Patho-Physiology Flashcards
Symptoms/signs of hypercalcaemia
Soft
Fatigue
Lack of concentration
Bone aches
Nausea and vomiting
Peptic ulcers
Rental stones
ECG changes
Hard:
Recurrent renal stones
Fractures/Dexa
Types of intestinal failure
Mechanical/length related
- short gut
- intestinal fistula
Absorptive
- mucosal disease
Functional
- dysmotility
- chronic obstruction
How does imiquimod work?
Immune enhancer - increased cytokines incl TNF-a and IFa
Leads to increase cytotoxic t-cell response
Aeitology of pilonidal disease
Unclear, but multiple theories
- acquired: thick hair falls into a deep natal cleft, were friction causes the hair to burrow under the skin and form tracts which can then become infected
- congenital: tracts are remanents of sinus tracts from coccyx
- some combination of above two
Risk factors
- coarse thick hair
- deep natal cleft
- poor skin condition
- young age
- smokers
How does VAC/ NPWT work
Optimises blood flow in the wound bed
Decreases local tissue swelling
Removes excessive fluid that can slow cell growth and proliferation in the wound bed
Decreases the numbers of bacteria
Alternating pressure also triggers cascade of intra-cellular signals that increase rate of cell division and formation of granulation tissue
Hypertrophic vs keloid scar
Both increase scar/ collagen disposition
Keloid
- extend beyond border of scar
- whorl pattern of collagen deposition
- increased ration type I:III collagen
Hypertrophic
- within scar
- always associated with trauma
- parallel collagen deposition
Actions of TNFa
Haemostasis
Increased vascular permeability
Enhanced endothelial proliferation
Fever
Increased collagenase production
Resorption of cartilage and bone
Release PDGF
PMN marination and cytotoxicity
Re-epithelisation
Production more IL-1
Broad stages of wound healing
Inflammation
Proliferation
Maturation
Factors that inhibit wound healing
Infection
Ischaemia
- circulation
- respiration
- local tension
DM
Ionizing radiation
Advanced age
Malnutrition
Vitamin Deficiency
- vitamin C
- vitamin A
Mineral deficiency
- zinc
- iron
Exogenous drugs
- docorubcin
- steroids
Definition: SIRS
Systemic inflammatory response syndrome
2 or more of
HR > 90
WCC <4 or >12
RR > 20
Temp >38 or <36
Caused by a dysregulated host imflammatory response to an injury or infection
Which organisms are commonly involved in OPSI?
Polysaccharide-encapsulated bacteria
SHiNE-SKiS
Streptococcus pneumoniae
Haemophilus influenza type B
Neisseria meningitidis
Escherichia coli
Salmonella
Kledseiella
Group B Streptococci
Presentation and treatment of OPSI
Short pro-drone phase
May not have clear primary source
Septic shock
DIC
Bilateral adrenal haemorrhage
Treatment:
Antibiotics (vanc and cefotaxime or ceftriaxone)
Supportive care
Pathophysiology of OPSI
Encapsulated bacteria
Occur because normal splenic immune function (maturation IgM, B lymphocytes and opsonins) do not occur
Hepatic acute phase proteins
CRP
c3 compliment
Haptiglobin
Fibrinogen
Anti-1 anti trypsin
Stimulated by IL6
Biochemical tests in DIC
Thrombocytopenia
Increased PT
Decreased fibrinogen
Increased d-dimer
Decreased Hb
SOFA score
Used in sepsis
Components:
BP/pressor requirement
Platelet count
Bilirubin
gCS
Creatinine
PaO2/FiO2
Mechanical ventilation
Factors which increase risk of variceal bleeding
Sepsis
High MELDNa (double digits bad)
Hx bleeding
Ongoing EtOH use
Size of varices
Lymphoedema
The chronic, progressive accumulation of protein rich fluid within the interstitium and the fibrous-adipose tissues which exceeds the capacity of the lymphatic system to transport the fluid
Can be primary (congenital) or secondary (acquired)
Common causes of secondary lymphoedema:
- infection with filariasis
- malignancy (disease and/or the treatment)
Disruption of lymph drainage leads to:
Dermal oedema
Hyperkeratosis
Epidermal palillomatosis and hyperplasia
Telengiectatic
Thickened upper dermis with fibrillation collagen and an increased number of fibroblasts
Staging 0-3
Staging or lymphoedema
Stage 0 (latent)
- at risk
Stage 1 (spontaneous)
- reversible pitting oedema
- soft
- may respond to elevation
Stage 2 (spontaneously irreversible)
- tissue fibrosis/induration
- swelling does not respond to elevation
- skin and tissue thickening; this makes Pitting difficult to assess
Stage 3 (lymphostatic elephantiasis)
- pitting oedema
- fibrosis
- skin changes
- dry skin and papillomas formation
Path phy of lipodermatosclerosis
Venous hypertension
Increased leukocytes in veins, migrate into surrounding tissues
Leukocyte activation - cytokines and pro-inflammatory cells
Collagen production leads to fibrosis of subcutaneous fat
Systemic effects of severe burns
Vascular permeability and oedema
Altered haemodynamics
Immunosuppression
Hypermetabolism
Decreased renal blood flow
Increased gut mucosal permeability
