MINISTRY OF HEALTH AND SOCIAL WELFARE
TECHNICIAN CERTIFICATE IN CLINICAL MEDICINE
NTA LEVEL 4
CONTINOUS ASSESSMENT 1
CMT04105: PATHOLOGY
CANDIDATE No. ………………............... DATE: …………………................
Time Allocated 2 hours
INSTRUCTIONS:
Read all questions carefully before answering
Follow the instructions given at the beginning of each section
Attempt all questions
Remember to write down your registration number on each page you use
Mobile phones or any other Unauthorized materials are not allowed in the examination room.
This paper consist of five sections. Attempt all questions
SECTIONS:
SECTION A: MULTIPLE CHOICE QUESTIONS (10 QUESTIONS) - 10 MARKS
SECTION B: MULTIPLE TRUE/FALSE QUESTIONS (4 QUESTIONS) -10 MARKS
SECTION C: MATCHING QUESTIONS (2 QUESTIONS) -10 MARKS
SECTION D: SHORT ANSWER QUESTIONS (8 QUESTIONS) -40 MARKS
SECTION E: ESSAY QUESTIONS (3 QUESTIONS) -30 MARKS
TOTAL = 100MARKS
SECTION A: MULTIPLE CHOICE QUESTIONS 10 MARKS
INSTRUCTIONS:
This section consists of ten (10) questions;
Respond by circling of the most correct answer
One mark will be awarded for each correct answer.
The branch of pathology that deals with organs and organ systems is called:
General Pathologyf
Histopathology
Systemic Pathology
Surgical Pathology
Forensic Pathology
Hypersensitivity reaction is one of the following environmental factors causing diseases:
Physical Agents
Chemical Poisoning
Nutritional Deficiency
Infection and Infestation
Hypersensitivity
One of the following is NOT a component of cellular event of acute inflammation:
Leukocyte Recruitment
Increased Vascular Permeability
Leukocyte Activation
Phagocytosis
Migration
Opsonization as used in acute in inflammation means:
Coating of microbes and target them for phagocytosis
Phagocytosis of microbes or dead cells
Chemotaxis of macrophages towards affected cells
Exudation of protein rich fluid during acute inflammation
Transudation of protein less fluid during acute inflammation
The most important opsonins in acute inflammation is
Immunoglobulin E (IgE) class
Immunoglobulin A (IgA) class
Immunoglobulin G (IgG) class
Immunoglobulin D (IgD) class
Immunoglobulin C (IgC) class
The patient was diagnosed with Asthma in the hospital. This is scenario best describes:
Immediate Type 1 hypersensitivity reaction
Antibody Mediated Type II hypersensitivity reaction
Immune Complex-Mediated (Type III) Hypersensitivity
Delayed-type hypersensitivity (DTH), initiated by CD4+ T cells.
Direct cell cytotoxicity, mediated by CD8+ T cells
The following components make up the Extra Cellular Matrix Except:
Collagens
Elastins
Fibroblast
Proteoglycans and hyaluronan
Adhesive glycoproteins
SECTION B: MULTIPLE TRUE/FALSE QUESTIONS 10 MARKS
INSTRUCTIONS:
This section consists of four (4) questions with five (5) options
Write the word “TRUE” and NOT letter ‘T’ for a correct statement and the word “FALSE” NOT letter ‘F’ for incorrect statement
Half (½) a mark will be awarded for each correct response
Stem cells are characterized by the following properties:
____FALSE________ Have replicative capacity to the stable cells
____TRUE_________ Have self-renewal capacity
____FALSE________ Have ability to enter GO phase of cell cycle
____TRUE_________ Have asymmetrical replication
____FALSE________ Can only occur during Embryonic Life
The characteristic findings of asthma, collectively called ‘airway remodelling’ includes:
____TRUE_________ Thickening of the basement membrane of the bronchial epithelium
____FALSE________ Lung collapse
____TRUE_________ Oedema in the bronchial walls
____TRUE_________ An increase in the size of the sub-mucosal glands.
____TRUE_________ Inflammatory infiltrate in the bronchial walls
The histologic spectrum of pneumonia includes
____TRUE_________ A fibrinopurulent alveolar exudates
____FALSE________ A Ghon's Focus seen as a result of enlarged regional lymphnodes
____TRUE_________ Mononuclear interstitial infiltrates
____FALSE________ Lymphocytic infiltration and presence of abundant kupffers cells
____TRUE_________ Granulomas and cavitation
SECTION C: MATCHING QUESTIONS 10 MARKS
Instructions:
This section consists of two (2) matching questions, each with five (5) options.
