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Haem - pathology > PT 2 > Flashcards

PT 2 Flashcards

1
Q
  1. What treatment can be used in chronic sickle cell to reduce freq crises?
A

Hydroxycarbamide: increases production of fetal Hb and reduces WBC in inflammatory state

(transfusion, stem cell transplant, painkillers, Abx for infections)

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2
Q
  1. Q. What complications of sickle cell?
A

Gallstones, leg ulcers, AVN of femoral head, splenic infarction, CKD

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3
Q
  1. Q. Sickle cell -Ix? What is seen
A

A. Neonate screening: 1st trimester: chorionic villus sampling, 3rd: cord blood or heel prick test at 5 days

B. FBC: low, reticulocytes high

C. Blood film: sickled erythrocytes

D. Hb electrophoresis: 80-95% Hb SS and absent Hb A

E. CXR: ? pulmonary infiltrate - sickle chest syndrome

F. U&E - ? renal impairment

G. Transcranial doppler US - measure velocity of blood flow in large intracranial vessels

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4
Q
  1. Q. Describe the absorption of vit B12
A

Terminal ileum, needs intrinsic factor from gastric parietal cells

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5
Q
  1. Q. What is pernicious anaemia? Sx?
A

A. Autoimmune - antibodies against parietal cells = reduced intrinsic factor = reduced B12 absorption = macrocytic anaemia (raised MCV)

B. Associated with other disease e.g. Addison’s disease

C. Sx: anaemia, paraesthesia, numbness leg>hands, cognitive changes, altered vision, sore mouth (glossitis, angular cheliosis)

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6
Q
  1. Q. What Ix test coagulation?
A

A. Prothrombin Time – marker of the extrinsic pathway: 9-12 seconds

B. Activated partial thromboplastin time - APTT – marker of the intrinsic pathway: 22-29 seconds

C. Von Willebrand Factor (absent in von Willebrand disease)

D. Platelets – usually 150-400 x109/L

E. Bleeding time – objective measure of how long it takes the patient to coagulate (not used commonly)

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7
Q
  1. Q. What treatments affect coagulation?
A

A. Warfarin - antagonises vit K dependent clotting factors (2, 7, 9, 10). Increased INR.

B. Heparin - inactivates factor Xa (reverse with protamine sulphate IV)

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8
Q
  1. Q. What occurs in haemophilia A/B? What Ix? Mx?
A

A. X-linked, A = factor VIII deficiency, B= factor IX

B. Sy/Si: Haemoarthrosis, secondary arthritis, spontaneous soft tissue bleeds, GI bleed, haematuria

C. Ix: Raised APTT, (intrinsic pathway) Normal PT, Normal vWF, Normal Platelets. CT/USS for suspected bleeds

D. Mx:
–Avoid NSAIDs and IM injections
–Minor bleed: Elevate and pressurise
–Major bleed: Replace missing factor to help correct clotting factors and improve haemostasis

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9
Q
  1. Q. What occurs in haemophilia A/B? What Ix? Mx?
A

A. Von Willebrand factor acts to prevent factor VIII from destruction

B. Autosomal dominant condition leading to mucocutanoeus bleeds and easy bruising

Ix: FBC; ↑APTT (intrinsic pathway); -PT; ↓vWF; ↑bleeding time

Large bleed Mx:
  Tranexamic acid
  DDAVP (vasopressin)
  vWF concentrate
  Cryoprecipitate
  FFP
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10
Q
  1. Q. What occurs in disseminated intravascular coagulation?
A

A. Pathological activation of the coagulation cascade - formation of microvascular thrombi and multi organ failure. Increased/exposed tissue factor on the epithelium. Consumption of fibrinogen, platelets and clotting factors - haemorrhage

B. Causes: Sepsis, haematological cancers, eclampsia, anaphylaxis, severe trauma/burns. Severe liver disease

C. Ix: prolonged PT/APTT, increased D-dimers, decreased fibrinogen

D. Blood film shows fragmented RBCs

E. Mx: Treat underlying; FFP; Cryoprecipitate

F. Cx: Massive haemorrhage; End organ failure; Death

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11
Q
  1. Q. What occurs in Glucose-6-phosphate dehydrogenase (G6PD) deficiency?
A

A. X linked, males in med, africa, middle/far east

B. Most are asyptomatic, may get oxidative crises (precipitated by drugs, fave beans, illness)

C. In attacks there is rapid anaemia and jaundice

D. Film shows bite and blister cells

Dx: enzyme assay

Tx: avoid precipitants, transfuse if severe

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12
Q
  1. Q. What occurs in aplastic anaemia?
A

A. Pancytopenia (reduction in RBC and WBC) and hypocellularity (aplasia) of the bone marrow (decreased in pluripotent stem cells, BM is replaced by fat)

B. Mostly idiopathic acquired, congen (fanconis), cytotoxic drugs/irradiation/drug reactions, infection (HIV, hepatitis, TB)

Ix: BM exam = hypocellular, FBC = pancytopenia, blood film

Tx:
blood and platelet transfusion, prophylactic Abx, BM transplant < 40 curative

> 40 - immunosuppression with anti-thymocyte globulin and ciclosporin

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13
Q
  1. Q. Name 3 causes of macrocytic anaemia > 100fl
A
  1. Alcohol excess - liver disease
  2. Folate deficiency - megaloblastic, folate (green veg, fruit, offal, body stores last 4months, absorbed in duo/jej), poor diet, alcoholics, pregnancy, elderly, malabsorption. Neural tube defects in pregnancy.
  3. Vitamin B12 deficiency - megaloblastic - found in meat, fish, dairy products, 4 yr stores in liver, binds to intrinsic factor in terminal ileum, caused: dietary vegans, malabsorption, congenital metabolic errors
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14
Q
  1. Q. What occurs in non-hodgkin’s lymphoma? Who? Why?
A

Adults, 80% are B cell origin, 20% T cell

RF: FHx, immunosuppression, H.pylori, EBV

Painless peripheral
lymphadenopathy + extra nodal more common than Hodgkin’s (skin, GI, BM - pancytopenia)

B symptoms - fever, sweats etc

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15
Q
  1. Q. Tx of non-hodgkin’s lymphoma
A

Blood: Beta-2 microglobulin and lactate dehydrogenase levels - prognostic

BM aspirate/trphine

Gastric lymphoma - eradicate H.pylori = cure

Aggressive e.g. large B cell = RCHOP (rituximab + combo chemo) - cure rates 60-70%

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16
Q
  1. Q. What occurs in thrombocytopenia?
A

A. Platelets involved in clotting/haemostasis. Adhere to endothelium via collagen and vWF, release platelet granules (ADP/fibrinogen/thrombin) leading to FIBRIN prodn, and platelet aggregation.

B. Too few platelets - mucosal bleeding (nose bleeds, gum), easy bruising, prupura

C. AE Reduced production: congenital, BM infiltration, decreased BM production (low B12/folate, aplastic anemia, HIV/TB)

D. AE increased destruction: immune, hypersplenism, drugs (heparin induced), consumption (DIC, TTP)

17
Q
  1. Q. What occurs in polycythaemia?
A

A. Too many RBCs

B. Primary (BM problem): Polycythaemia Rubra Vera (PRV) - overactive BM, increased RBC, WBC, plts CF: hyperviscocity, thrombosis, itching, splenomeg, plethoric apperance, Tx: aspirin, venesection, BM suppression (hydroxycarbamide)

C. Reactive/secondary: EPO excess, altitude, lung disease

Haem - pathology (5 decks)

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