Hi all!
specially for those YOG volunteers who missed the 2nd FPATH REV Lec.
topic 2.6 on amyloidosis will not be tested for exam

also things tested will not be limited to just the questions cher went through during rev lec.

AY 2007/2008 SUPPLEMENTARY EXAMINATION
(April Semester)

Al. (a) State FIVE characteristics used to describe diseases. (5 marks)

Answers can be found in: Topic 1.1, slide #5.

ANY 5
· Aetiology means cause
· Pathogenesis means mechanism
· Clinical manifestations means structural & functional features of disease
· Complications and sequelea means secondary effects
· Prognosis means outcome
· Epidemiology means incidence

(b) Choose the appropriate information from the article given below and match it to suitable characteristic mentioned above in the description of peptic ulcer. (5 marks)

Topic 1.1 Slides #6-18

Prognosis (Pathogenesis) Complication Manifestation Aetiology <Epidemiology>

<Peptic ulcer is common all over the world.> <It is estimated that 5-10% of individuals in the United States suffer from peptic ulcers during their lifetime.> Peptic ulcers occur principally in the duodenum and stomach. Best estimates suggest that <in American population, about 2% of males and 1.5% of females have peptic ulcers.> The fundamental prerequisite for peptic ulceration is mucosal exposure to gastric acid and pepsin. There is a very strong association with H. pylori infection. Most peptic ulcers cause epigastric gnawing or burning pain related to meals. The pain tends to be worse at night and occurs usually 1 to 3 hours after meals. Bleeding is the result of erosion of a blood vessel by the ulcer and occurs in about 30% of patients with peptic ulcer. Perforation occurs in about 5% of peptic ulcer patients and is most common with anterior duodenal ulcers. (Secretion by H. pylori of a urease that generates free ammonia and a protease that breaks down glycoproteins in the gastric mucus.) (H. pylori also elaborate phospholipases which damage surface epithelial cells and may release bioactive leukotrienes and eicosanoids.) (Breakdown of mucosal defence is much more important than excessive acid production.) Chronic gastritis associated with H. pylori infection is a major risk factor for gastric carcinoma. Early gastric cancer restricted to the mucosa and submucosa has a 5 year survival rate of about 85%.


AY 2009/2010 MAIN EXAMINATION
(April Semester)

Al. (a) Outline the SEVEN categories of diseases. List an example for each category. (7 marks)

1.1 #19-23

Congenital
· Genetic – eg. Albinism; Down’s syndrome
· Non-genetic – congenital rubella syndrome leading to congenital heart disease, blindness and deafness
Acquired
· Inflammatory – appendicitis
· Vascular – shock
· Growth disorders – neoplasia
· Injury and disordered repair - …
· Metabolic and degenerative disorders – diabetes mellitus; Alzheimer’s disease

(b) For each of the conditions below, list ONE clinical laboratory discipline that
would be directly helpful to diagnose the condition. Include in your answer a
relevant investigative test. (5 marks)

1.2 #6-19

(i) Breast cancer

Cytopathology: fine-needle aspiration
Or Histopathology: surgical biopsy

(ii) Liver dysfunction

Clinical chemistry: …
Histopathology: …

(iii) Leukemia

Haematology: complete blood count

(iv) HIV/AIDs

Immunology: …
Microbiology: …

(v) Respiratory acidosis

Clinical chemistry: …


A2. An injured mountaineer was found with a gaping wound. He was rushed to
hospital for emergency treatment.

(a) Scenario A: The mountaineer died from his injuries. State the type of autopsy to be
performed. Describe the associated routine autopsy procedures. (6 marks)

1.3 #31-32

(b) Scenario B: The mountaineer survived. Describe the wound healing process. (6 marks)

2.4 #11-17

By 2nd intention (gaping/big wound) Describe (get from notes)


AY 2009/2010 SUPPLEMENTARY EXAMINATION
(Apr Semester)

A2. (a) Differentiate between idiopathic and iatrogenic diseases. State any ONE
example of iatrogenic diseases. (3 marks)

1.1 #24
Idiopathic: unknown cause (disease) --> eg. …
Iatrogenic: disease induced by a medical practitioner’s words or actions --> eg. …

