
what is Helicobater Pylori
- The major cause of ulcers
* Second most common cause is NSAIDs
peptic ulcer treatment
Eradication therapy if H Pylori detected – Antibiotic therapy Antacid H2 – Receptor antagonists eg Ranitadine PPI eg Omeprazole Discontinue NSAIDS/Aspirin Dietary Advice Smoking cessation Diarrhoea and constipation
what is constipation
‘difficult or infrequent defecation’
Common complaint
Normal bowel habits – 1-3 times per day - once per week
Causes of constipation
Neurogenic disorders
Large Intestine
Neural pathways/neurotransmitters altered
Parkinson’s disease
Personal Habits
Low fibre diet
Highly refined (Processed) foods (white bread, snacks, cakes etc)
Sedentary lifestyle
Excessive use of antacids (Calcium carbonate)
Opioid Analgesics
Problems with constipation
Serious Can lead to perforation of the bowels Can cause death Pain Straining Cardiac issues Bradycardia (Valsalva manoeuvre) MI
Assessment and Treatment of constipation
Subjective data Bowel habits Bristol Stool Chart Objective data Abdominal Assessment PR exam Abdominal X-Ray/Barium Enema Treatment Manage underlying disorder Increase fluid/fibre intake Laxatives/stool softeners/enemas
what is diarrhoea
‘increase in the frequency of defecation and the fluidity and volume of faeces’ (Craft & Gordon 2015 p796)
More than 3 stools/day – Abnormal
Stool volume normal adult – 200grams/day
types of diarrhoea
Osmotic diarrhoea
Produces large volumes
Caused by:
Lactase and pancreatic enzyme deficiency
Excessive ingestion of synthetic sugars (artificial sweeteners)
Secretory diarrhoea
Excessive mucosal secretion
Caused by:
E-Coli
Clostridium Difficile (C-Diff)
Small volume diarrhea can also occur being caused by chromes disease, faecal impaction or ulcerative cholitis
Problems with diarrhoea
Acute or chronic
Pain is problematic
If caused by bacterial infection can cause fever, cramping and bloody stool
Steteral is fat in stool, lign of malabsorption syndrome, stool specimen must be taken to rule out any of these
Acute
Fatigue, thirst, nausea, headache
Chronic
Dehydration
Electrolyte imbalance
Excessive loss of potassium and sodium- can have systemic effects on ther systems
assessment and treatment of diarrhoea
Assessment and treatment Subjective data Bowel habits Bristol Stool Chart Exposure to contaminated food Travel Objective data Abdominal Assessment Stool specimen Abdominal X-Ray Treatment Fluid Resus Treat causal factors eg. Antibiotics for bacterial infection Nutritional support/balance
difference between acute and chronic pancreatitis
Acute Mild disease Alcoholism /biliary tract obstruction Enzyme outflow blocked – leak into pancreatic tissue - Causes inflammation - Causing Systemic effects • Cardiac • Coagulation • Renal MODS ( multiple organ dysfunction syndrome)
Chronic Due to structural and functional impairment Alcoholism Smoking Lesions caused by • Fibrosis • Strictures • Pancreatic cysts Risk Pancreatic Cancer
assessment for treatment of pancreatitits
Subjective data
• Pain
• Time
• Hx – Pain post eating
Objective data
• Lab tests
• Pancreatic amylase- indicator for pancreatitis
• Serum Lipase- indicator for pancreatitis
• CRP (inflammatory marker may be indicative of systemic inflammation… although test not specific to pancreatitis)
what is gantroenteritis and its causes
Inflammation of stomach and small intestine
Causes: • Bacteria • Viruses • Parasites • Toxins
what are the primary mechanisms of gastroenteritis
2 primary mechanisms
Production of exotoxins Invasion and ulceration of mucosa
Explain the 2 primary mechanisms of gastroenteritis
2 primary mechanisms
