Pathology

Question 1

Which of the following is NOT TRUE regarding noncoding DNA?
A. It consists of a minority of the genome
B. It functions to regulate gene expression
C. It can be injured by exposure to radiation
D. dysregulation can lead to disease

Answer 1

ANS: A
Rationale:
 The human genome contains 3.2 billion DNA base pairs. Yet, within the genome there are only about 20,000 protein-encoding genes (1.5%). 98.5 % of the human genome does not encode proteins
 There are 5 major classes of functional non-protein sequences in the human genome
1- Promoter and enhancer regions (provide binding sites for
transcription factors
2- Binding sites for factors that organize and maintain higher order
chromatin structures
3- Noncoding regulatory RNAs
4- Mobile genetic elements (e.g. transposons)
5- Special structural regions of DNA (telomeres and centromeres)

Question 2

In which of the following conditions is edema caused by both increased hydrostatic pressure and decreased plasma colloid pressure?
A. Lymphatic obstruction
B. Malnutrition
C. Prolonged cirrhosis
D. AOTA

Answer 2

C. Liver cirrhosis

There is a stepwise fashion to edema, reduced intravascular volume, renal hypofusion, and secondary aldosteronism

Primary defect: low plasma protein levels

Question 3

Increased vascular permeability is a mechanism of edema in which of these?
A. acute inflammation
B. Angiogenesis
C. Burns
D. A and B only
E. AOTA

Answer 3

AOTA

Angiogenesis: contraction of pericytes from where the new vessel forms
Acute inflammation: induced by histamine, kinins, and other mediators

Question 4

What kind of cells are “heart failure cells” seen in chronic pulmonary congestion?
A. Cardiac myocytes
B. RBCs
C. Fibroblasts
D. Lymphocytes
E. Macrophages

Answer 4

Macrophages

Extravasated RBCs and plasma proteins in the alveoli are phagocytosed and digested by macrophages; the accumulated iron is stored as hemosiderin. These hemosiderin-laden macrophages (heart failure cells) are telltale signs of previous episode of pulmonary edema.

Question 5

In normal hemostasis, the initial vascular response is mediated by:
A. Platelet mediators
B. Reflex neurogenic response
C. Endothelial cell derived
factors
D. Plasmaproteins
E. AOTA

Answer 5

Reflex neurogenic response

General sequence of events leading to hemostasis:
Arteriolar vasoconstriction: occurs immediately and markedly reduces blood flow to injured areas. It is mediated by reflex neurogenic mechanisms and may be augmented by the local secretion of factors such as endothelin.
Primary hemostasis: the formation of the platelet plug.
Disruption of the endothelium exposes subendothelial von Willebrand factor (vWF) and collagen, which promote platelet adherence and activation.
Secondary hemostasis: deposition of fibrin. Vascular injury exposes tissue factor (TF) at the site of injury. TF is a membrane-bound procoagulant glycoprotein that is normally expressed by subendothelial cells in the vessel wall, such as smooth muscle cells and fibroblasts. Tissue factor binds and activates factor VII, which culminates in thrombin generation. Clot stabilisation and resorption: polymerized fibrin and platelet aggregates undergo contraction to form a solid, permanent plug that prevents further hemorrhage.

Question 6

Lymphatic obstruction is a result of which of the following conditions?
A. Trauma
B. Surgery
C. Infection D. Malignancy E. AOTA

Answer 6

AOTA

Trauma, fibrosis, invasive tumors, and infections agents
can all disrupt lymphatic vessels and impair the clearance of interstitial fluid, resulting in lymphedema in the affected part of the body.

Question 7

Which of these events occur in platelet activation?
A. Change in shape of platelets
B. Release of secretory granules
C. Release of thromboxane
D. NOTA
E. AOTA

Answer 7

AOTA

• Platelets rapidly change shape: ‘spiky sea urchins’
• Secretion of granule contents:
• Activated platelets secrete thromboxane A2, a potent inducer of platelet aggregation

Question 8

Tissue plasminogen, which is an anticoagulant factor, is derived from which of these cells?
A. Endothelial cells
B. Macrophages
C. Platelets
D. Fibroblasts
E. RBCs

Answer 8

Endothelial cells

Question 9

The most common cause of DVT (deep vein thrombosis)
A. Disseminated cancer
B. Protein C deficiency
C. Immobilization
D. Pregnancy
E. Chronic alcohol use

Answer 9

Immobilization

Lower extremity DVTs are often associated with hypercoagulable states. Common predisposing factors include bed rest and immobilization, because these reduce the milking action of the leg muscles, resulting in stasis.

Question 10

Which of these coagulation factors are affected by prolonged antibiotic use?
A. Factor VII
B. Factor IX
C. Factor X
D. Prothrombin
E. AOTA

Answer 10

AOTA

Vit K is a cofactor in hepatic carboxylation of procoagulants: Factors II (prothrombin), VII, IX, X and protein C and
protein S

Question 11

Deficiency of von Willebrand factor is associated with which of the following?
A. Hypercoagulability of blood
B. Stasis
C. Predisposition to infections
D. Corpulmonale
E. Bleeding tendencies

Answer 11

Bleeding tendencies

Von Willebrand factor plays an important role in platelet adhesion to the cellular matrix. Patients with Von Willebrand disease have defects in platelet function despite having normal platelet counts

Question 12

This part of the heart, being the major user of O2 and nutrients, is the most likely site of a mural thrombi arising from a myocardial infarction
A. Left atrium
B. Left ventricle
C. Right atrium
D. Rightventricle
E. Aorta

Answer 12

Left ventricle
Most systematic emboli (80%) arise from intracardiac mural thrombi, 2/3 of which are associated with left ventricular wall infarcts and another 1⁄4 with left atrial dilation and fibrillation.