Week 2 - Lecture 3 - Clinical Models Flashcards
burn injuries
caused by a trauma injury
burn injuries cause an inflammatory response
- in the skin
- in other integumentary structures
6 functions of the skin
protection : 1st line of defence -physical barrier
body temperature regulation
cutaneous sensation
metabolic functions (vitamin D activation)
blood reservoir
excretion
Burn pathophysiology
burns are caused through
direct contact with excessive heat, radiation, caustic chemicals or electricity
- heat will denature proteins causing irreversible cellular damage
all burns result in acute inflammatory response
burn severity is correlated with exposure type and time of the affected surface area
Burn pathophysiology classification
superficial partial thickness (first degree)
epidermal damage only
vasodilation of dermal blood vessels
increased capillary permeability
- localised redness, warmth, oedema (swelling) pain
do not result in cell necrosis or scarring
extracellular matrix remains intact
healing is rapid
Deep partial thickness( second degree) burns
epidermal and upper dermal damage epidermal and dermal layers separate - fluid accumulates, blisters appear loss of function: 1st line of defence Tissue necrosis are common, tissue fibrosis, scarring healing occurs within 2-4weeks
Full thickness (3rd degree) burns
entire thickness of skin involved
-epidermis, dermis, subcutaneous
skin gray- white, cherry red, or blackened
not painful (nerve ending destroyed)
healing is difficult due to extensive tissue loss
skin grafting usually necessary
regeneration of epithelial cells impaired
scarring is extensive
loss of elasticity leads to contractors
loss of skin function: multiple complications (in severe burns)
microorganism invasion -infection body fluids shifts - impaired blood circulation, oedema (swelling) dehydration and electrolyte imbalance - leads to renal shutdown and circulatory shock overwhelming metabolic demand - increased risk of malnutrition temperature regulation problems
Burn pathophysiology cont’
significant hemodynamic changes - changes in the flow of blood in tissues and organs
poor perfusion
- problematic for vital organs
- constant flow of oxygen required
inadequate blood in circulation can lead to hypovolemic shock
fluid volume replacement required
Access for microorganisms in burns means
significant risk for sepsis development
- bacterial infection of the blood
significant risk for septic shock
- massive inflammatory response due to bacterial toxins in blood
in full thickness burns : dead tissue and exudate convert into an eschar
- thick coagulated crust made from dead skin
- requires surgical removal to prevent further microorganism growth within the dead tissue
extensive demand on metabolic and reparative processes
- increased energy, oxygen, protein needs
- not sufficient nutrients available will lead to tissue wasting, hypoxia and infection
burn diagnosis
wound depths are classified according to the affected tissue layers
brun clinical manifestations
depend on depth of burn injury
superficial- partial thickness burns show the 5 signs of inflammation
deep partial thickness burns
- blistering occurs, erythema, pain, oedema, serous exudate
full thickness burns
- erythema, eschar, oedema, exudate
- destroyed nerve endings inhibit pain response from burn penetration area
- not pain free : nearby tissue suffer from partial thickness burn
- pain perception according to bull’s eye
surface area of 9
slide 15
critical burn if
> 25% of body has second degree burns or
10% of body has third degree OR
if the face, hands, feet or respiratory passages bear third degree burns
burn treatment
increased survival rates
minor and moderate burns
- remove source of injury
- stop burning process
- chemical burns flushed with plenty of water
- wound can be cleared with water
- antimicrobial ointment applied
- dressing
changing dressing frequently helps debridement
what is debridement
the mechanical removal of debris and necrotic tissue
burn treatment for moderate and major burns
emergency medical admission
includes any third degree burns to the face, hands, feet or respiratory system
respiratory passageway burns may lead to suffocation
-specialised intervention
initial focus
-stabilise airways, breathing and circulation
- fluids : replace water and sodium, restore circulation
nutrition: increased metabolic demand
antibiotics : infection
analgesics : pain management
wound management for major burns
removing necrotic tissue
closing wounds
preventing infection
hydrotherapy to cleanse the wound, remove dead tissue and exudate
