WHO 2017 Classification of tumours of Salivary Glands

General Pathology Multiple choice questions (MCQ)

1. Regarding cell injury and death

a)       Initially there is a reduction in cell size during cell necrosis

b)      Apoptosis is associated with an inflammatory response

c)       Necrosis results from caspases sequestered in mitochondrial membranes

d)      Cellular swelling and fatty change indicate reversible cell injury

2. In which of the following organs is steatosis NOT seen

a)       Heart

b)      Kidney

c)       Lung

d)      Liver

3. Dystrophic calcification can occur in

a)       Coagulative necrosis

b)      Caseous necrosis

c)       Enzyme necrosis of fat

d)      All the above

4. Cholesterol and its esters are

a)       Metabolised in a loosely regulated system within cells

b)      Are seen as xanthomas within monocytes in tendons

c)       Accumulate in macrophages in the gallbladder known as cholesterosis

d)      Are seen in the media propria of the aorta in atherosclerosis

5. Progressive atrophy of the brain in later adult life is thought to be part due to

a)       Decreased workload

b)      Loss of innervation

c)       Diminished blood supply

d)      Loss of endocrine stimulation

6. Inflammation is

a)       Fundamentally a destructive response acutely

b)      Is characterised by exudation of fluid and migration of neutrophils

c)       Results in scarring thru regeneration of native parenchymal cells

d)      Is activated by Toll like receptors on microbes

7. The most common mechanism for the formation of leaky endothelium in inflammation is

a)       Endothelial retraction

b)      Direct endothelial injury

c)       Leukocyte mediated endothelial injury

d)      Endothelial cell contraction

8,Regarding mediators of inflammation

a)       Histamine is a preformed vasoactive mediator causing arteriole vasoconstriction

b)      Histamine is considered to be the principle mediatory of the immediate transient phase of increased vascular permeability

c)       Nitric oxide has dual actions in inflammation, it relaxes vascular smooth muscle and also promotes the cellular response in the inflammatory response

d)      Platelet activating factor is found unique to platelets

9. In leukocyte migration thru blood vessels in inflammation

a)       Extravasation of the leukocyte occurs in the order of: adhesion to the wall, margination and then rolling of the leucocyte across the endothelial wall.

b)      Selectins are the primary molecule who play roles with neutrophil activation

c)       Integrins are  involved in firm adhesion of the leucocyte to the cell wall

d)      Endothelial cells will take 6-12hrs before they express their selctin ( E selectin ) in inflammation

10. Regarding some inflammatory patterns

a)       When mesothelial cells of the peritoneum, pleural and pericardial linings secrete fluid it is usually of a fibrinous nature

b)      A serous exudation consists primarily of neutrophils, liquefactive necrosis and oedematous fluid

c)       When there are large vascular leaks or an associated procoagulant stimulus you commonly see a suppurative exudate

d)      Ulcers can only occur when tissue necrosis and the resultant inflammation is on or near a surface

11.In chronic inflammation, all are true except

a)       It can be caused by prolonged exposure to toxic agents

b)      It involves mononuclear inflammatory cells

c)       It may contribute to the formation of atherosclerosis

d)      It primarily involves tissue destruction

12. The complement system

a)       Most critical step is the proteolysis of the 3^rd component C3 to C3a

b)      Is only involved in innate immunity reactions

c)       Causes decreased vascular permeability, chemotaxsis and opsonization of leukocytes

d)      Is a loosely controlled pathway

13, Regarding wound healing,

a)       The inflammatory response in primary healing is more intense than in secondary healing 

b)      At 1 week , the wound strength is 20% of that of unwounded skin

c)       Wound contraction is due in part to fibroblast contraction

d)      In primary union, collagen fibres appear with granulation tissue

14.The most important cause of delay of healing is

a)       Inadequate blood supply

b)      Infection

c)       Foreign body presence

d)      Poor nutritional state of the patient

15. Regarding the extracellular matrix, which is NOT CORRECT?

a)       Fibronectin in its plasma form is involved in blood clot stabilisation

b)      Laminin is the most abundant glycoprotein in the extracellular matrix

c)       Vit D is required for the hydroxylation of procollagen to collagen

d)      The cross linking of collagen is important in providing tensile strength to a wound