Bacteria/ virus cause inflammation and tissue damage
Production of exotoxins- bacteria can produce and excrete an exotoxin that enters the gastric lumen causing damage and inflammation, exotoxins impair absorption and can cause secretions of significant amounts of electrolytes and water into bowel resulting in diarrhoea and fluid loss common bacterial endotoxins seen in clinical practice- staphylococcus, e coli and clostrium differseal Invasion and ulceration of mucosa- other bacteria such as salmonella and cert e coli strains directly damage the GI tissue causing ulceration of the small bowel and colon causing bleeding, fluid loss and as in exotoxin cause producing significant electrolytes and water into bowel resulting in diarrhoea
gastroenteritis manifestations
GI Effects • Anorexia • Nausea & Vomiting • Abdominal Pain • Cramping • Diarrhoea • Loud bowel sounds/gurgling
general effects of gastroenteritis
- Malaise/weakness
- Muscle aches
- Headache
- Dry skin/mucous membranes
- Poor skin turgor
- Orthostatic hypotension
- Tachycardia
- > Temp/ pyrexia
assessment and treatment for gastroenteritis
Diagnosis • Lab tests after 48hrs severe symptoms o U & E (urea and electrolytes) o Acid base • ABG’s • Stool Sample
Treatments • Usually self limiting • Medications o AB’s – specific organism o Antidiarrheal drugs • Fluid Replacement therapy
what is a stoma
Intestinal ostomy surgically created opening between intestine and abdominal wall – allows the passage of faecal material
Name depends on location
Ileostomy – ostomy made of ileum and small intestine
Colostomy – ostomy made in the colon
Can be temporary or permanent
reasons for stomas
IBD (inflammatory bowel disease)
• Ulcerative Colitis
• Crohns
(more common for these conditions to have ileostomy )
Cancers
Tumors
(more common for these conditions to have colostomy )
Bowel Obstruction- used for treatment
care considerations for stomas
- Pre-operative education
- Role of the stomal therapist
- Check the stoma as part of the post op observations
- Expect it to be red with moderate oedema and a small amount of bleeding
- Stoma bag will be in situ
- Bowel will be slow to regain normal peristalsis due to the anaesthesia.
what do antiemetics do
- Symptom Control
- Nausea
Chemoreceptor trigger zone in the 4th ventricle, activated by CSF blood borne emetics, chemical toxins and drugs
Also mediated by neurotransmitter 5HT which is released from afferent nerve pathw in stom and small in. it communicates with emetic center in medullar
Chemoreceptor trigger zone doesn’t nduse vom, just relays messages to the emetic center via neurotransmitters such as acetyl choine, 5HT, histamine and dopamin
Medications to control Nausea and Vomiting MOA
- Act principally by blocking neurotransmitters in emetic centre, the cerebral cortex, the CTZ or the vestibular apparatus ( VA is in the ear and it deals solely with balance so for example when we’re looking at medications that are used to control the nausea that comes with seasickness that’s where the vestibular apparatus comes into it )
- Dopamine antagonists
- Muscarinic receptor antagonists
- 5-HT3 –receptor antagonists
Dopamine Antagonists examples
• Metoclopramide, prochlorperazine, domperidone
Mechanisms of Hormone Regulation
Secretion Patterns Diurnal Patterns Pulsatile and cyclic Patterns Dependent on Circulating substances All hormone release operate within feedback loops to maintain internal environment Triggers for hormone release Chemical factors Endocrine factors Neural control
Regulation of Target Cell Sensitivity
The sensitivity of a target cell to its hormone is related to the number of receptors per cell.