(b) Differentiate the purpose/ function of the following laboratory disciplines.
Include ONE laboratory test for each laboratory discipline. (6 marks)

I Haematology and Clinical chemistry
II Histopathology and Cytopathology

1.2 #6-19
Haematology
· Study of disease of bone marrow & blood & blood transfusion
Clinical chemistry
· Detection, measurement and interpretation of chemical substances in blood and body fluids
Histopathology
· Diagnostic interpretation of tissue samples/ macroscopic examination of tissue to study the manifestation of disease
Cytopathology
· Diagnostic interpretation of cells, single cells or clumps of cells dissociated from the surrounding tissues/ focuses on the relationship between structure and function within a cell and how it is affected by diseases

And any ONE Lab test each, eg:
· Haematology: haemoglobin concentration/ red cell count/ packed cell volume/ mean cell volume, mean cell haemoglobin/ mean cell haemoglobin oncentration
· Clinical chemistry: blood gases: oxygen, carbon dioxide/ electrolytes: sodium, potassium/ urea/ creatinine/ hormones
· Histopathology: tissues/ organs/ abnormal lumps/ mass removed during surgery or Biopsy for gross/ macroscopic examination
· Cytopathology: Microscopic examination of stained smears/ fine-needle aspiration/ Pap smear

(c) Differentiate between congenital disease with structural abnormality from an acquired disease with functional abnormality. Name an example for each type. (3 marks)

1.1 #13-14; 19-23
· Congenital disease with structural abnormality. Anatomical abnormalities attributable to events prior to birth, not necessarily genetic pr inherited.
· Eg Cleft lip
· Acquired disease with functional abnormality: Disease of physiological dysfunction due to an event after birth.
· Eg. Diabetes mellitus

A3. Assume that the following tissues/organs have undergone necrotic changes due to
different types of injuries, answer the questions that follow:

I Kidney
II Brain
III Adipose tissues near the pancreas
IV Toes (uninfected)

For EACH tissue/organ listed above, (12 marks)

2.2 #16-24

(a) predict the type of necrosis,

(b) state the cause of necrosis, and

(c) describe the microscopic or gross morphology of the affected organs/tissues.

I Kidney
(a) Coagulative necrosis
(b) Ischemia / Hypoxia
(c) ANY ONE:
· Firm texture/ preservation of tissue architecture
· Acidophilic, coagulated (clumping of cytoplasm) aneucleate cells
· Membrane integrity preserved

II Brain
(a) Liquefactive necrosis
(b) Ischemia / Hypoxia
(c) ANY ONE:
· Liquid, viscous mass/ cyst

III Adipose tissues near the pancreas
(a) fat necrosis
(b) acute pancreatitis/ pancreatic injuries releases activated pancreatic lipases cause focal fat destruction
(c) ANY ONE:
· Fat call membrane liquefied
· Visible chalky white area

IV Toes
……….

AY 2007/2008 MAIN EXAMINATION
(April Semester)

A3. (a) With reasons, provide the appropriate nomenclature of the benign and
malignant neoplasms derived from the following tissues/organs. (6 marks)

· Cartilage

· Liver

2.9 #6-7

Cartilage
· Benign: Chondroma; Malignant: Chondrosarcoma
· Benign mesenchymal tumours are named after the cell or tissue of origin suffixed by ‘-oma’.
· Malignant mesenchymal tumours are designated sarcomas, prefixed by the name that describes the cells of tissues of origin which is cartilage.

Liver
· Hepatic adenoma; Hepatocellular carcinoma
· Benign tumours of glandular epithelium are named after the cell or tissue of origin suffixed by “adenoma”
· Malignant tumours of glandular epithelium are designated adenocarcinoma, prefixed by the name that describes the cell of tissue of origin which is liver.


(b) Differentiate lymphatic metastasis and transcoelomic metastasis. (4 marks)

2.9 #16-17

Lymphatic metastasis
· Malignant cells are carried by the lymphatics to the regional lymph nodes · Pattern of lymph node involvement follows the natural route of drainage Eg. CA breast ( upper outer quadrant) spread to axillary lymph nodes

Transcoelomic metastasis
· Malignant cells spread to peritoneal, pleural & pericardial cavities
· Peritoneal effusion (ascites) primaries in ovaries or due to any abdominal tumours OR Pleural & pericardial effusion are common conseqences of the breast/ lung neoplasms

A6. (a) Explain the type and pathophysiology of edema in the following patients.