16. The causes of liver steatosis do not include:

a)       Alcohol abuse

b)      Protein malnutrition

c)       XI-antitrypsin deficiency

d)      CCl4

17.Regarding metastatic calcification, which of the following is not a cause?

a)       Renal failure

b)      Paget’s disease

c)       Sarcoidosis

d)      Hypoparathyroidism

18. Depletion of AtP cause all EXCEPT

^a)                 efflux of Ca²⁺

b)      efflux of K

c)       influx of Na⁺

d)      decrease pH cells

19.The most common causes of fatty liver in the developed world  are

a)       Hypercholesterolaemia and lipid storage diseases

b)      Alcohol abuse and hypercholesterolaemia

c)       NAFLD and alcohol abuse

d)      NAFLD and hypercholesterolaemia

20   .Examples of intracellular accumulations of lipid do NOT include

a)       Niemann-Pick disease type C

b)      Atherosclerosis

c)       Xanthomas

d)      Amyloidosis

21. .Regardig white cell extravasation in acute inflammation which of the following pairs are incorrect

a)       P selectin: neutrophil rolling

b)      ICAM: neutrophil rolling

c)       E selectin neutrophil rolling

d)      CD34: neutrophil rolling

22.Which of the following disorders are examples of chronic leukocyte induced injury

a)       Arthritis

b)      Asthma

c)       Atherosclerosis

d)      Septic  shock

23.Leukotrienes does not mediate the following actions

a)       Vasoconstriction

b)      Chemotaxis

c)       Increased vascular permiability

d)      Vasodilatation

24.Which is NOT true regarding blood clot formation?

a)       The clot contains red cells, fibrin, fibronectin and complement

b)      Within 24 hours of injury, macrophages migrate in along the fibrin scaffold

c)       Neutrophils release proteolytic enzymes that clean out debris and bacteria

d)      Platelet adhesion and aggregation, and formation of the clot leads to inflammation

25.          Which of the following is true about formation of granulation tissue:

a)       Granulation tissue forms around day 6 from proliferation of fibroblasts and vascular endothelial cells

b)      Characteristic histological feature is presence of new small blood vessels (angiogenesis) and proliferation of fibroblasts

c)       The new vessels in angiogenesis are tight and restrict passage of plasma proteins.

d)      There is a similar amount of granulation tissue in wounds healing by both primary and secondary intention

26.          The following complications of healing are true, except:

a)       Hypertrophic scars result from accumulation of granulation tissue

b)      Keloid scars grow beyond the boundaries of the original wound and don't regress

c)       Dehiscence, common after abdominal surgery, is due to increased abdominal pressure

d)      Wounds can ulcerate because of inadequate vascularisation

27.          Which is NOT true regarding wound healing?

a)       A scar is composed of fibroblasts, collagen, elastic tissue and other ECM components.    

b)      Wound contraction is important in healing by secondary intention.

c)       The initial matrix of fibrin, fibronectin and type I collagen is ultimately replaced by type III collagen.

d)      The tensile strength after one week in an incisional surgical wound is about 10% of unwounded skin.

28. Which of the following is not an example of peripheral immunologic tolerance?

a)       Anergy

b)      Thymic deletion

c)       Suppression by regulatory T-cells

d)      Antigen sequestration

29. Regarding mitochondrial alterations, which is true?

a)       In cell hypertrophy, there is corresponding increase in mitochondrial size.

b)      Mitochondrial myopathies are associated with increased numbers of morphologically abnormal mitochondria

c)       Oncocytomas are malignant tumours consisting of cells with abundant enlarged mitochondria

d)      Hepatocytes in alcoholic liver disease assume megamitochondria -> extremely large, normally shaped mitochondria (abnormal shapes)

30.Regarding lysosomes which is incorrect?

a)       Primary lysosomes are membrane bound

b)      Contain hydrolytic enzymes

c)       Are synthesised in the smooth endoplasmic reticulum

d)      May persist in the cell as residual bodies

Wait for the answers

Acute inflammation - General Pathology Multiple Choice Questions (MCQ) - With Answers