Target cells adjust to levels of hormones by increasing or decreasing the number of receptors
upregulation and down regulation
Protein Based Hormones moa
First Messenger
Endocrine gland to target cell
Second Messenger
From receptor to cytoplasm and nucleaus
Function of Thyroxine
Regulates protein, fat and carbohydrate usage in all cells Regulates metabolic rate of all cells Controls body heat production Increases blood glucose levels Maintain growth hormone secretion
Regulation of Thyroid Hormone Secretion
increased energy requirements ->
hypothalamus releases thyrotrophin- releasing hormone->
anterior pituitary gland releases TSH->
thyroid gland to release thyroid hormone->
thyroid hormone targeting most body cells->
adequate levels of thyroid hormone in the blood
what does the pineal gland do
Melatonin – regulation of circadian rhythms
what does the thymus gland do
Development of T-lymphocytes
what hormones to the testes and ovaries do
Secrete hormones that have role in reproduction
elimination of peptide hormones and catecholamines
Degraded by enzymes in the blood or tissues
Excreted by kidney and liver
elimination of steroid hormones
Bound to protein carriers and inactive in bound state
Unbound hormone conjugated in liver rendering them inactive
Excreted in bile or urine
elimination of thyroid hormones
Unbound hormone rendered inactive through removal of amino acids in tissues
Conjugated in the liver and eliminated in the bile
reasons for hormone alterations
Feedback systems that fail to function properly
Feedback systems that respond to inappropriate signals
Endocrine gland may fail to produce adequate amounts of hormone
Endocrine gland may produce and release too much hormone
Hormones may be degraded once in circulation
Hormones may be inactivated by antibodies prior to reaching target cell
Ectopic hormone production
Abnormal receptor function
Altered intracellular response to the hormone at the target cell
Alterations to Pituitary Function
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Diabetes insipidus
Nephrogenic Form – inadequate response of the renal tubules to ADH, such as pyelonephritis
explain syndrome of inappropriate antidiuretic hormone secretion (SIADH)
High levels of circulating ADH
Associated with symptoms of water intoxication (increase in water retention by the kidneys or increased total body water hyponatraemia and concentrated urine
Diagnosis based on – low serum osmolality and hyponatraemia, urine hyper osmolality, urine sodium excretion matches intake, normal adrenal and thyroid function, absence of conditions that alter fluid volume status
explain diabetes insipidus
Insufficiency of ADH polyuria and polydipsia
Neurogenic Form – absence of ADH, damage to the hypothalamus, pituitary and can be seen with brain tumours
Alterations to adrenal function
Hyperfunction Hypofunction - Hyperaldosteronism - Hypercortisolism - Hypoadrenalism - Adrenal Crisis
explain adrenal hyperfunction
Hyperfunction
Hyperaldosteronism
Hypercortisolism
explain adrenal hypofunction
Hypofunction
Hypoadrenalism
Explain Hyperaldosteronism
Excessive aldosterone secretion
Primary hyperaldosteronism
Excessive secretion from the adrenal cortex
Secondary hyperaldosteronism
Caused by extra-adrenal stimulus (RAAS)
Increased levels of aldosterone result in
Increased renal sodium and water reabsorption hypervolaemia and hypertension
Renal excretion of potassium
explain Hypercortisolism
Excessive levels of serum cortisol
Chronic hypercortisolism leads to Cushing’s syndrome
Causes
Exogenous – administration of glucocorticoids (most common)
Endogenous – ectopic adrenocorticotrophic hormone secretion (adults), adrenal tumours (children)
Cushing’s Disease – excess production of ACTH from pituitary
manifestations of Hyperaldosteronism
Manifestations – hypertension, hypokalaemia (assoc. with muscle weakness, cramping and headache)
Manage hypertension and hypokalaemia, correct underlying cause.
manifestations of Hypercortisolism
- thin extremities, easy bruising, trunk obesity, pendulous abdomen, hyperpigmentation, puple striae, supraclavicular fat pad, moon face
explain hypoadrenalism
Primary adrenal insufficiency (Addison’s disease)
Hyposecretion of cortisol, aldosterone and androgens
Caused by autoimmune adrenalitis, adrenal infection, metastatic disease, adrenal haemorrhage, congenital adrenal hyperplasia, bilateral adrenalectomy.
