The Normal Cell - EmergencyPedia
1 PATHOLOGY
The Normal Cell
1. What is the function of the smooth endoplasmic reticulum
a. protein synthesis
b. steroid synthesis – this one
c. mitosis
2. Pinocytosis
a. is a way of transporting large molecules – no small molecules.
b. adds to cellular membrane
3. Mitochondria repeat – read bloody alberts, we still haven’t
4. Regarding SER
a. For protein synthesis
b. Contains electron chain thingy enzymes
c. For lipid synthesis – yes
d. Extracellular pathway through cell – er….
5. Ribosomes
a. have 3 subunits – no, 2 subunits
b. have 30% DNA – no, RNA -65%- and proteins -35%-
c. synthesise haemoglobin – synthesise globin. Not heme group though…
6. Which cell type is found predominantly in the periarteriolar sheaths in the white pulp of the spleen & (somewhere in lymph nodes)
a. B lymphocyte found in the white pulp of the spleen
b. Neutrophil
c. Mast cell
d. T lymphocyte – periarteriolar sheath of the spleen
e. Macrophages
7. Smooth endoplasmic reticulum
a. is the site a cell steroid production – this one
b. is the site of cell protein synthesis
is the site of cellular cytochrome oxidases
8. Pinocytosis
a. adds to the cell membrane
b. involves the uptake of soluble macromolecules – yes only large molecules
9. Which cell organelle has no basement membrane
a. mitochondrium
b. RER
c. lysosome
d. centriole
e. –Lysozyme _ yes, as this is the enzyme
10. Regarding Mitochondria
a. are self replicative - yes
b. are present in RBC – no, produce enery by fermentation
c. responsible for protein synthesis - no
d. have no membrane – have two membranes
11. Regarding centrioles
a. are responsible for spindle formation in mitosis - indeed
12. Which substance is not subject to passive diffusion
a. PO4 - this one?
b. Na
c. K+
d. H20
e. Cl
13. Regarding ribosomes
a. There are 3 subunits - no, 2
b. they are 65% DNA - 65% RNA
c. They synthesize haemoglobin - globin
d. They contain 30% DNA - 35% protein
14. What is the function of the smooth endoplasmic reticulum; which is incorrect
a. steroid synthesis - yes, and lipid synthesis
b. drug detoxification / cytochrome P450 - yes
c. protein synthesis - INCORRECT
d. role in carbohydrate metabolism - yes
2 Cell Injury & Adaptation
1. Regarding dystrophic calcification; which is correct (deposition of crystalline calcium in damaged tissues – causes major pathology)
a. causes organ dysfunction – yes,
b. multiple myeloma is a cause – no, this is metatstatic calcification
c. associated with hypercalcaemia – no this is metastatic calcification
2. Regarding atrophy; all are correct except?????
a. persistance of residual bodies - true
b. decreased myofilaments - correct
c. decreased rough endoplasmic reticulum - correct
d. decreased autophagic vacuoles - WRONG, increased numbers
e. decreased smooth endoplasmic reticulum - correct
3. Which of the following is an example of hypertrophy
a. increase in liver size after partial hepatectomy – hyperplasia
b. increased size of female breast –hypertrophy in lactation, hyperplasia in puberty and pregnancy
c. increased respiratory epithelium in response to vitamin A deficiency – squamous metaplasia
d. increase in size of female uterus during pregnancy – partially hypertrophy, partially hyperplasia PROBABLY THIS ONE
e. ?? endometrial – just hyperplasia
4. Hyperplasia
a. Increased mitotic bodies
b. Due to increased function demands - true
c. Distractor
5. Regarding atrophy, all are correct except
a. Persistance of residual bodies
b. Decrease myofilaments
c. Decrease rough endoplasmic reticulum
d. Decreased autophagic vacuoles – increased vacuoles
e. Decreased smooth endoplasmic reticulum
6. Which of the following is an example of hypertrophy
a. Increase in liver size after partial hepatectomy
b. Increase size of female breast
c. Increase respiratory epithelium in response to Vitamin A deficiency – metaplasia (squamous)
d. Increase in size of female uterus in pregnancy – yes
e. ??endometrial
7. Repeat Q regarding wound healing and time frames…‘What occurs at the same time?’
a. Neutrophils and basal epithelial mitoses – both neutrophils and epithelial cells are there in days 1-2,
b. Tensile strength and granulation tissue – false – tensile strength is from collagen, laid down by fibroblasts, later.
