Patho-Physiology

Question 1

Symptoms/signs of hypercalcaemia

Answer 1

Soft
Fatigue
Lack of concentration
Bone aches
Nausea and vomiting
Peptic ulcers
Rental stones
ECG changes

Hard:
Recurrent renal stones
Fractures/Dexa

Question 2

Types of intestinal failure

Answer 2

Mechanical/length related
- short gut
- intestinal fistula
Absorptive
- mucosal disease
Functional
- dysmotility
- chronic obstruction

Question 3

How does imiquimod work?

Answer 3

Immune enhancer - increased cytokines incl TNF-a and IFa
Leads to increase cytotoxic t-cell response

Question 4

Aeitology of pilonidal disease

Answer 4

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

Question 5

How does VAC/ NPWT work

Answer 5

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

Question 6

Hypertrophic vs keloid scar

Answer 6

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

Question 7

Actions of TNFa

Answer 7

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

Question 8

Broad stages of wound healing

Answer 8

Inflammation

Proliferation

Maturation

Question 9

Factors that inhibit wound healing

Answer 9

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

Question 10

Definition: SIRS

Answer 10

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

Question 11

Which organisms are commonly involved in OPSI?

Answer 11

Polysaccharide-encapsulated bacteria

SHiNE-SKiS
Streptococcus pneumoniae
Haemophilus influenza type B
Neisseria meningitidis
Escherichia coli
Salmonella
Kledseiella
Group B Streptococci

Question 12

Presentation and treatment of OPSI

Answer 12

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

Question 13

Pathophysiology of OPSI

Answer 13

Encapsulated bacteria

Occur because normal splenic immune function (maturation IgM, B lymphocytes and opsonins) do not occur

Question 14

Hepatic acute phase proteins

Answer 14

CRP
c3 compliment
Haptiglobin
Fibrinogen
Anti-1 anti trypsin

Stimulated by IL6

Question 15

Biochemical tests in DIC

Answer 15

Thrombocytopenia
Increased PT
Decreased fibrinogen
Increased d-dimer
Decreased Hb

Question 16

SOFA score

Answer 16

Used in sepsis

Components:
BP/pressor requirement
Platelet count
Bilirubin
gCS
Creatinine
PaO2/FiO2
Mechanical ventilation

Question 17

Factors which increase risk of variceal bleeding

Answer 17

Sepsis
High MELDNa (double digits bad)
Hx bleeding
Ongoing EtOH use
Size of varices

Question 18

Lymphoedema

Answer 18

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

Question 19

Staging or lymphoedema

Answer 19

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

Question 20

Path phy of lipodermatosclerosis

Answer 20

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

Question 21

Systemic effects of severe burns

Answer 21

Vascular permeability and oedema
Altered haemodynamics
Immunosuppression
Hypermetabolism
Decreased renal blood flow
Increased gut mucosal permeability