Secondary adrenal insufficiency
Hyposecretion of pituitary ACTH hyposecretion of cortisol
Caused by exogenous treatment with glucocorticoid therapy which suppresses ACTH production
hypoadrenalism manifestations
Mild to moderate – weakness, fatigue, anorexia and weight loss
Moderate – nausea, vomiting, diarrhoea
Severe – hypotension leading to vascular collapse and shock
explain adrenal crisis
Life threatening condition develops from inadequate cortisol levels
Causes
Sudden cessation of glucocorticoids (steroids)
Illness
Infection
Trauma or surgery
Stressful periods
Early Intervention is essential – parenteral hydrocortisone
alterations in pancreatic function
diabetes mellitus
alterations of thyroid function
hyperthyroidism nodular thyroid disease thyroiditis thyrotoxic crisis hypothyroidism postpartum thyroiditis
explain hyperthyroidism
Graves’ Disease – autoimmune condition
An abnormal immune response triggers antibodies against the TSH receptor
Manifestations – Thyrotoxicosis (tachycardia, palpitations, nervousness, insomnia, heat intolerance, moist skin, tremor, lid retraction in the eye, increased SBP, increased cardiac contractility and weight loss)
Goitre – diffuse or enlarged gland caused by stimulation of thyroid cells increasing the size and vascularity of the thyroid gland.
Exophthalmos (protrusion of the eyeball), periorbital oedema, extraocular muscle weakness leading to diplopia – TSH receptors on tissue within the orbit
what is Thyroiditis
Thyroiditis – inflammation of the thyroid tissue due to viruses, trauma, medication or during the postpartum period
what is Thyrotoxic crisis
Thyrotoxic crisis – thyroid storm (rare but dangerous)
- hyperthermia, tachycardia, high output heart failure, agitation or delirium, nausea and vomiting or diarrhoea
explain hypothyroidism
Decreased production of thyroid hormone by the thyroid gland
Primary causes
Congenital defects
Defective hormone production
Loss of thyroid tissue after surgery or radioactive treatment
Primary hypothyroidism
Acute thyroiditis – bacterial infection
Subacute thyroiditis – nonbacterial inflammation
Autoimmune thyroiditis – Hashimoto disease
Painless thyroiditis
alterations to parathyroid hormones
hyperparathyroidism
hypoparathyroidism
explain hyperparathyroidism
Hyperparathyroidism
Primary hyperparathyroidism – single parathyroid adenoma
Secondary hyperparathyroidism – compensatory response to chronic hypocalcaemia
Tertiary hyperparathyroidism – increase in number of parathyroid cells and loss of sensitivity to circulating calcium can autonomous secretion.
explain hypoparathyroidism
Damage to parathyroid glands during thyroid surgery
pancreas endocrine function
Produce hormones secreted into bloodstream
Involved in nutrient balance (blood glucose levels) and gastrointestinal functions
Insulin produced by beta cells
Glucagon produced by alpha cells
Somatostatin by delta cells
what is gluconeogenesis
the formation of glucose, especially by the liver from carbohydrate sources such as amino acids and the glycerol portion of fats
what is Glycogenolysis
breakdown of stored glucose to increase the blood glucose levels
what is Glucagon
hormone produced by the alpha cells, stimulating the breakdown of glycogen in the liver, the formation of carbohydrates in the liver and the breakdown of lipids in both the liver and adipose tissue
3 main categories of diabetes mellitus
Type 1 Diabetes Mellitus
Characterised by an absolute insulin deficiency
Type 2 Diabetes Mellitus
Insulin resistance with an accompanying deficiency in insulin production
Gestational Diabetes
explain type 1 diabetes
Autoimmune Destruction of the Beta (β) cells in the Islets of Langerhans
Severe or absolute lack of insulin caused by the loss of β cells
Slowly progressive autoimmune T-cell mediated disease that destroys the β cells
Concurrent abnormal production by alpha (α) cells with an increase production of glucagon.
