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1

The following are true about RET protooncogene except

D;

Point mutation in RET extracellular domain in MEN 2A


Point mutation in RET cytoplasmic domain in MEN 2B
Somatic rearrangement of RET in Sporadic medullary carcinoma
RET protein is a receptor for Human epidermal growth factor

Regarding Adiponectin, which is false:

D; Increased in metabolic syndrome Expl: Adiponectin is an anti


inflammatory cytokine produced exclusively by adipocytes. It enhances
insulin sensitivity and inhibits many inflammatory processes. In liver it
inhibits gluconeogenesis. It increases glucose transport into muscles and
also enhances fatty acid oxidation by activation of AMP kinase. It is
reduced in metabolic syndrome.

It is an anti inflammatory cytokine produced exclusively by adipocytes


Inhibits gluconeogenesis
Enhances fatty acid oxidation
Increased in metabolic syndrome

The following are true about Epigenetics except:

D; All of the above

It includes changes in gene expression by mechanisms other tha changes in the


underlying DNA sequence
May remain through cell divisions for the remainder if the cells life
May also last for multiple generations
All of the above

The following are true about Nanobodies except:

C; Susceptible to heat and Ph They are more resistant to heat and pH


Ref: en.wikipedia.org/wiki/nanobodies

They are single domain antibodies composed solely of a pair of heavy chains
They are fully functional antibodies
Susceptible to heat and pH
Can be used as oral nanobody pills for treatment of IBD and Ca colon

The bone morphogenetic protein expressed in the hippocampus is:

BMP3

D; BMP8b
BMP1  involved in cartilage development
BMP2  induces bone and cartilage formation; key role in osteoblast
differentiation
BMP3  induces bone formation
BMP4  formation of teeth, limbs and bone from mesoderm; also plays
role in fracture repair
BMP5  cartilage development
BMP6  joint integrity in adults
BMP7  osteoblast differentiation; renal development and repair
BMP8a  bone and cartilage development
BMP8b  expressed in the hippocampus
BMP10  trabeculation of embryonic heart
BMP15  oocyte and follicular development

BMP4
BMP8a
BMP8b

All of the following are stimulators of angiogenesis except

D; IFN

VEGF
FGF
TGF

IFN
The following are features of healing by primary intention except:

C; Healing process slow

Wound edges directly next to one another


Minimal scarring

Healing process slow


Most surgical wounds are examples

The following are true about Dariers disease except:

D; All of the above

Autosomal dominant mutations in ATPA2 gene


Also known as Keratosis follicularis
Increased susceptibility to cutaneous bacterial and viral infections
All of the above

Accumulation of lipofuscin granules in cells is typically seen in which of the


following conditions?

A; Atrophy
Atrophy is often associated with increased destruction of subcellular
components by autophagy. The cellular components are digested by the
lysosomal enzymes. Some of the cell debris resist digestion and persist as
insoluble material in the lysosomes. Lipofuscin granules represent
undigested material that results from lipid peroxidation.

Atrophy
Hypertrophy
Hyperplasia
Apoptosis

10

After a thrombus is formed in an area of vascular injury, the propagation of the


thrombus to normal arteries is prevented in part by the action of

D; Thrombomodulin
Thrombomodulin is present on intact endothelium and binds thrombin,
which inhibits coagulation by activating protein (Robbins)

Tumor necrosis factor


Platelet factor 4
Calcium
Thrombomodulin

11

Which of the following is true about Early secretory phase of endometrium

A; For subnuclear vacuolation to be regarded as evidence of ovulation, it


should be present in atleast 50% of the glands
bMid secretory and midproliferative phase
cLate secretory phase
dEarly proliferative phase
Explanation:

PHASE

DAY
S

SURFACE
EPITHELIU
M
Thin
regenerating

GLANDS

STROMA

Early
Proliferativ
e phase

4th
to
7th
day

Straight short
narrow

Compact
with some
mitotic
activity
and large
nuclei

Mid
Proliferativ
e phase

8th
to
10th
day

Columnar

Longer curved

11th
to
14th
day

Undulant
surface

Tortuous glands
with active growth
&
pseudostratificatio
n

Variable
stromal
edema
Numerous
mitosis in
naked
nuclei of
stroma
Moderatel
y dense
actively
growing
stroma

Late
Proliferativ
e phase

Upto 36 hours after ovulation, there are no changes.

