Pathology Flashcards
What are the stages of acute inflammation
- change in vascular calibre
- increased vascular permeability
- formation of extracellular matrix
- Outcome
What is the triple response of Lewis
The reaction to a sharp injury:
flare-capillary dilation=red line
flush-arteriolar dilatation= red spreads
wheal-extravasation of fluid to interstitum causes oedema
What is present in exudate
-proteins
-neutrophils
-immunoglobulins
-coagulation factors
describe the role of neutrophils in the acute inflammatory response
-in formation of the exudate:
neutrophils become marginalised and adhere to the endothelium via expression of paired adhesion molecules on both the neutrophils and the endothelium (complement, leukotrienes, IL, endotoxins, TNF). They move in ameboeic fashion and chemotaxis to areas of inflammation and phagocytose oppsonized micro-organisms lysosomal products which further help increase vascular permieability/ cause pyrexia/ cause proteolysis
name the chemical mediators of acute inflammation
-Histamines
-cytokines
-prostaglandins
-lysosomal compounds
-leukotrienes
-nitric oxide
which inflammatory mediators cause increase in vascular permeability
-histamines
-lysosomal compounds
-prostaglandins
-nitric oxide
other functions of prostaglandins
platelet aggregation/ deaggregation
Also cause contractions during menstruation
(Made from arachadonic acid)
function of cytokines
attracts leucocytes to areas of inflammation
(Made by macrophages and T cells)
function of nitric oxide
toxic to bacteria
Name the plasma factors/ systems that preduce inflammatory mediators
complements
kinnins
coagulation system
fibrinolytic system
Which factor activates kinnins, coagulation and fibrinolytic systems
Factor 12
Describe the events that occur when kinnin system is activated
-activated by factor 12
prekallikrein–>kallikrein
kallikrein cleaves kininogen to release bradykinin
Function of bradykinin
-controls vascular permeability
-chemical mediator of pain
What is the difference between PT/ INR and APTT
PT & INR-assess extrinsic pathway
APTT-assesses intrinsic pathway
of coagulation cascade
causes of DIC
-Sepsis
-severe immune reactions:
Transfusion reactions
Organ transplant
Rxn to toxins (eg venom)
-Severe damage to major organs:
trauma
shock
liver disease
acute panc
Burns
Major surgery
-obstetric issues (amniotic fluid embolism, placental abruption)
-cancer
Pathogenesis of DIC
Due to both coagulation cascade and fibrinolytic pathway
coag= multiple microthrombi form= fibrin and platelets used up
fibrinolytic= plasmin breaks down fibrin clots= increased fibrin degredation products (FDP)
HAEMORRHAGE
Describe the serum findings of DIC
-low fibrin
-low platelets
-raised FDP
-prolonged PT/ APTT
What is the critical mediator of DIC
TISSUE FACTOR (transmembrane glycoprotein)
Which blood test in the coag profile is affected by warfarin administration
prolonged PT
Which blood test in the coag profile is affected by ASPIRIN administration
prolonged bleeding time
Which blood test in the coag profile is affected by HEPARIN administration
prolonged APTT
What are oncoviruses
Viruses that cause cancer and can be prevented by vaccination
What are the mailgnancies caused by EBV
-Burkitts lymphoma (non-Hodgkins B-cell)
-Hodgkins lymphoma
-post transplant lymphoma
-nasopharyngeal carcinoma
Which oncoviruse causes cervical/ vulval/ penile/ oropharyngeal/ anal cancer
HPV 16/18
Which oncoviruses cause hepatocellular carcinoma
Hep B/C
What cancer does HPV-8 cause
Kaposi’s sarcoma
What cancer does Human-T lymphotrophic virus-1 cause
-Tropical spastic paraparesis
-Adult T cell leukaemia
What cells are seen in thalassaemia microscopy
Target cells
basophilic stippling
When is basophilic stippling evident in blood films
thalassaemia
lead poisoning
What cells are seen on a blood film in sickle cell anaemia
Target cells
What cells are seen on a blood film in haemolytic anaemia
spherocytes
Spherocytosis-common haemolytic anaemia (due to abnormal RBC cell membrane allowing Na and water in giving it a round shape)