c. Neutrophils and granulation tissue – no, neutrophils are replaced by macrophages on day 3, when gran. tiss begins to appear
8. Which is an example of hypertrophy?
a. the pregnant uterus - yes
b. tissue with a high capillary to myocyte ratio – decreased in cardiac hypertrophy
c. the breast at puberty - hyperplasia
d. the liver post hepatectomy - hyperplasia
9. Which of the following is not associated with atrophy
a. decreased smooth endoplasmic reticulum
b. decreased rough endoplasmic reticulum
c. decreased autophagic vacuoles - yes
10. Examples of hyperplasia include
a. glandular epithelium of pubertal breasts – yes, after puberty the cells don’t increase in number, just in size.
11. Hypertrophy
a. occurs after partial hepatectomy - hyperplasia
b. increases function of an organ exponentionally – probably not
c. is triggered by mechanical and trophic chemicals - true
d. occurs after denervation - false
e. is usually pathological - false
12. All the following are features of apoptosis EXCEPT
a. cell swelling - this one, cell just shrinks nicely, without causing damage to surrounding cells
b. chromatin condensation - is
c. formation of cytoplasmic blebs - is
d. lack of inflammation - is
e. phagocytosis of apoptotic bodies - is
13. Dystrophic calcification
a. is formed only in coagulative necrosis - false
b. does not occur on heart valves - false
c. rarely causes dysfunction – false, eg heart valves
d. is rarely found on mitochondria – false, forms first in mitochondria
e. is formed by crystalline calcium phosphate mineral - true
14. Irreversible cell injury is characterised by
a. dispertion of ribosomes – no, this is in reversible injury
b. cell swelling - reversible
c. nuclear chromatin dumping- clumping, reversible
d. lysosomal rupture - TRUE
e. cell membrane defects - ALSO TRUE
15. Metaplasia
a. can be caused by vitamin B12 deficiency – vit A def in lungs
b. preserves mucus secretion in the respiratory tract - ??
c. is typically an irreversible process - reversible
d. is the process that occurs in Barrett’s oesophagitis - true
e. is an increase in the number and size of cells in a tissue - change from one cell type to another
16. Dysplasia
a. is a feature of mesenchymal cells – don’t think so
b. inevitably progresses to cancer – can, not always
c. is characterised by cellular pleomorphism – yes and also loss of uniformity, architertural orientation loss and anarchy, usually in epithelia – yes. Hyperchromasia, Mitotic Figures
d. is the same as carcinoma in situ – no - - this is when is marked and full thickness then it is CIS
e. is not associated with architectural abnormalities – no
17. Metastasis
a. unequivocally prove malignancy - yes
b. is the most common presentation of melanoma – change in a mole?
c. is proven by lymph node enlargement adjacent to a tumor – not by TNM staging
d. of breast is usually to supraclavicular nodes – axillary node
e. all of the above
18. Metastatic calcification occurs in (repeat) – stomach, kidney, lungs, arteries. In conditions causing hypercalcemia
3 Tissue Renewal & Repair
1. With regard to wound healing
a. neutrophils proliferate at the wound margins at the same time as epithelial proliferation occurs –no, neutrophils arrive first.