Hyperglycaemia and ketonaemia can result from insulin deficiency however the excess of glucagon facilitates the other metabolic alterations seen in diabetes.
clinical manifestations of type 1 diabetes
Classical Presentation Polyphagia (increased hunger) Polydipsia (increased thirst) Polyuria (increased urine production) Weight Loss Ketoacidosis Sweet Smelling Breath
type 1 diabetes assessment and management
Urinalysis Presence of classic signs and symptoms Management Aim Avoid swings in insulin and glucose levels Mimic body’s natural patterns Monitoring Blood Glucose Levels Long Term – Glycolated haemoglobin A1c The future Islet cell transplantation
explain type 2 diabetes
Currently around 1.7 millions Australians have diabetes (of which 85% have Type 2 diabetes)
280 Australian develop diabetes every day (1 every 5 minutes)
Total annual cost in Australia is approx. $14.6 billion
Fastest growing chronic disease in Australia
Fasting hyperglycaemia occurs despite insulin being available
Cellular Insulin resistance
No ketoacidosis
Gradual increase in hyperglycaemia
Metabolic Abnormalities
Insulin resistance
Increased glucose production by the liver
Impaired secretion of insulin by β cells
Type 2 – Risk Factors History of diabetes in parents or siblings Obesity Physical inactivity Race/ethnicity
type 2 diabetes clinical manifestations
Slow onset Hyperglycaemia – polyuria and polydipsia Blurred vision Fatigue Paresthesia Skin infections
type 2 diabetes management
Changes in diet and exercise
Hypoglycaemic medication possibly in combination with insulin
explain gestational diabetes
Occurs during pregnancy and resolves once the infant and the placenta have been delivered
Glucose intolerance appears during pregnancy
New routine screening and screening of high risk women
Family history of diabetes
Some ethnic groups have a higher risk
Advanced maternal age
History of large babies
Prior history of gestational diabetes or polycystic ovary syndrome
Overweight prior to pregnancy (BMI >35)
Women on corticosteroids or antipsychotics
complications of diabetes
Alterations in Blood Glucose Alterations in cardiovascular system Neuropathies Increased susceptibility to infection Peridontal disease
4 metabolic problems of diabetic ketoacidosis
Hyperosmolality from hyperglycaemia and dehydration
Metabolic acidosis from an accumulation of ketoacids
Extracellular volume depletion from osmotic diuresis
Electrolyte imbalances (potassium and sodium) from osmotic diuresis
what increases risk of diabetic ketoacidosis
Increased risk during physical or emotional stress – surgery, illness, infection, trauma, omitted insulin
Occurs in Type 1 Diabetes
DKA – Manifestations and Treatment
Manifestations – flushed skin, increased thirst, fruity breath, decreased BP, increased HR, Kussmauls Respirations, confusion, Nausea, vomiting, abdominal pain, fatigue, weight loss, blurred vision
Treatment Immediate medical intervention Primary Survey – Prioritise ABC IV hydration Regular Insulin Potassium Replacement Continuous cardiac monitoring
Explain Hyperosmolar Hyperglycaemic State
Plasma Osmolality >340 mmol/kg
Elevated Blood Glucose levels >33.3mmol/L
Altered Levels of consciousness
Precipitating Factors – infection, therapeutic agents or procedures, acute or chronic illness.