· Patient " U with malnutrition (4 marks)

· Patient "V" suspected with tumour metastasis in the lymphatic vessel

2.5 #9-10
Patient U with malnutrition
· Hypoalbuminaemic edema resulting from reduced protein intake due to malnutrition: hypoalbuminaemia reduces the plasma oncotic pressure.
· So that H­­2O cannot be sucked back into the capillary or oncotic end & remains in tissue leading to edema.
Patient V with tumour metastasis in the lymphatic vessel
· Lymphatic edema due to obstruction of lymphatic drainage by tumour (s); some fluids normally leave capillaries and drain into lymphatic channels
· When there is lymphatic obstruction, it will prevent drainage of H­­2O from tissues causing edema.

(b) Contrast the pathogenesis of amyloidosis in the following patients. (6 marks)
· Patient "W" diagnosed with multiple myeloma

· Patient "X" suffering from rheumatoid arthritis (Not tested)

B2. (a) Describe suppuration and repair and organisation. (8 marks)

2.7 #14-18
Suppuration
· Means formation of pus which is a mixture of living, dying and dead neutrophils and bacteria
· Cellular debris and sometimes globules of fat
· Occurs when there is infection caused by pyogenic bacteria such as Staph aureus.
· Strep pyogenes, Neisseria or coliforms

Repair and Organisation
· Means replacement by granulation tissue
· Occurs when large amounts of fibrin are formed
· Occurs when substantial volume of tissue become necrotic or if dead tissue is not easily digested
· Occurs when exudates and debris cannot be removed or discharged

(b) A patient was suspected with inflammation of the appendix for 2 hours.

(i) With reasons, propose the appropriate medical term for this case. (2 marks)

2.7 #2
Acute appendicitis. Acute as t occurs 2 hrs; appendicitis means inflammation of the appendix

(ii) Explain the possible macroscopic features of the above case. (5 marks)

­2.7 #7
· Redness of the appendix due to dilatation of blood vessels within the damaged area
· Appendix will be swollen due to edema from accumulation of fluid
· The patient will have fever due to release of endogenous pyrogens from polymorphs and macrophages
· The patient will feel pain resulting from stretching and distortion of tissues due to edema and release of chemical mediators such as bradykinin, prostaglandins and serotonin.

(iii) Explain the microscopic features of the tissue taken from the above
appendix. (2 marks)

2.7 #8
· Neutrophil infiltration
· Of the mucosa and the wall of appendix

(iv) Describe THREE early stages of inflammation that could have occurred around the blood vessels of the above appendix. (3 marks)

2.7 #9
· Alterations in vascular calibre that leads to an increase in blood flow
· Increased vascular permeability and the formation of fluid exudate
· Emigration of the neutrophil polymorphs into the extravascular space and formation of the cellular exudates


AY 2008/2009 SUPPLEMENTARY EXAMINATION
(Apr Semester)

A3. (a) State the purposes of inflammation and characteristics of chronic
inflammation. (6 marks)

2.7 #2; 2.8#2
· To localise and eliminate the injurious agent and
· To restore the tissue to normal structure and function.
· Chronic inflammatory response is characterised by lymphocytes, plasma cells and macrophages and proliferation of blood vessels and connective tissue.
· It is of prolonged duration: weeks or months
· It leave behind areas of permanent tissue damage.