2. With regard to wound healing
a. Neutrophils proliferate at the wound margins at the same time as epithelial proliferation occurs
3. Platelets
a. contain alpha and beta granules – no, alpha and delta granules – fibrinogen, fibronecton, factors 5 and 8, plt factor 4, PDGF, TGF-beta in alpha granules. Delta granules – dense – contain ADP, ATP, histamine, calcium, serotonin and adrenaline
b. are biconcave discs – true
c. contain a nucleus - false
d. are found in the plasma at levels of 200-500 per microliter – no, 150-400 million per microlitre
e. are the main source of thrombin – no – liver.
4. Macrophages may secrete
a. histamine
b. seretonin
c. prostaglandins
d. oxygen free radicals - yes
5. Which of the following cells cannot phagocytose
a. Neutrophils - can
b. Eosinophils – can
c. macrophages - can
d. T-cells – not phagocytic
6. The most common peripheral circulating lymphocyte is
a. B-cell
b. T-cell – nearly 70% of lymphocytes in periph smear are T cells… T helper >cytotoxic
7. Mast cell
a. may discharge independent of IgE - yes - direct injury (e.g physical or chemical), cross-linking of IgE receptors, or by activated complement proteins
b. release lysosymes – degranulate.
8. Metastatic calcification occurs in
a. old lymph nodes - no
b. gastric mucosa - yes
c. atherosclerotic vessels – no, that’s dystrophic,
d. damaged heart valves – no, dystrophic
9. Concerning the repair of a well opposed, clean surgical incision
a. dermal appendages destroyed by the incision usually recover - unlikely
b. new collagen begins to accumulate after the first week – no, on day 5
c. granulation tissue does not occur – false – begins to appear by day 3
d. there is an initial inflammatory response -TRUE
e. 15% of original tissue strength is attained after 1 week – no, 10% at week 1
10. With respect to wound healing
a. neutrophils proliferate at the wound margins at the same time as epitheleal proliferation occurs
11. Which occurs first in fracture healing
a. neutrophil invasion – yes (to organise the haematoma)
b. procallus formation, - no, second (within organised haematoma)
c. woven bone ossification – woven bone laid down to form fracture callus
d. lamellar bone ossification – all changed to lamellar bone to restore strength
e. collagen deposition –procallus is changed to fibrocartilaginous callus
12. Subchondral necrosis
a. is rarely idiopathic – no, most cases of bone necrosis are idiopathic or after corticosteroid administration
b. associated with diving injuries – true – nitrogen bubbles – bone ischaemia
c. rarely involves ischaemia – false – all forms of bone necrosis result from ischaemia
13. In bone fracture healing
a. woven bone forms in the periosteum of the medullary cavity – no.
b. osteoblasts lay down woven bone over the procallous to repair the fracture line - yes
c. PTH acts directly on osteoclasts to increase absorption – false – indirect, through RANKL release by osteoblasts
d. Haematoma at the fracture site plays little role in the development of procallous - false
e. Inadequate immobilisation aids the formation of normal callous- false
14. In healing by primary intention
a. there is a large tissue defect – no.
b. the tissue defect cannot be reconstituted - no
c. it involves excessive granulation tissue - no
d. an epitheleal spur forms on the first day
4 Acute & Chronic Inflammation
1. Which occurs first in acute inflammation
a. arteriolar dilation – 2nd
b. arteriolar constriction – this occurs, for a few seconds
c. oedema – 3rd, after extravasation of fluid and protein
d. leucocyte margination – 5th. Leucocytes adhere to the vascular endothelium then leak out into the interstitium
e. stasis of blood flow – 4th after the fluid has left the vasculature
2. Regarding chronic inflammation
a. is characterised by hyperaemia, oedema and leucocyte infiltration – this is acute inflammation