Hyperglycaemia increased urine output plasma volume decreases and glomerular filtration rate decreases glucose is retained and water lost increase in glucose and sodium lead to increased serum osmolality severe dehydration intracellular water reduced in all tissue including brain
HHS – Manifestation and Treatment
Manifestations - Flushed skin, increased thirst, decreased BP, increased HR, lethargic, nausea and vomiting, abdominal pain, fatigue, weight loss, malaise, extreme thirst, seizures
Treatment Similar to DKA Primary Survey – ABCDE Intravenous fluid Potassium replacement Insulin administration
Hypoglycaemia – Manifestations
Autonomic Nervous System • Hunger • Shakiness • Nausea • Irritability • Anxiety • Rapid Pulse • Pale, cool skin • Hypotension - sweating
Impaired Cerebral Function • Strange or unusual feeling • Slurred Speech • Headache • Blurred Vision • Decreasing levels of consciousness • Difficulty in Thinking • Inability to concentrate • Seizures • Change in emotional behaviour • Coma
Hypoglycaemia – Treatment
Mild
15 g rapid acting or simple sugar (fruit juice, lollies, honey)
Followed by a meal with complex carbohydrates
Review diabetes management plan if occurring frequently
Severe
Blood glucose <3mmol/L
Conscious and alert – 10-15g of oral carbohydrate
Altered consciousness – parenteral glucose or glucagon
Long-term complications of diabetes mellitus
Microvasculature
Neuropathies
Nephropathies
Retinopathies
Macrovascular Coronary artery Cerebrovascular Peripheral arterial disease Foot ulcers
Diabetic Neuropathies
Thickening of the walls of the nutrient vessels supplying the nerve
Demyelination process affecting the Schwann cell
Somatic Neuropathy
Distal symmetric polyneuropathy Autonomic Neuropathy Disorders of vasomotor function Decreased cardiac responses Inability to empty the bladder Gastrointestinal motility problems Sexual dysfunction Kidney Enlargement Nephron hypertrophy and Hyperfiltration
Diabetic Nephropathies Risk Factors
– genetic or familial predisposition, elevated BP, poor glycaemic control, smoking, hyperlipidemia and increased albumin excretion.
Diabetic neuropathies Affect on Glomeruli
Capillary basement membrane thickening
Diffuse glomeruli sclerosis
Nodular glomerulosclerosis
Diabetic Retinopathies
Abnormal retinal vascular permeability Microaneurysm formation Neovascularisation and associated haemorrhage Scarring Diabetic macular oedema Retinal detachment
discuss diabetic foot ulcers
Sensory Neuropathy is a major risk factor
Impaired pain sensation, not aware of constant trauma to feet
Motor Neuropathy
Weakness of intrinsic muscles of the foot may result in deformities
Full foot exam at least once a year
Assessment of protective sensation, foot structure and biomechanics, vascular status and skin integrity
diabetic infections
Soft tissue infections of the extremities Osteomyelitis Urinary tract infections Pyelonephritis Candidal infections of the skin and mucous surfaces Dental caries Periodontal disease Tuberculosis
diabetes nursing diagnosis
Risk of impaired skin integrity related to diabetic neuropathies
Risk of Infection
Risk of injury related to neuropathies, visual deficit, hyperglycaemia
Risk of sexual dysfunction related to peripheral neuropathy
Risk of impaired coping related to the chronic nature of diabetes
Risk of knowledge deficit related to self care
Risk of falls related to neuropathies
Risk of feelings of powerlessness related to chronic nature of diabetes
what is insulin
Body’s main fuel storage hormone
Secreted in response to raised levels of glucose in the blood
Ensures tissues and cells have sufficient chemical substrates for energy, storage, anabolism and repair
Within 30-60 seconds of absorption of glucose after a meal insulin release is increased
Fall in blood glucose inhibits insulin secretion
Rapidly absorbed in the gut if given orally, with a half life of only a few minutes
when is insulin replacement needed
Human insulin has all the properties and actions of the natural hormone – synthetically engineered
Treatment of Type 1 diabetes and treatment of type 2 during emergencies, in stressful situations, during pregnancy or as an adjunct to oral hypoglycaemic agents
insulin formulations
Ultra Short Acting (or rapid acting)
Clear, onset of action 0-20 min, peak 60-90mins, Duration 3-5hrs
Apidra, Humalog, Novorapid
Short Acting
Clear, onset of action 30mins, peak 2-4hrs, Duration 6-8hrs
Actrapid, Humulin R, Hypurin Neutral
Intermediate Acting
Cloudy – gently shaken or rotated prior to use
Onset of action – 90mins, Peak 4-10hrs, Duration 12-24hrs
Protaphane, Humulin NPH, Hypurin Isophane
Long Acting
Have either no peak or only a slight peak, duration up to 24hrs
Lantus or Levemir
different insulin dosing regimens
Basal-bolus regimen
Split mixed regimen
describe the Basal-bolus dosing regimen
Dose of short acting insulin given before each meal
Intermediate or long acting insulin at bedtime
Mimics the bodies natural rhythms of insulin release
describe the split mixed insulin dosing regimen
Total daily dose is estimated and split
One third short acting and two thirds intermediate or long acting.