skin grafting for full thickness burns
- full thickness burns use the replacement healing process
- unable to undergo re-epithelialisation
-transplanted tissue supports cellular regeneration
-decrease infection
-minimise scarring
long term rehab (tertiary prevention)
severe scarring contractures (shortening and hardening of tissues) deformity and immobility chronic pain depression, psychological issues
What is arthritis
inflammatory disorders that involves damage to articular cartilages of synovial joints
acute forms of arthritis : caused by bacteria via traumatic joint wound - treated with antibiotics
arthritis caused by chronic inflammation
- RA
-Gouty arthritis
OA is not caused by inflammation
function of synovial joints
articulation : site where two or more bones meet
function of joints
-give skeleton mobility
-hold skeleton together
synovial joints
- highly vascular
- two layer synovial membrane
- connective tissue layer
- synovial cell layer : fluid production
- bone separated by fluid filled joint cavity
- freely movable
- include limb joints; most joints of body
common target for inflammation
RA pathophysiology
RA is systemic autoimmune disease
chronic inflammation of synovial membranes and synovial hyperplasia
-increased synovial fluid production
-swelling and thickening of synovial membrane
-joint erosion
-pain
onset between 36-50 years
RA affect 0.8% of adults worldwide
F= 3x more
autoimmune =
the immune system attacking healthy tissue
Etiology of RA
involves a combination of
- genetic susceptibility
- environmental factors are also linked to RA (eg. smoking, infections)
- immune triggering event (currently unknown)
- subsequent autoimmunity against synovial cells
lymphocytes and plasma cells (WBCs) in the synovial membrane and cartilage produce antibodies
- our circulating antibodies in our immune system bind to these antibodies(or other antigens or proteins in the synovial membrane)
these complexes of antibodies and antigens form immune complexes and present in the synovial
these immune complexes trigger the complement system and exaggerate the inflammatory response
excess production/release of inflammatory mediators means
RA patho
vascular response/cellular response of inflammation
production of destructive enzymes, health tissue damage
synovial cells adapt to this damaging environment through rapid regeneration ( hyperplasia)
synovium is altered and causes what
RA patho
mild oedema
accumulation of cells of chronic inflammation
acceleration of angiogenesis (new blood vessel formation)
accumulation of fibrin (fibrous protein in connective tissue)
At this point, minimal damage to the joint
remissions and exacerbations for RA
pannus formation : granulation tissue
- formed over inflamed synovium
- pannus produce enzymes that break down cartilage and erode adjacent bone
- irreversible erosion process
Fibroblasts try to replace damaged connective tissue layer : lead to fibrosis in the joint capsule
-impaired and debilitating fixation of joint : ankylosis
limited joint movement leads to decreased workload – muscle tissue atrophy
inflammatory cells irritate surrounding muscle
- muscle spasm
RA clinical manifestations
Most RA inset is insidious Severity : mild to debilitating joint swelling is symmetric and widespread - any number of joints pain and stiffness redness, heat and swelling decreased mobility
malalignment/deviation is common for long standing RA
-combination of cartilage, bone erosion and fibrosis
systemic manifestations during exacerbations
- low grade fever, fatigue, anorexia, weight loss, weakness
- granulomas (nodules) can form on blood vessels
RA diagnostic criteria
no definitive test
history and P/E -morning joint stiffness lasting over 1 hour arthritis of 3 or more joints areas arthritis of the hand joints symmetric arthritis rheumatoid nodules
several diagnostic tests
increased likelihood with positive findings:
Erythrocyte sedimentation rate (ESR) : elevated
C-reactive protein (CRP) : elevated
Presence of rheumatoid factor (IgG)
Presence of antinuclear antibodies (ANA)
Presence of inflammatory products
in synovial fluid
radiographic visualisation of joint damage
many of the tests are not specific
-false positives and false negatives
RA treatment
balance between pharmacologic and non-pharmacologic approach
pharmacologic :
-drugs that induce remission
-anti-inflammatory drugs (NSAIDs)
Immunosuppressant drugs (DMARDs- disease modifying antihirheumatic drugs)
Non-Pharmacologic
- rest/activity balance (to suppress inflammation)
- physical therapy exercises to promote joint mobility, physiotherapy