b. monocytes use the same chemotactic pathway as neutrophils - yes
c. is always preceded by acute inflammation - no
d. most frequently results in resolution - no
3. The first thing to occur in acute inflammation is
a. vasodilation
b. increased permability
c. diapedesis
d. vasoconstriction – this one
e. stasis
4. Regarding chronic inflammation ???
a. monocytes have a half life of 5 days - ?in blood about 1 day, in tissue – months to years
b. frequently follows acute – ‘may follow acute, but frequently occurs insidiously’ (Kotram)
c. frequently resolves – don’t think so
d. characterised by increased vascular permeability and oedema – this is acute
5. Factor C5a ???
a. is chemotactic for neutrophils –yes. Also anaphylotoxin – causes mast cell degranulation
b. stimulates arachidonic acid metabolism – yes. Stimulates lipoxygenase in neutrophils and monocytes
c. same factors that are chemotactic for neutrophils as for macrophages - yes
6. Mast cells
a. are derived from thymus – from bone marrow, made from same precursors as basophils
b. can degranulate without IgE – yes by anaphylotoxins (c3a, c5a), tissue injury, heat, cold, IL1, IL6
c. are only found in mucosal membranes – no found in most tissues near blood supply
7. Regarding chronic inflammation ???
a. monocytes have a half live of 5 days – 1 day in blood, months/years in tissue
b. frequently follows acute - no
c. frequently resolves - no
d. characterised by increased vascular permeability and oedema – no this is acute
8. Factor C5a
a. is chemotactic for neutrophils - yes
b. stimulates arachodonic acid metabolism - yes
c. same factors that are chemotactic for neutrophils as for macrophages - yes
9. Bradykinin
a. formed from pre kallikrein – no kallikrein is the enzyme that breaks it from its precursor molecule
b. causes vasodilation – yes. Released by venules, cause vasodilation and inc. permeability. Receptors GProtein coupled. Mediate chronic pain (B1) and vasodil (B2)
10. What is released by macrophages
a. O2 radicles - yes
11. Mast cells
a. Predominantly in circulation – no in tissue
b. Originate in thymus – no – from bone marrow, mature in tissue
c. Can degranulate without IgE stimulation – this one
12. Which is not chemotactic
a. Histamine – has to be this.
b. C5a – no, this is chemotactic
c. Leukotriene B4 – also chemotactic (product of lipooxygenase pathway
d. Bacterial polypeptides – these are the most common exogenous chemotactic agents
e. Cytokines – all chemotactic
13. phagocytosis
a. occurs in 2 steps – three steps – 1. recognitioin and attachment, 2. engulfing, 3. killing
b. C5a is an opsonin – no – C3b, IgG, certain plasma lectins, esp mannose binding lectin
c. IgM is a potent opsonin - no
d. Bacterial killing occurs by mainly O2 dependant mechanisms - true.
e. Doesn’t occur without opsonisation – false,
14. Regarding Chronic inflammation
a. Freq follows acute inflammation – can do, can occur alone
b. Characterised by oedema, stasis, etc - acute
c. Frequently resolves - no
d. Chemotactic factors for monocytes same as for neutrophils - true
15. Regarding fatty change - which is incorrect
a. May result from protein malnutrition - true
b. Fatty acids are oxidised in the mitochondria - true
c. May result from diabetes mellitus - true
d. May represent unmasking of normal cell fat content - false
Which of the following is an example of an oxygen dependent process?
e. Halogenation – this one – peroxide – myeloperoxidase – halide system = most efficient PMN killing mech
f. MBP
16. What is the correct order of events in acute inflammation
a. v/c, v/d, margination, …… - yes
17. Question regarding Complement pathway….need to know about C3a and C5a effects, and also what initiates the classic and alternative pathways – C3a, 5a – anaphylatoxins – chemoattractant – pro-inflammatory, C3b opsonises – macrophage phagocytosis of microbe, C5b – forms MAC – cell lysis
18. In acute inflammation which event occurs first
a. arteriolar dilatation – 2nd
b. arteriolar constriction – this one.