Two thirds before breakfast and one third before evening meal
insulin administration care considerations
Obtain blood glucose level as ordered – to monitor response to insulin and adjust dose as required.
Always verify the name of the insulin being given – each insulin has a different peak and duration and the names can be confused
Gently rotate the vial containing the agent and avoid vigorous shaking – ensure uniform suspension of insulin
when should you not use an insulin vial
Checks prior to Administration
Do not give insulin if:
The clear insulin has turned cloudy
The expiry date has been reached
The insulin has been frozen or exposed to high temperature
Lumps or flakes are seen in the insulin
Deposits of insulin are seen on the inside of the vial which cannot be dissolved with gentle shaking or rotation
The vial has been open for longer than a month.
how is insulin prescribed
Insulin should be prescribed on insulin chart with full dosage instruction
how is insulin stored
Vials and Pens are for individual patient use only
Unopened insulin should be stored in a fridge (2-8 deg C)
Insulin in use can be stored at room temperature (below 25 deg C) for up to 28 days
Label the date and time of opening when insulin is first used
Should be discarded if out of fridge for more than 28 days
Do not use if insulin has expired
what type of diabetes can use oral hypoglycemics
Oral Hypoglycaemics- only for type 2 diabetes
drug groups of oral hypoglycemics
Biguanides
Sulfonylureas
Thiazolidindiones
Choice of drug depends on;
Patients weight
Pancreatic, renal and liver function
- Response to trialled medications
example of a biguanide
metformin
metformin MOA
Mechanism of action
Increase glucose uptake and utilisation in skeletal muscle ( reducing resistance to insulin)
Reduce glucose production in the liver (gluconeogenesis)
Reduce low and very low density lipoproteins
Increase insulin sensitivity via increasing number of receptors and affinity for receptors
Does not affect β cells – does not increase insulin release and not as likely to cause hypoglycaemia.
Less likely to cause weight gain and improves lipid profile
metformin Adverse Reactions and Administration
Absorbed after oral dose from length of GIT
Half life (5-10 hours)
Excreted unchanged in urine
Adverse Reactions
GI upset – N&V, anorexia and diarrhoea (common)
metformin contraindications
Patients with GI problems, severe liver or kidney disease (increases risk for lactic acidosis which can be a fatal adverse effect)
Pregnancy category C – preferred to use insulin during pregnancy
metformin dosage and administration
Orally with meals
500mg once or twice daily, max. 1gm three times daily.
example of Sulfonylureas
Glibenclamide, glipizide, glicazide, glimepiride
what do Sulfonylureas do
Enhance release of insulin from β cells in pancreas
Increase the cellular sensitivity to insulin in the body tissues.
Decrease glycogenolysis and gluconeogenesis
Reduce blood concentration in people with a functioning pancreas
describe Glibenclamide
Glibenclamide
Inactivated in the liver
Elimination half life (2-10hours) – variable
Adverse Reactions
Hypoglycaemia and weight gain
GI effects (N&V, abdominal distress) - common
Glibenclamide Dosage and Administration
Average Dose 2.5-20mg/day before breakfast
Doses over 10mg daily – remainder taken in the evening
Dosage individualised based on blood glucose levels
Glibenclamide administraion care considerations
Monitor response carefully – blood glucose monitoring is the most effective method
Monitor individuals during times of trauma, pregnancy or severe stress – may need to arrange to switch to insulin coverage as it is easier to titrate.