- splints to allow joint to rest and prevent deformities
- heat/cold therapy (to suppress inflammation)
- surgery : synovial membrane removal, joint replacement
function of the stomach
organ of protection : first line of defence
-very acidic environment - pH 1.5-3.5
digestion
-gastric secretions
- mucus, gastric acid, enzymes, hormones, intrinsic factors
absorption: water and alcohol
cells form tight junction
- protect tissues against corrosive gastric acid
acute gastritis
inflammation in the gastric mucosa
cause :
ingestion of irritating substances (medications, alcohol, microorganisms)
-develops over short period
-reversible if causative agent removed
acute gastritis pathophysiology
ingestion of irritating substances and/or poor gastric perfusion results in acute inflammation of the gastric mucosa
gastric epithelial cell become necrotic
gastric acid erodes underlying tissue
acute inflammatory response
- mild erythema (redness)
- severe gastric perforation
- gastric acid escape and corrodes nearby tissue
acute gastritis clinical manifestations
dependant on severity - mild to severe abdominal pain -ingestion (heartburn) loss of appetite nausea vomiting mild haemorrhage and vomiting blood
severe haemorrhage and perforation : lead to shock and medical emergency
Acute gastritis diagnosis
history and P/E
- medication taking (aspirin/NSAIDs) alcohol, contaminated food
- other potential causes of ischemia
- abdominal tenderness
endoscopic examination : presence ulcers in the mucosa
stool analysis (presence of blood in stool)
haemoglobin/ hematocrits level, complete blood count (anaemia)
Acute gastritis treatment
prevent the injury (discontinue ingestion of irritating substances)
buffer or decrease production of gastric acid
prognosis is good
chronic gastritis
unrelenting injury
- chronic infection : helicobacter pylori
- autoimmunity
Gastric epithelial and mucosal cell atrophy
gastric acid production impaired
helicobacter pylori is most prevalent
asia
developing countries
50% of world’s population has been infected
pathological effect occur in 10-20% infected individuals
H. Pylori : gram negative bacteria
person to person, saliva, stool
ingested and multiplies on epithelial surface and mucus barrier
produce enzyme that neutralises the pH 1.5-3.5 gastric acid
H. pylori survives and produces toxin
toxins destroy mucosal barrier - injury
intense inflammation triggered (CG pathophysiology)
neutrophils, macrophages try to contain the infection
ongoing phagocytosis, immune response triggered
H.Pylori is contained in the epithelial cells
- no erosion of the gastric mucosa
-epithelial cells and glands adapt and atrophy
-gastric acid production and secretion is impaired
Chronic gastritis autoimmune pathophysiology
parietal cell secrete HCI)
- antibodies against parietal cells : gastric acid secretion impaired
intrinsic factor (IF) is needed for B12 absorption
-antibodies against IF: B12 absorption is impaired
- B12 required to promote DNA synthesis in RBCs
impaired DNA synthesis – decrease in RBCs
Low haemoglobin levels
-pernicious anaemia (pernicious = deadly)
chronic gastritis clinical manifestations
H.Pylori infection - most infected : symptomatic carrier - pathological effect occur in 10-20% of infected individuals -dyspepsia (vague discomfort of the upper abdomen or chest) nausea heartburn loss of appetite vomiting
autoimmune
- can be asymptomatic
- first sign : pernicious anaemia (deficiency in intrinsic factor, unable to absorb B12, abnormal RBCs production)
- – weakness, fatigue, light-headedness
- dyspepsia, vague abdominal pain, vomiting, anorexia, nausea
Chronic gastritis diagnosis
H.Pylori
- endoscopic examination
- biopsy of gastric tissue
- breath test for presence of a specific enzyme
- H.Pylori breaks urea into NH3 and CO2
- CO2 content measured
- Presence of antibodies in blood
autoimmune
- biopsy of gastric tissue and histologic examination
- antiparietal or anti-intrinsic factor antibodies in blood
- existing autoimmune process
- low B12 level in blood
Chronic gastritis treatment
H.Pylori infection
multiple antibiotics for chronic infectious processes
proton pump inhibitors (raise pH) to help healing
H.Pylori can lead to chronic ulcers and gastric cancer
Autoimmune
- immunosuppressive drugs
- administration of B12 intramuscularly
- autoimmune gastritis can lead to gastric cancer
inflammatory bowel disease (IBD)
chronic, relapsing inflammatory bowel disorders of unknown origin (idiopathic)
- genetic aetiology
- autoimmunity (immune reactions to intestinal flora)
- alterations of epithelial barrier functions