c. oedema
d. leucocyte migration – 3rd
e. blood flow stasis
19. The first vascular response to injury is
a. slowing of the circulation – stasis – prior to leucocyte margination
b. venular dilation
c. recruitment of vascular beds
d. capillary engorgement
e. arteriolar vasoconstriction – this one
20. Leucocytes move into the tissues from the vasculature (extravasation )
a. by the action of actin and myosin -???
b. predominantly as monocytes on the first day post injury – no – PMNs.
c. in response to C3b - no
d. in response to the Fc fragment of IgG - no
e. largely in the arterioles - venules
21. Regarding chemical mediators of inflammation
a. histamine is derived from plasma – no mast cell granules,
b. C3b is within macrophages – part of complement system
c. The kinin system is activated in platelets – no, plasma based / endothelium
d. Nitric oxide is preformed in leukocytes
e. seretonin is preformed in mast cells – true, along with histamine, also from platelets and basophils
22. Chronic inflammation is
a. always preceded by acute inflammation - no
b. characterised by hyperemia, oedema and leukocyte infiltration - no
c. most frequently results in resolution - no
d. the factors underlying monocyte infiltration are the same as for acute inflammation – this one
23. In the triple response the reactive hyperemia is due to 1. red reaction due to capillary dilation, a direct response to pressure. 2. wheal, local oedema due to increased permeability 3. flare, due to arteriolar dilation
a. blushing
b. excersise
c. arteriolar dilation – this one
d. inflammatory mediators
e. still present after sympathectomy
24. Vascular hyperemia
a. is caused by inflammatory mediators
b. results in cyanosis
c. results in oedema – this one
d. results in brown induration
25. Macrophages are derived from
a. monocytes – this one – monocytes stimuated to become macrophages by chemokines in circulation
b. T-cells
c. B-cells
d. Eosinophils
e. Plasma cells
26. With respect to the changes in acute inflammation, which occurs first
a. Arteriolar dilatation
b. Arteriolar constriction – this one
c. Edema
d. Leucocyte margination
e. Stasis of blood flow
27. Regarding chronic inflammation
a. Is characterised by hyperaemia, edema, and leucocyte infiltration – acute
b. Monocytes use the same chemotactic pathway as neutrophils – this one
c. Is always preceded by acute inflammation – no
d. Most frequently results in resolution
28. The first thing to occur in acute inflammation is
a. Vasodilation
b. Increase permeability
c. Diapedesis
d. Vasoconstriction – this
e. Stasis
29. What is released by macrophages
a. oxygen free radicals – this
b. eicosanoids
5 Fluid & Haemodynamics
1. Non inflammatory oedema – ‘transudate’
a. has a high protein content – protein poor
b. is caused by low levels of aldosterone – increased aldosterone as per CCF (renin-ang system activated by low renal perfusion)
c. has a SG > 1.012 – 0.012 – 80% – according to small robbins. 20-40% in big robbins
e. 20% get DIC – 50% get it
10. Factor VIII (lordy!)
a. Bound to large vWF – yes, large = multimers
b. Joins with inactive factor V to activate thrombin – this is Factor X
c. Useful in haemophilia B – no. factor VIII and Factor IX (defic of which=hemophilia B) join forces to activate Factor X
d. 50% of normal activity gives mild disease – yes
e. monitored by PT – no, PTT
11. Regarding clotting cascade
a. Tissue thromboplastins activation intrinsic cascade – extrinsic
b. Thrombin can activate prothrombin – no
c. Clot retraction is independent of platelets – must be dependent on platelets
d. Increased plasminogen activator extends thrombus – activates plasminogen – ie dissolves clot
e. Thrombomodulin can bind and activate thrombin – ‘modifies thrombin’ - cofactor in activation of Protein C