       

    True and False type MCQ's

     01.Acute inflammation

a.     Heal by suppuration with abscess formation

b.     Completely heal by resolution

c.      Heal with fibrosis

d.     Heal with regeneration

e.     Leads to amyloidosis

        

02  Regarding acute inflammation

a. Active hyperaemia is due to increased venous pressure

b. Increased pressure is due to gaps in basement membrane

c. Prostaglandin is an endogenous mediator of increased venous pressure

d. Excess proteins are removed by lymph

e. Cellular inflammatory exudates has low O2 tension

03. Regarding acute inflammation

a. Active hyperaemia is due to arteriolar relaxation

b. Angiotensin is an endogenous mediator causing increase in permeability

c. Monocyte infiltration is an active process

d. Increased permeability is due to gaps in the basement membrane

e. Proteins are taken into the lymphatics by pinocytosis

04. Regarding acute inflammation

a. It does not depend on the structure of the tissue affected

b. Mild acute inflammation is healed by the granulation tissue formation

c. In mild acute inflammation the cardinal signs of inflammation cannot be seen

d. Dilation of blood vessels are due to stimulation of autonomic innervation of arterioles

e. In severe inflammation cell necrosis may occur

05. Regarding acute inflammation

a. Migration of monocytes is a passive process

b. Fibrin network forms a mechanical barrier to the spread of bacteria

c. Promotion of immunity is due to antibody mediated immunity as well as cell mediated immunity

d. Slowing of blood flow preceded by active hyperaemia

e. Formation of granulation tissue leading to fibrosis is a recognized sequale

06. “Triple response” of acute inflammation is characterized by

a. Redness of the injury followed by reflex vasodilation

b. Local tissue wheal representing swelling

c. Development of heat

d. Involvement of both a local nerve reflex and a histamine response

e. Increased reaction due to a mixture of polypetides

07. Effects of acute inflammation include

a. Prevention of local tissue injury by dilution of the toxin

b. Prevention of spread of organism by forming a fibrin network

c. Maintaining long term immunity by promoting antibody formation

d. Destruction of microorganisms due to heat

e. Healing of the injury by promoting immobility due to pain

08. Cells that take part in acute inflammation include

a. Plasma cells

b. Mast cells

c. Lymphocytes

d. Polymorphonuclear leucocytes

e. Macrophages

09. Exudate occurs as a result of

a. Increased capillary permeability

b. Direct action of prostacycline and complement

c. Chemical mediators

d. Axonal reflex via substance P

e. Prostaglandin action

10. In acute inflammation oedema is produced by

a. increased capillary permeability

b. Direct reflex

c. Neural reflex

d. Antibody reactions

e. Increased intravascular pressure

11. Substances important in the increased vascular permeability of acute inflammation include

a. Globulin permeability factor

b. Cortisol

c. Histamine

d. Plasma kinines

e. Seratonin

12. Essential features of abscess formation are

a. Eosinophil leucocytosis

b. Destruction of tissue

c. Pyaemia

d. Septicaemia

e. Neutrophil leucocytosis

13. Regarding chronic inflammation

a. Important feature is production of vascular granulation tissue

b. Nature of the lesion depend on the intensity and persistence of the stimulation

