3 Flashcards
- Q. What regulates platelet production?
A. Thrombopoetin: produced mainly by the liver binds to platlet and MK receptors
B. ↓plts = less bound TPO = ↑ free TPO able to bind to MK = ↑ Plt prodn
- Q. What activates platelets to aggregate?
A. Exposure to collagen, adhesion to vWF via GP1b and IIb/IIa, release of alpha-granules containing PDFG, fibrinogen, vWF, PF4
B. (Adhesion-release-aggregation-procoagulant effect-healing via PDGF))
- Q. How can platelets be investigated?
A. Number – FBC
B. Appearance – Blood film
C. Function – PFA (response to aggregating agents e.g. ADP, collagen), Bleeding time (unreliable
D. Surface proteins: flow cytometry
- Q. What can cause excessive bleeding?
A. Injury, vascular disorders (weak collagen, age), low platelets, abnormal platelet function, defective coagulation
- Q. Describe the differences in the clinical patterns between platelet type v haemophiliac type
A. Platelet dysfunction: clinical features • Mucosal bleeding: epistaxis, gum bleeding, menorrhagia • Easy bruising • Petechiae, purpura • Traumatic haematomas B. Haemophiliac type bleeding • Increasing bleeding with trauma • Joint and muscle bleeds • Depends on severity of deficiency
- Q. Name some causes of impaired platelet function
A. Congenital: platelet disorders, von Willebrand disease
B. Acquired: uraemia, drugs
- Q. Name some causes of thrombocytopenia: decreased platelet production
A. Congenital thrombocytopenia: absent, reduced, malfunctioning megakaryocytes
B. Reduced platelet production
- Q. Name some causes of thrombocytosis: increased platelet production
A. Autoimmune: immune thrombocytopenia, primary or secondary
B. Hypersplenism: portal HTN, splenomegaly
C. Drug related immune destruction: e .g. HIT heparin induced thrombocytopenia
D. Consumption of platelets: DIC-blood platelets activate, TTP, HUS, HELLP, major haemorrhage
- Q. What is the role of neutrophils in the innate immune system?
A. Phagocytosis, degranulation, form neutrophil extracellular traps (web-like structures of DNA which trap and kill extra-cellular microbes), release cytokines
- Q. What is the definition of fibrile neutropenia? Who is at risk of this?
A. Temp > 38degrees, in a pt with a neutrophil count <1.0 x 10^9/L
B. 2-21% mortality if untreated
C. Recent chemo, stem cell transplant, haemotalogical conditions (myelodysplasia, aplastic anemia, autoimmune, leukaemia), some drugs, bone marrow infiltrate
- Q. Describe the presentation of febrile neutropenia
A. Pyrexia > 38 degrees + rigors, infective symptoms, signs of deterioration (confusion/less responsive, hypotensive/tachycardiac/tachypnoeic)
- Q. What signs and symptoms are associated with malignant spinal cord compression?
A. Back pain
B. Weakness/numbness in legs
C. Inability to control bladder/bowel
D. Saddle paraesthesia
- Q. What would be seen on examination? (Malignant spinal cord compression)
A. Uni/bilateral leg weakness B. Paraesthesia – may be sensory level C. Decreased perineal sensation D. Decreased anal tone – PR exam E. In acute cord compression, tone and reflexes be reduced
- Q. Describe the management of malignant spinal cord compression
A. Strict bed rest, high dose steroids, analgesia, urgent MRI whole spine
- Q. What is tumour lysis syndrome?
A. Metabolic disorder due to break down of malignant cells
a. High uric acid (nucleic acid catabolism), hyperkalemia (cardiac instability, muscle cramps), hyperphosphatemia leads to hypocalcaemia
B. Uric acid crystals form in renal tubules
C. Calcium phosphate is also precipitated in the kidneys
D. Hypocalcaemia is due to calcium chelation caused by hyperphosphatemia
E. Treatment: aggressive hydration