EARLY SECRETORY PHASE


DAY
POD 2

FEATURES
Subnuclear vacuolation in >50 % glands with
nuclear pseudostratification

POD 3

Subnuclear vacuoles and nuclei uniformly


aligned; Scattered mitotic figures

POD 4

Vacuoles luminal position; Mitotic figures rare

POD 5

Vacuoles infrequent; Secretion in lumen of


gland

[POD = Post Ovulatory Day]

MID SECRETORY PHASE


DAY
POD 6

FEATURES
Peak of acidophilic intraluminal secretion

POD 7

Beginning of stromal edema

POD 8

Maximal stromal edema

LATE SECRETORY PHASE


DAY
POD 9

FEATURES
Prominent spiral arteries (due to
predecidualisation of periarterial stromal cells)

POD 10 Thick periarterial cuffs of predecidual cells


POD 11 Islands of predecidual cells in superficial
compactum
POD 12 Beginning coalescence of predecidual islands

For subnuclear vacuolation to be regarded as evidence of ovulation, it should be


present in atleast 50% of the glands
Presence of stromal edema
Presence of stromal predecidualisation
Short straight narrow glands

12

True about Gamna Favre body

Small intracytoplasmic inclusion bodies found in LGV


Deposits of calcium in cerebral capillaries
Minute bodies found in the blood in psittacosis
Hyaline or colloid masses scattered throughout the pars nervosa of pituitary gland

A; Small intracytoplasmic inclusion bodies found in LGV


bHarting body
cCoccoid X bodies
dHerring bodies

13

The most common and most important mechanism in the pathogenesis of


endometriosis is:

D; Metaplastic change of secondary mullerian system


Metaplastic change of secondary mullerian system represented by pelvic
mesothelium is the most common and most important mechanism
Ref: Ackerman Pathology Pg 1577

Origin from congenital mullerian or wolfian rests


Endometrial implantation
Lymphatic / hematogenous spread
Metaplastic change of secondary mullerian system

14

All of the following are true about Malignant mixed mullerian tumours except:

D; Most commonly seen in premenopausal women


Also called Carcinosarcomas, most commonly presents with
postmenopausal bleeding
Ref: Robbins Pg 1088

Endometrial adenocarcinomas with malignant stromal differentiation


Stromal cells stain positive for epithelial cell markers
Usually metastasize as adenocarcinoma
Most commonly seen in premenopausal women

15

The following are true about leiomyoma except

D; They are considered as smooth muscle tumors of uncertain malignant


potential
dleiomyosarcoma
Ref: Robbins 1089-1090

It represents a clonal neoplasm


The normal myometrium of leiomyoma containing uterus expresses higher levels of
estrogen receptors
Dysregulations of the high mobility proteins HMGIC and HMGIY contribute to the
development of these tumors
They are considered as smooth muscle tumors of uncertain malignant potential

16

The latest theory of origin of Brenner tumour is:

A; Origin from surface epithelium of ovary or cysts derived from them


through metaplasia
Ref: Robbins1098, Ackerman1671

Origin from surface epithelium of ovary or cysts derived from them through
metaplasia
Origin from Walthard cell rests
Implantation of transitional epithelium
None of the above

17

Which of the following is false about dysgerminoma:

D; None of the above


A, b, c are true
Ref: Robbins1101

Ovarian counterpart of seminoma of testis


Most of these tumours have no endocrine function
All dysgerminomas are malignant
None of the above

18

Teeth are often present in a mature solid teratoma of ovary, the teeth tend to be
located in a well defined nipple like structure covered with hair known as:

A; Rokitanskys protuberance
Ref: Ackerman1687

Rokitanskys protuberance
Marchal body
Arantius protuberance
None of the above

19

A 50-year-old childless woman noticed a blood-tinged vaginal discharge twice in


the past month. Bimanual pelvic examination reveals a normal-sized uterus with
no palpable adnexal masses. There are no cervical erosions or masses. She has
hypertension and type I diabetes mellitus and is on treatment with insulin. An
endometrial biopsy is most likely to show:
Adenomyosis