c. Most of the migrating cells into the injured tissue are mononuclear cells

d. It gives rise to serious effects by narrowing orifices and tubes

e. Fibrosis tissue formation always have harmful effects

14. Regarding chronic inflammation

a. Microorganisms ingested by macrophages are destroyed by it

b. In autoimmune thyroiditis it serves a useful function

c. In arteritis, fibrous tissue formation strengthens the arterial wall

d. Presence of large numbers of lymphocytes suggest hypersensitivity

e. Production of vascular granulation tissue is important feature

15. Malignant disease may complicate the chronic inflammatory conditions

a. Sarcoidosis

b. Ulcerative colitis

c. Chronic osteomyelitis

d. Asbestosis

e. Schistosomiasis

16. Granulomas are characteristically found in

a. Beryllium pneumonitis

b. Leprosy

c. Tuberculosis

d. Syphilis

e. Coccidiodomycosis

17. Granuloma is a type of inflammatory reaction characteristic of

a. Tuberculosis

b. Rheumatoid arthritis

c. Regional ileitis

d. Staphylococcal pyaemia

e. Sarcoidosis

18. Cells which may be found in granulomas

a. Plasma cells

b. Giant cells

c. Lymphocytes

d. Epithelioid cells

e. Macrophages

19. Epithelial cell granulomas are seen in

a. Typhoid fever

b. Crohn’s disease

c. Foerign body reactions

d. Tuberculosis

e. Alcoholic hepatitis

20. Caseous granuloma are seen in

a. Tuberculosis

b. Lupus vulgaris

c. Sarcoidosis

d. Foreign body granulomas

e. Inflammatory bowel disease

 Answers will be Uploaded soon

Embolism

Embolus Definition

A detached intravascular solid, liquid  or gaseous mass that is carried by the blood to a site distant from its origin.

Embolism

Occlusion or obstruction of a vessel by an embolus

Causes and Types of emboli

• Thrombi: Thromboembolism
• Microemboli
• Fragments of atheromatous plaques-Atheroemboli
• Bone marrow and bone fragments
• Fat emboli
• Air/nitrogen emboli
• Aminiotic fluid
• Tumour
• Foreign body emboli: IV catheters
• Parasitic emboli

Where emboli lodge depend on their size, their origin, and relevant cardiovascular anatomy.

Those arise in the venous system can travel through the right side of the heart to end up in pulmonary circulation.

Those arise in the left side will block the systemic arteries, and the clinical effect will depend on the organ involved, be it brain, kidneys, spleen, or periphery of the limbs.

Categories of Embolism

• Systemic embolism- Arise in arterial system eg: thromboemboli in arterial system and left heart, atheroemboli, fat, tumor
• Pulonary embolism- Arise in venous system thrombi in right heart and deep venous thrombosis, all except atheroemboli.
• Paradoxical-  By right to left shunt- ASD and VSD
• Retrograde

Pulmonary embolism

Thrombo-emboli often originate in the deep veins and pass in the venous circulation through right side of heart.

The outcome of pulmonary embolism depends on the size of the blood vessel blocked & presence of pre-existing lung diseases.

Massive pulmonary embolism

Massive coiled pulmonary emboli  are impacted in a main pulmonary artery at bifurcation (Saddle embolus).

This leads to acute right heart failure and sudden death. 

Obstruction of medium sized artery

Dual blood supply protects lung from effects of pulmonary arterial embolism.

No infarctions are seen.

There will be local haemorhage but no damage to pulmonary frame work.

Patient may be asymptomatic or breathlessness  or haemoptysis may present

Emboli in small peripheral arteries

Smaller emboli in periphery can lead to infarctions of the lung as there are no collateral supplies to pulmonary arteries in end arteries.

Area affected is often small but may produce symptoms if multiple

Patient has dyspnoea if these are multiple.

If the bronchial blood supply is impaired

Emboli lodging in medium sized arteries can lead to infarctions.

Since the blockage is proximal the infarcted area is large extending as a cone with the base towards the surface and apex at the blocked artery.

Infarcted area is red due to haemorhage  and congestion.

Infarcts are common in lower lobes and are often multiple.

Microscopy

Bloked blood vessel.

Infarcted area shows haemorhage  with loss of nuclear staining.

But still the alveoli can be identified.

The main pulmonary trunk and pulmonary arteries to right and left lungs are seen here opened to reveal a large "saddle" pulmonary thromboembolus. Such an embolus will kill your patient.

Here is another large pulmonary thromboembolus seen in cross section of this lung. The typical source for such thromboemboli is from large veins in the legs and pelvis

This pulmonary thromboembolus is occluding the main pulmonary artery. Persons who are immobilized for weeks are at greatest risk. The patient can experience sudden onset of shortness of breath. Death may occur within minutes.

This pulmonary embolus is adherent to the pulmonary arterial wall. If the patient survives, the thromboembolus will organize and, for the most part, be removed.

A pulmonary infarct is hemorrhagic because of the dual blood supply from the non-occluded bronchial arteries which continue to supply blood, but do not prevent the infarction.