(b) Define amyloid. Outline the pathogenesis of secondary amyloidosis resulting
from chronic inflammation. (6 marks) (Not tested)

AY 2009/2010 MAIN EXAMINATION
(April Semester)

A5. (a) Describe the pathological conditions in the circulatory system that would
promote thrombus formation. (8 marks)

3.1 #10-14
· Endothelial injury
· Leads to exposure of platelets and release of tissue factors that activate coagulation cascade.
· Altered blood flow (ANY 2 below)
· Turbulence in arteries will damage the endothelial layer. OR form counter-current; OR form small pockets of blood stasis
· Blood stasis in veins will promote thrombus formation
· Will disrupt laminar flow of blood and bring platelets into contact with endothelium; OR Will prevent dilution of activated clotting factors due to blood stasis
· Hypercoagulability
· Examples of acquired or genetic aetiology that promotes blood coagulation by increasing thrombin activity; OR decrease inactivation of clotting factors; OR promote fibrin formation

(b) Explain the FOUR possible consequences of a thrombus. (4 marks)

3.1 #21
· Propagation: More platelets and fibrin accumulate to block blood vessels
· Embolization: thrombi dislodge from origin and move to distal sites
· Dissolution: removal of thrombi by fibrinolytic activity
· Organization and recanalization: induce inflammation and fibrosis that blood vessels may be recanalized

AY 2008/2009 MAIN EXAMINATION
(April Semester)

B2. Mr and Mrs X were badly injured in a motor accident. Mr X suffered abrasions to his face and limbs while Mrs X suffered haemorrhagic shock.

(a) Explain haemorrhagic shock and describe the stage of systemic compensation. (6 marks)

3.3 #8;10
· Haemorrhagic or hypovolemic shock due to inadequate blood or plasma volume caused by haemorrhage.
· Decreased cardiac output à reflex sympathetic stimulation
· --> increases the heart rate & peripheral vasoconstriction
· --> maintains blood pressure in brain and myocardium
· --> peripheral vasoconstriction --> cold and clammy skin
· --> vasoconstriction in renal arterioles --> decreases pressure and rate of glomerular filtration --> decreases urine output
Note: you can’t use “-->” during the exams.

(b) Mrs X could deteriorate into decompensation stage if help is delayed. Describe the stage of decompensation. (4 marks)

3.3 #12
· Reflex peripheral vasoconstriction fails
· --> widespread vasodilation and stasis à progressive fall in blood pressure (hypotension)
· --> cerebral hypoxia à acute brain dysfunction (loss of consciousness, edema, neuronal degeneration)
· --> myocardial hypoxia --> diminution of cardiac output and death
Note: you can’t use “-->” during the exams.

(c) Mr X was hospitalized and treated for his wounds. Explain the factors that the hospital can control to ensure proper wound healing for Mr X. (10 marks)

2.4 #18-19
· Prevent infection
· as it would cause delay in wound healing
· by prolonging the inflammation pjae & increasing local tissue injury.
· Provide proper nutrition
· as protein deficiency & vit. C deficiency inhibits collagen synthesis & retard healing.
· Minimise use of steroid,
· which results in poor wound strength due to diminished fibrosis.
· Minimise local pressure or torsion
· which may cause wounds to pull apart.
· Remove fragments of steel of glass or even bone as they impedes healing.

AY 2008/2009 SUPPLEMENTARY EXAMINATION
(Apr Semester)

Al. (a) Explain atheroma, arteriosclerosis and atherosclerosis. List any THREE of
the aetiology of atherosclerosis. (6 marks)

3.4 #5-8
· Atheroma: fibrofatty plaque/ raised focal plaque within the intima/ core of lipid and a covering fibrous cap.
· Arteriosclerosis: thickening and loss of elasticity (hardening) of the arteries from any cause.
· Atherosclerosis: thickening of the artery resulting from deposition of specific artheromatous lesions.
Aetiology (any THREE)
· Hypertension
· Cigarette smoking
· Diabetes mellitus
· Hyperlipidemia (genetic/ acquired)

(b) State the THREE components of atheromatous plaques. Describe the
consequences/sequelae of complicated plaques. (6 marks)

3.4 #23-24
Components
Any one of each
· Cells including smooth muscle cells, macrophages and other leukocytes
· Connective tissue matrix: collagen, elastic fibers and proteoglycans
· Intracellular and extracellular lipid deposits
Complication/ Sequelae (any THREE): plaques may develop the following changes
· Calcification
· Ulcerated lesions may develop thrombosis
· Rapture of the plaque may discharge debris into the bloodstream as cholesterol emboli
· Haemorrhage into the plaque
· Aneurysm: arteries weakened by extensive plaque formation