- abnormal cell responses in the immune system
most common in small and large intestines
-can occur anywhere in the GI tract
most common form of IBD
- Crohn’s disease
- ulcerative colitis
Function of the small intestine
primary function : digestion and absorption
- enzymes of villi : digestion
- epithelium of mucosa : absorption
- lamina propria : infection-fighting, immune response
- Labile cells : cells divide
Crohn’s disease pathophysiology
idiopathic chronic inflammatory disease
-family history, environmental factors (smoking, diet, microorganisms)
affects any part of the digestive tract from mouth to anus
most common in small intestine
recurrent condition
cont’ pathophysiology of Crohn’s
28000 in australia
non-continuous penetrating ulcerations and fibrosis (skip lesions)
ulcerations can produce longitudinal and transverse inflammatory tissues that extend into the lymphatics
Crohn disease patho pt. 3
inflammation begins in the mucosa and submucosa
- increased permeability and vascular changes
- oedema and fibrosis
- cellular response
- granulomas form to wall off effected areas
-bowel segment become further inflamed
-interior surface thicken - oedema, fibrosis, granuloma
- can lead to bowel obstruction
- ingested food can’t pass through - critical condition
-ulcers (due to poor perfusion) form and lead to - fistula : abnormal passage between 2 segments of bowel or epithelial tissue
- abscess : pocket of purulent exudate, containing pus
external surfaces can form adhesions, limiting bowel function
Crohn disease clinical manifestations
rapid stool transition time intestinal oedema fibrosis loss of absorptive function symptoms depend on location of affected area - abdominal pain - diarrhoea -malnutrition -blood in stool - bowel obstruction systemic manifestations - fever - weight loss - fatigue - anaemia may result from malabsorption of vitamin B12 and folic acid
Crohn disease diagnostic criteria
history and P/E
- difficult to differentiate from ulcerative colitis
- similar risk factors and theories of causations as ulcerative colitis
endoscopic examination to check mucosa involvement
radiography/CT to check abscesses, fistulas, obstruction
stool cultures to rule out infection
Crohn disease treatment
treatment is symptomatic (symptom management)
pharmacologic treatment
- suppress inflammation
- suppress immune response
dietary changes
- acid foods that irritate bowel
- during exacerbation
- high in calories and protein
- low in fat and fibre
surgical treatment
- remove damaged bowel
- repairs fistula
increased risk of colorectal cancer
ulcerative colitis
chronic inflammatory disease of the colon
- only in large intestine
- does not affect other GI tract
- mainly mucosal layer (can extend to submucosa)
idiopathic disease
- suggested causes : infectious, immunologic (anticolon antibiotics), dietary, genetic
australia : around 33000
UC pathophysiology
chronic inflammation begins in rectum and ascends the descending colon
continous superficial areas of ulcerations (does not skip)
- inflammation invades superficial mucosa : friability (easily bleeds)
mucosa erythematous and granular
hemorrhagic lesions, abscesses, necrotic tissue, ulceration
-repeated cycle of ulceration alternating with the deposition of granulation tissue during the healing phase
- pseudopolyps raised inflammatory tissue
perforation, obstruction, and massive haemorrhaging can result
UC clinical manifestations
symtoms are related to large intestine irritability and friability
functional losses are related to the extent of inflammation
most common symptoms
- diarrhoea
-rectal bleeding
-abdominal pain
systemic manifestations fever weight loss fatigue anaemia
UC diagnosis
History and PE
-diarrhoea (10 to 20/day) bloody stool, cramping
-severity is based on the number of bowel movement with rectal bleeding
mild- <4 day no systemic manifestations
moderate - >4 day no systemic manifestations
severe - >4 days, systemic manifestations, low blood albumin
endoscopic examination : mucosal erythema (redness)
radiographs
- colonic dilation, ulceration, perforation, obstruction
complete blood count (anaemia)
UC treatment
treatment is symptomatic (symptoms management) pharmacologic treatment - suppress inflammation - suppress immune response -antidiarrheal medication
dietary changes - healthy diet (avoid milk, caffeine, spicy food) -adequate fluid intake Surgical treatment - if perforation or obstruction occur
increased risk of colon cancer, higher than crohn’s
differential diagnosis crohn;s and UC
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