Match the items from column B with those in column A by writing the letter of the correct response in the space provided. USE CAPITAL LETTERS Only.
Each correct response is awarded one (1) mark.
Each item from column B is used only once.
1: Match the following clinical description from column A with the type of necrosis from column B:
SECTION D: SHORT ANSWER QUESTIONS 40 MARKS
INSTRUCTIONS:
This section consists of eight (8) questions.
Write your answer in the space provided
Write a readable handwrite; DIRTY WORK IS NOT ALLOWED.
Mention three(3) general features of chronic inflammation
_________________________________________________________________________________________________________________________________________________________________________________________________________________________________
Answer ( 3 marks) @ 1 mark
Mononuclear cell infiltration
Tissue destruction or necrosis
Proliferative changes
Mention the cardinal signs of inflammation
____________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
___________________________________________________________________________
Answer ( 5 marks) @ 1 mark
Pain and tenderness(dolour)
Swelling(tumour)
Redness(rubor)
Hotness(colour)
Loss of function or reduced efficiency (function laesa)
Outline the components of Exudates
_______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
Answer ( 5 marks) @ 1 mark
Water
Proteins (immunoglobulins), albumin and fibrinogen in severe cases
Hormones
Natural antibacterial opsonin
Cells-White blood cells (WBCs)
Outline five(5) growth factors used in cellular proliferation and mitosis
_______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
Answer: Any five(5) points @ 1 marks
Epidermal
Transforming (alpha, beta)
Hepatocyte
Vascular Endothelial
Platelet Derived
Fibroblast
Keratinocyte
Cytokines (TNF, IL-1, Interferons)
Immune Complex-Mediated (Type III) Hypersensitivity diseases are among the commonest diseases in Tanzania. Mention five(5) diseases caused by the hypersensitivity reaction:
_______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
Answer
Acute serum sickness (as a result of blood group incompatibility)
Acute post-streptococcal glomerulonephritis
Polyarteritis nodosa (PAN)
Reactive arthritis
Systemic lupus erythematosus (SLE)
SECTION E: GUIDED ESSAY QUESTIONS 30 MARKS
INSTRUCTIONS
This section consists of three (3) questions which are to be answered in a narrative way
Write your answer in the back of the page; each question should start on a new page.
Mr X 60 years old came to the hospital with a complain of swelling and pain after being bitten with bees. Describe the type of inflammation using the following subheadings( Definition, Signs of Inflammation, Causes, Components and Outcomes Of Inflammation)
Answer 10 marks
Definition: (1 mark)
It is a rapid response to injury or microbes and other foreign substances that is designed to deliver leukocytes and plasma proteins to sites of injury.
Signs of Inflammation Any Four(4) points @ 0.5 marks
Acute inflammation has five cardinal features as follows:
• Pain and tenderness (dolour):
This is an early symptom in acute inflammation
The pain in acute inflammation is due to direct nerve injury, tissue irritation by chemicals and agents released by cells involved in acute inflammation and pressure due to accumulating exudates compressing nerves
• Swelling (tumour)
This is due to local accumulation of inflammatory exudates
Vascular changes occur within the affected area, which cause accumulation of fluid and white blood cells to escape from the intravascular compartment to the interstitial tissue in the inflamed area
• Redness (rubor)
This is due to local increase in blood flow to the inflamed zone, increased permeability and blood flow give red coloration
The coloration is less prominent feature among dark skinned individuals
• Hotness (colour)
Inflamed area feels warmer than the surrounding areas due to increased blood flow to the affected area.
• Loss of function or reduced efficiency (function laesa)
Inflamed tissue or organ cannot perform its function as efficiently as a normal tissue
Temporary or permanent structural damage to the tissue may lead to loss of function
Causes of acute inflammation Any four (4) points @ 0.5 marks
Infections (bacterial, viral, fungal, parasitic) are among the most common and medically important causes of inflammation
Trauma (blunt and penetrating)
Physical and chemical agents (thermal injury, e.g. burns or frostbite; irradiation; some environmental chemicals) injure host cells and elicit inflammatory reactions.