Ensure that the individual is following diet and exercise modifications – increase effectiveness of the drug and decrease adverse effects.
what is immunity
- Immunity is a protection from disease or more specifically infectious disease.
- Immune Response is the collective and coordinated response of the cells and molecules that make up the immune system.
• Two defence mechanisms that protect the body
- Innate immunity – early and rapid response
* Adaptive immunity -later but highly effective
presence of innate vs adaptive immunity
• Innate immunity is something already present in the body. • Adaptive immunity is created in response to exposure to a foreign substance.
specifity of innate vs adaptive immunity
I- Non-specific A- Specific
response of innate vs adapt immunity
I- Fights any foreign invader A- Fights specific infection
response time innate vs adaptive immunity
I- Rapid A- Slow (1-2 weeks)
time span innate vs adaptive immunity
I- Once activated against a specific type of antigen, the immunity remains throughout the life. A- The span of developed immunity can be lifelong or short.
inheritance innate vs adaptive immunity
I- • Innate type of immunity is generally inherited from parents and passed to offspring. A- Adaptive immunity is not passed from the parents to offspring, hence it cannot be inherited.
decribe innate immunity
- Components – skin, mucous membranes, phagocytic leukocytes (neutrophils and macrophages), specialised lymphocytes (natural killer cells) plasma proteins (including the proteins of the complement system)
- Rapid Response within minutes to hours
- Aim to prevent establishment of infection, deeper tissue penetration of microorganisms
describe adaptive immunity
- Components – two group of lymphocytes and their products (including antibodies)
- Recognise numerous microbial and non-infectious substances and develop a specific response for each
- Substances that illicit an adaptive response are called antigens
- Develops a memory – so able to respond more rapidly and effectively on next exposure
- Two type
- Humoral Immunity
- Cell mediated immunity
humeral vs cell mediated immunity
Humoral Immunity
• Mediated by antibodies produced by B lymphocytes
• Antibodies secreted into circulation and mucosal fluid where they act to eliminate microbes or toxins.
• Prevent organisms from colonising in body tissues
Cell mediated Immunity
• Defends against intracellular microbes such as viruses
• Mediated by T lymphocytes
• May active phagocytes to destroy microbes
• Other mays kill host cell harbouring microbes
phagocytic cells
macrophages, granulocytes and dendritic cells
role of macrophages
- Engulf and kill invading microorganisms (innate response)
- Dispose of pathogens and infected cells targeted for disposal (adaptive response)
- Induce inflammation, scavenger cells
role of granulocytes
- Neutrophils (phagocytosis –destroy them using degenerative enzymes –innate immunity),
- basophils and eosinophils (role unclear)involved in allergic reactions
role of dendritic cells
- Capture foreign agents and transport them to peripheral lymphoid organs
- Antigen presenting cell (present molecule to B and T lymphocytes to initiate adaptive response)
b lymphocytes role
• Only cells capable of producing antibodies (mediate humoral immunity)
t lymphocyte role
- Cell mediated immunity
- Helper T cells – help B lymphocytes produce antibodies and help phagocytic cells destroy ingested pathogens
- Cytotoxic T cells – kill or lyse intracellular microbes
natural killer cells role
- Innate immune response
- First line of defence against viral infections
- Also recognises and kills tumour cells, abnormal body cells and cells infected with intracellular pathogens
what are Immunoglobulins
• Immunoglobulins – protein compounds found in body fluids produced by B lymphocytes
types of immunoglobin
- IgG
- IgA
- IgM
- IgD
- IgE
immunoglobin IgG
• Most abundant, most protective activity against infection