C; Adenocarcinoma
Ref: Robbins

Leiomyosarcoma
Adenocarcinoma
Choriocarcinoma

20

False about sarcoma botyroides:

D; None of the above


Ref: Robbins1071-1072

It is a type of embryonal rhabdomyosarcoma


Cambium layer of Nicholson contains crowding of tumour cells beneath the non
neoplastic squamous epithelium
Seen in children younger than 5 years
None of the above

21

Which of the following is not seen in Alzheimers disease:

D; None of the above


A, b, c, d are true

Neurofibrillary tangles
Amyloid angiopathy
Granulo vacuolar degeneration
None of the above

22

Loss of normal external contour of the cerebral convolutions is known as:

B; Polymicrogyria
Ref: Robbins1354

Megalencephaly
Polymicrogyria
Microcephaly
Scaphocephaly

23

False about agenesis of corpus callosum:

D; Patients with this defect has maximum deficits with


neuropsychological testing
Ref: Robbins Pg 1355

Can be seen in clinically normal individuals


Bat-wing deformity of lateral ventricles on imaging studies
It is seen in Aicardi syndrome
Patients with this defect has maximum deficits with neuropsychological testing

24

Charcot-Bouchard microaneurysms:

A; Occurs in cases of chronic hypertension, ruptures leading to

intracerebral hemorrhage
Ref: Robbins Pg 1366
Occurs in cases of chronic hypertension, ruptures leading to intracerebral hemorrhage
Saccular aneurysms of intracranial vessels more than 300 m diameter
Pulmonary artery aneurysm adjacent to or within a tuberculous cavity
Bronchial artery aneurysm adjacent to or within a tuberculous cavity

25

True about Foix-Alajouanine disease are all except:

D; Associated with rapidly progressive neurological symptoms


Ref: Robbins Pg 1368

Venous angiomatous malformation of spinal cord and overlying meninges


Angiodysgenetic necrotising myelopathy
Associated with ischemic myelomalacia
Associated with rapidly progressive neurological symptoms

26

True about Bulbospinal atrophy are all except:

B; Autosomal dominant disorder


Expl: X-linked adult onset disease due to expansion of CAG repeat in the
androgen receptor gene
Ref: Robbins Pg 1397

Degeneration of lower motor neurons in the spinal cord and brainstem


Autosomal dominant disorder
Affected individuals manifest androgen insensitivity with gynecomastia, testicular
atrophy and oligospermia
Nuclear inclusions containing aggregated androgen receptor is seen
Also called as Kennedy syndrome

27

A brain tumour from a 14 year old male child on microscopic examination is


seen to be composed of bipolar cells with long thin GFAP positive hair like
processes. Rosenthal fibres and microcysts are also present. He is most probably
suffering from:
Pilocytic astrocytoma

A; Pilocytic astrocytoma
Ref: Robbins Pg 1403

Pleomorphic xanthoastrocytoma
Medulloblastoma
Oligodendroglioma

28

Stiff-man syndrome is seen as a paraneoplastic syndrome in some cases of breast


carcinoma. The antigen targeted here is:

C; Amphiphysin
aRetinal degeneration in Small cell lung cancer
bLambert Eaton myasthenic syndrome
dSubacute cerebellar degeneration
Ref: Robbins Pg 1411

Recoverin
Presynaptic calcium channel
Amphiphysin
Yo

29

True about Rasmussens syndrome are all except:

D; None of the above


A, b, c are true
Ref: Ackerman Pg 2484

It is a form of chronic encephalitis


Intractable unilateral focal seizures, progressive cerebral hemiatrophy with
hemiparesis
Characterised by antibodies to Glutamate R3 receptor
None of the above

30

False about Lhermitte-Duclos disease:

D; None of the above


A, b, c are true
Ref: Ackerman Pg 2550-2551

Dysplastic gangliocytoma of the cerebellum


MRI shows regionally thickened and abnormally T2 bright cerebellar folia without
associated contrast enhancement
Variable replacement of granule cell layer by a disorganised array of large neurons and
aberrant myelination of the overlying molecular layer
None of the above