12. Passive hyperaemia caused by(what the fuck?)
a. Exercising muscle
b. Inflammatory mediator release
c. Arteriolar dilatation
d. Blushing
e. Portal hypertension – this one – venous obstruction
13. Post mortem features of clot include
a. Lines of Zahn
b. The absence of RBC's in supernatant – this one
c. Adherence to vascular walls
14. What best defines the pathophysiology underlying shock and the resultant
a. Widespread tissue hypoxia as a result of decreased blood volume/effective blood volume
b. Lactic acid production
c. Low cardiac output
d. Decrease blood volume
e. Cellular hypoxia resulting from impaired tissue perfusion – this one
15. White infarcts
a. May be transiently red – can only be this one
b. Occur in the untestine – no, heart, kidney, spleen
c. Result from venous occlusion – arterial occlusion
d. Are always septic – no
e. Occur predominantly in the liver – no
16. Central pathophysiological feature of shock
a. hypotension
b. decreased blood volume
c. cellular hypoxia at a tissue level – this one
d. infection
e. cardiac failure
17. Septic shock may cause all of the following EXCEPT
a. myocardial depression – decreased contractility
b. vasoconstriction – vasodil
c. DIC – yes
d. ARF – yes
e. ARDS – yes
18. Shock results in
a. decreased capillary hydrostatic pressure – no idea
19. The process of blood coagulation involves
a. prothrombin activator converting fibrinogen to fibrin – thrombin converts it
b. alpha 2 macroglobulin – inhibits thrombin, therefore no
c. the action of antithrombin 3 to promote clotting – erm…ANTIthrombin
d. the action of plasmin on fibrin – no
e. the removal of peptides from each fibrinogen molecule – must be
20. DIC is associated with
a. thrombocytosis – thrombocytopenia
b. a bleeding diathesis presentation in a patient with malignancy – yes
21. With respect to the clotting cascade – complement?
a. the alternative pathway is stimulated by Ag-Ab interaction – microbe / polysaccharides
b. C3bBb inhibits the final common pathway – alternative pathway activator
c. As
d. As
e. C5a initiates arachadonic acid metabolite release from neutrophils – anaphylotoxic, yes
22. With regard to embolism
a. arterial emboli most often lodge in the viscera
b. pulmonary emboli are rarely multiple – no
c. amniotic fluid emboli are associated with the highest mortality – think so – 20-40%
d. all emboli consist of either gas or solid intravascular mass – no, amniotic fluid?
e. most pulmonary emboli produce signs of respiratory distress – no
23. Regarding the veins of the lower limb
a. thrombosis in the superficial veins is a common source of emboli – no, DEEP VT
b. phlegmasia alba dolens is associated with iliofemoral vein thrombosis - yes
c. dermatitis is a common consequence of Buergers disease – don’t think so
d. varicosity development has no genetic component
e. 20% of venous thrombi commence in superficial veins
24. Post mortem features of clot include
a. adherence to vascular walls
b. absence of red cells in supernatant – this one
c. lines of Zahn
25. Air embolism – focal ischaemia in brain and other tissues
a. is fatal as air is non-compressible so does not leave the heart
b. 200 ml is the lethal dose - 100ml for clinical symptoms
26. Amniotic fluid embolism
a. is associated with a greater than 80 % mortality – yes according to little robbins
27. Fat embolism syndrome is assocoated with
a. mortality of greater than 20 % - fewer than 10% have any clinical findings
b. petechial rash, non-thrombocytopenic – yes – in 20-50% of patients
28. Non-inflammatory oedema
a. has a high protein content – this is INFLAMMATORY (due to increased vasc perm)
b. has a SG of greater than 1.012 – again – inflammatory >1.012, non-inflamm thrombin
32. Which are features of a clot at post mortem?
a. lines of Zahn –no this is where blood clots while flowing…
b. adherence to vascular walls - no
c. Supernatant resembling chicken fat - yes
d. absence of red cells in the supernatant – yes.
33. Which is a feature of non-inflammatory causes of oedema (there’s are table)
a. Aldosterone level low - high
b. Right atrial pressure high – yes – CCF is most common cause
c. protein is high - low
d. SG < whatever that ridiculous number is - ................
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