Systemic embolism

Systemic emboli travel in the internal circulation, commonly originating in the left side of the heart.

Arterial emboli, unless very small, nearly always cause infarction. Emboli to the lower limb may produce gangrene of a few toes or of the entire limb.

Sources of emboli

Heart

1. Ischemic heart disease-mural thrombi, aneurisms,, hypokinetic segments
2. Arrhythmias
3. Valvular- Rheumatic hreart
4. Myocardial - Myocarditis
5. Intra cardiac lesions-
6. Myxomas

Arterial System

• Ulcerated atheromatous plaque
• Aortic aneurisma
• Venous shunts in dialysis patients

Sites of lodgement

• Coronary arteries
• Cerebral Arteries
• Renal Arteries
• Splenic Arteries
• Retinal arteries
• Mesentric Arteries
• Limb arteries
• Embolous at the bifurcation of the aorta

Cerebral emboli cause death or infarction unless the embolus lodges in an area that receives adequate collateral supply through the circle of Willis.

A special type of systemic embolus comprises the infected material from vegetations on the heart valves in infective endocarditis. These produce septic infarcts and large abscesses in the affected tissues.

Paradoxical embolus: Venous thrombi that pass through a right–to-left congenital cardiac anomaly

 

Bone marrow emboli

Common in patients who suffered major trauma eg. RTA

Attempted cardiac resuscitation  with rib fractures can lead to this.

Any thing that fractures bones can release bone marrow into venous circulation, resulting in pulmonary emboli.

Clinical significance unclear

Embolism of fragments of atheromatous plaques

Ulcerated atheromatous plaques can cause thrombosis on surface of it or cause embolism of fragments

Cholesterol clefts are seen in the embolus

Fat embolism

Fat from marrow cavities of long bones or from soft tissues can also enter the circulation as a result of severe trauma.

‘Fat embolism syndrome’ characterized by respiratory problems, haemorhagic skin rash, and mental deterioration  24-72 hours after the injury.

The syndrome results from mechanical blockage of vessels, chemical injury to vessels of lung producing pulmonary oedema and activation of coagulative pathway to cause DIC.

Causes of fat embolism

·         Severe trauma with fractures of long bones

·         Damage to fatty tissues

·         Diabetes mellitus

·         Pancreatitis

·         Hyperlipidaemia

Laboratory investigations

·         Urine deposit: fat globules

·         Sputum: fat globules

·         Blood picture :DIC and thrombocytopenia

Air embolism

Large quantities of air within the circulation can act as emboli by forming a frothy mass that can block vessels or become trapped in the right heart chambers to impede pumping.

Over 100 ml of air is needed to produce problems. Lesser amounts dissolve in plasma.

Air can either enter the circulation from

Atmosphere: cut injuries of neck and thorax allowing air to be sucked in.

Air forced into the uterine vessels during badly performed abortions and deliveries,

Produced within circulation: decompression sickness in deep sea divers

Acute decompression sickness

N2 or He will dissolve in blood and tissues at high pressures.

As the diver surfaces, the pressure is reduced and gas begins to come out as minute bubbles.

If rapid this causes air embolism (lodge in brain and skeletal muscle).

Platelets adhere to nitrogen bubbles causing DIC.

Pain around joints, skeletal muscle, respiratory distress coma and death.

Treatment of decompression sickness

·         Early stages, by putting the victim in a decompression chamber pressure will dissolve the bubbles where the high pressure will redissolve the bubbles and allow a slow, controlled decompression.

·         The chronic form, Caisson disease, produces multiple areas of ischaemic necrosis in the long bones

Amniotic fluid embolism

Uncommon but life threatening forms of embolisation.

Amniotic  fluid is forced into the circulation as as a result of traring of the placental membranes and rupture of uterine wall or cervical veins.

Emboli are a mixture of fat, hair, mucous, meconeum and squamous cells from the fetus

Commonly lodge in the alveolar capillaries

Clinically, respiratory failure, cerebral convulsions and coma. Often excessive bleeding due to DIC

Tumour emboli

This is an important mechanism of tumour spread.

Unlikely to have immediate CVS effects