Tissue necrosis (from any cause), including ischemia (as in a myocardial infarct) and physical and chemical injury
Foreign bodies (splinters, dirt, sutures)
Immune reactions against environmental substances or against self tissues (hypersensitivity)
Components of acute inflammation Each component 1.5 marks( 3 marks)
Acute inflammation has two major components which are:
Vascular changes (1.5 marks)
Alterations in vessel caliber resulting in increased blood flow (vasodilatation) and structural changes that permit plasma proteins to leave the circulation (increased vascular permeability)
Transient Vasoconstriction
This is a very short event lasting for a few seconds
Arteriolar Vasodilatation
This is a predominant feature in acute inflammation.
This occurs due to increased blood flow and engorgement of the down-stream capillary beds.
This vascular expansion is the cause of the redness (erythema) and warmth characteristically seen in acute inflammation.
Increased Vascular Permeability
In the early phase of inflammation, arteriolar vasodilatation and increased volume of blood flow lead to a rise in intravascular hydrostatic pressure, resulting in movement of fluid from capillaries into the tissues. This fluid, called a transudate, is essentially an ultra filtrate of blood plasma and contains little protein.
Cellular events (1.5 marks)
This is the emigration of the leukocytes from the microcirculation and accumulation in the focus of injury (cellular recruitment and activation) which involves three distinct steps which are leukocyte recruitment, Activation and Phagocytosis.
Outcomes Of Inflammation Four(4) points @ 0.5 marks
Resolution
Complete healing when tissue damage is minimal or process is short lived and the tissue has the ability of regeneration.
Progression
The acute inflammation can progress to chronic inflammation when the tissue damage is extensive or when the exudates is not completely eliminated or cleared.
Fibrosis
This occurs when there is extensive tissue damage, exudates are not timely cleared and tissue involved has no capacity to regenerate.
Spread
Direct e.g.cellulitis
Lymphatic-lymphangitis progressing to acute lymphadenitis
Blood vessels
Pyaemia-spread of pyogenic organisms in infected micro-thrombi via the blood stream possibly giving rise to secondary (metastatic) abscesses.
Septicaemia-multiplication of organisms in the blood stream in the absence of adequate host defenses.
Death
It results from Septicaemia, e.g. endotoxic shock and its complications
Involvement of vital organs, e.g. encephalitis, myocarditis
Describe wound healing using the following sub headings (Definition, Phases of wound healing, Types of wound healing and Sequence of events in wound healing)
ANSWER ( 10 marks)
Definition: 1 marks
Wound Healing is a complex and dynamic process of restoring cellular structures and tissue layers.
Phases of wound healing: 3 points @ 1 mark
Wound healing process can be divided into 3 distinct phases
Inflammatory phase
Proliferative phase
Remodelling phase
Within these three broad phases is a complex and coordinated series of events that includes chemotaxis, phagocytosis, granulation, collagen degradation, and collagen remodeling. In addition, angiogenesis, epithelization, and the production of new glycosaminoglycans and proteoglycans are vital to the wound healing.
Types of wound healing 3 points @ 1 mark
There are three categories of wound healing which are:
Primary wound healing
This is also known as healing by first intention.
Occurs within hours of repairing a full-thickness surgical incision when edges of the wound are in aposition.
Delayed primary wound healing
Occurs if the wound edges are not reapproximated immediately.
By the fourth day, phagocytosis of contaminated tissues is well underway, and the processes of epithelialisation, collagen deposition, and maturation are occurring.
Secondary healing
This is also known as healing by secondary intention.
Secondary healing results in an inflammatory response that is more intense than with primary wound healing.
In addition, a larger quantity of granulomatous tissue is fabricated because of the need for wound closure.
Sequence of events in wound healing: 3 points @ 1 mark
Sequence of events in wound healing has the following phases:
Initial phase (Hemostasis)
Following vasoconstriction, platelets adhere to damaged endothelium and discharge adenosine diphosphate (ADP), promoting thrombocyte clumping, which dams the wound.
Second phase (Inflammation)
Polymorphonuclear leukocytes (PMNs) engorging the wound.
Third phase (Granulation): This phase consists of subphases which are fibroplasia, matrix deposition, angiogenesis and re-epithelialization.
Fourth phase (Remodelling): The wound undergoes constant alterations which can last for years after the initial injury occurred.
