Pharmacotherapy Principles and Practice, Fourth Edition
The most trusted guide of its kind for decades, Pharmacotherapy: A Pathophysiologic Approachis the go-to text for students and practitioners seeking clear, objective coverage of corepathophysiologic and therapeutic elements.
Complete Test Bank Pharmacotherapy Principles And Practice 4th Edition Questions & Answers with rationales (Chapter 1-102)
Test Bank for Pharmacotherapy Principles And Practice 4th Edition Chisholm-Burns | Complete Chapters 1 - 102 | Questions and Answers with explanation | PDF format | Latest 2022
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Voorbeeld van de inhoud
Hematological Disorders
Venous Thromboembolism (VTE)
Introduction:
Þ Venous Thromboembolism (VTE) encompasses of Deep Vein Thrombosis (DVT)
and Pulmonary Embolism (PE).
Þ It causes cardiovascular death and disability as well as psychological
illnesses and emotional distress.
Epidemiology:
Þ It is estimated that 3,00,000 to 8,00,000 new cases of VTE occur each
year with 60,000 to 80,000 deaths attributed to DVT or PE.
Þ Out of the new cases, up to 30% of patient die within 30 days and one-
fifth suffer sudden death due to PE, 30% go and develop recurrent VTE
within 10 years.
Þ Data from the Atherosclerotic Risk in Communities (ARIC) study reported
a 9% 28 days fatality from DVT and 5% fatality from PE.
Þ The mean incidence of first DVT in general population is 5 per 10,000
persons year.
Deep Vein Thrombosis (DVT):
Þ DVT is characterized by formation of thrombus in the deep-seated veins of
the body, specially in the lower extremities.
Þ Sites:- Larger veins in the legs at or above the knee:-
o Popliteal vein
o Femoral vein
o Iliac veins
Þ Lower extremity DVT begins in the calf and propagates proximally to the
popliteal vein, femoral vein and to the iliac vein.
Þ Leg DVT is more common than upper extremity DVT which is often
precipitated by pacemakers, internal cardiac defibrillators or indwelling
central venous catheter.
Þ Superficial vein DVT presents with erythema, thrombosis, tenderness and
palpable cord.
Pulmonary Embolism (PE):
Þ It is defined as an embolism in which emboli occlude pulmonary arterial tree.
Þ Mechanism:
o DVT undergo fragmentation ® Thrombo- emboli are carried through the
progressively large vascular channels ® to the right side of the heart
® to right ventricle ® pulmonary arterial vasculature.
,Types of PE:
a. Low Risk PE(65-75%):
Þ It has excellent prognosis.
Þ No hypotension, No RV dysfunction
b. Sub- massive DVT (20-25%):
Þ Right ventricular dysfunction despite of normal systolic arterial pressure.
c. Massive PE (5-10%):
Þ Hallmark:- Dyspnea, Hypotension, syncope and cyanosis
Etiology:
1. Patient Factors:
Þ Advanced age
Þ Obesity
Þ Varicose vein
Þ Previous DVT
Þ Family H/O DVT
Þ Transient additional risk factors:
o Pregnancy/ puerperium
o Estrogen containing oral contraceptives
o Immobility (long distance travel >45 hours)
o Surgery
o Medical illness
2. Surgical Conditions:
Þ Major surgery, especially >30 min duration.
Þ Abdominal and pelvic surgery, especially for cancer.
Þ Major lower limb orthopedic surgery:- Joint replacement and hip fracture
surgery.
3. Medical conditions:
Þ Myocardial infraction/ Heart failure.
Þ Inflammatory bowel disease.
Þ Malignancy (Anti- cancer chemotherapy)
Þ Nephrotic syndrome
Þ COPD
Þ Pneumonia
Þ Stroke, paraplegia
Þ Any high dependency admission.
4. Hematological disorders:
Þ Polycythemia rubra vera
Þ Essential thrombocytopenia
,Þ Deficiency of natural anticoagulants:- Antithrombin, Protein-C, Protein-
S.
Þ Gain of function of prothrombotic mutation, factor- V Leiden, prothrombin
gene G20210A mutation.
Þ Myelofibrosis
Þ Antiphospholipid syndrome
Pathophysiology:
Þ DVT is caused by same etiological factors that favours arterial and cardiac
thrombosis.
Þ These include:
o Endothelial injury
o Stasis
o Hyper- coagulation
Virchow’s triad
Endothelial injury Stasis Hypercoagulation
Damage to Accumulation of
Intima of the vein Coagulation factors
Activation of fibrin
Platelet adhesion
Primary platelet plaque
Further aggregation of platelets
Platelets and fibrin accumulate are grows upright the stream forming
Corline thrombus
Further growth of thrombus forms Occluding thrombus
, Consecutive clot
Matured thrombus
DVT
Mechanism of PE:
DVT undergo fragmentation ® Thrombo- emboli are carried through the
progressively large vascular channels ® to the right side of the heart ® to
right ventricle ® pulmonary arterial vasculature.
Clinical Features:
1. Deep vein thrombosis (DVT):
Þ Edema (m/c)
Þ Leg pain
Þ Tenderness
Þ Cramp (Charley Horse) in lower leg.
Þ Local warmth with erythema
Þ Homan’s Sign:- Calf pain on dorsiflexion
Þ Palpable, tender, indurate, cord like venous segment
Þ Variable discoloration of lower extremities.
Diagnosis:
1. History taking:
Þ H/O previous surgical conditions specially of lower extremities.
Þ H/O of medical illnesses
Þ Family history of DVT or PE.
Þ H/O pregnancy
Þ H/O malignancy
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