31

A rod shaped structure within the cytoplasm with zipper like striations and
sometimes a bulbous end, which is positive for CD1a and S-100 seen in
Langerhans cells of the skin, is known as:
Birbeck Granules

A; Birbeck Granules

Babes-Ernst granules
Acidophil granules
Keratohyaline granules

32

A condition characterised by apocrine glands in the scalp, a type of heterotopia,


is known as:
Nevus sebaceous of Jadassohn

A; Nevus sebaceous of Jadassohn

Nevus araneus
Suttons nevus
None of the above

33

The sudden appearance of or increase in number and size of seborrheic


keratosis in association with internal malignancy is called as:
Jaccouds sign

C; Leser Trelat sign

Kernigs sign
Leser Trelat sign
Maisonneuve sign

34

Sucquet-Hoyer canals

A; Specialised arteriovenous anastomosis present in the acral skin


bSacral canal
cVomerorostral canal

Specialised arteriovenous anastomosis present in the acral skin


Continuation of vertebral canal through sacrum
Canal between the vomer and sphenoidal rostrum
None of the above

35

All of the following are warning clinical signs of melanoma except:

D; Loss of pain in a pre-existing mole


Ref: Robbins Pg 1235

Enlargement of a pre-existing mole


Development of a new pigmented lesion
Irregular borders
Loss of pain in a pre-existing mole

36

Which of the following type of skin adnexal tumours has apocrine type of
secretion:
Trichoepithelioma

B; Syringocystadenoma papilliferum
Ref: Robbins Pg 1240

Syringocystadenoma papilliferum
Syringoma
Trichofolliculoma

37

True about malignant melanoma are all except:

C; S-100 is a much more specific marker than HMB-45

It is positive for Vimentin, S-100, HMB-45 and Melan-A


HMB-45 is a much more specific marker than S-100
S-100 is a much more specific marker than HMB-45
HMB-45 is negative in desmoplastic type of malignant melanoma

38

An enlarging cutaneous horn that has been present for one year projects 0.5 cm
from the base on the left lateral cheek of the face of a 50 year old patient. This
lesion is excised, and microscopic examinationshows basal cell hyperplasia.
Some of the basal cells show nuclear atypicalities. This is associated with
marked hyper- keratosis and parakeratosis. Which of the following lesions best
accounts for these findings:

C; Actinic keratosis
Expl: Actinic keratosis occurs on sun-exposed areas and is considered a
precursor of squamous cell carcinoma. When the atypical basal cells
occupy the entire thickness of the epidermis, the lesion transforms into a
carcinoma in situ. The presence of a hyperkeratotic layer is characteristic.
Occasionally, so much keratin is produced that a cutaneous horn is
formed. Ref: Robbins

Verruca vulgaris
Keratoacanthoma
Actinic keratosis
Seborrheic keratosis

39

Which of the following is true:

D; All of the above

Thrombin time is the time taken for clotting to occur when thrombin is added to
plasma
Partial thromboplastin time is the time from factor XII to fibrin clot formation
Prothrombin time is the time from factor VII activation to fibrin clot formation
All of the above

40

Testicular tumour with a very poor prognosis

D; Lymphoma of testis

Embryonal cell carcinoma


Endodermal sinus tumour
Leydig cell tumour
Lymphoma of testis

41

Pharmacologic agents that inhibit 5-reductase and diminish


dihydrotestosterone (DHT) synthesis in the prostate have the greatest effect on
which of the following prostatic lesions?

D; Nodular hyperplasia
The presence of androgens is the major hormonal stimulus to glandular
and stromal proliferation that results in nodular prostatic hyperplasia.
Ref: Robbins

Acute prostatitis
Adenocarcinoma
Chronic prostatitis
Nodular hyperplasia

42

The following are true about Reed-Sternberg cells except:

D; Does not possess clonal chromosomal abberations


Ref: Robbins Pg 686-690

RS cells are neoplastic giant cells derived from the germinal centre or post germinal
centre B cells
They undergo a peculiar form of cell death in which the cells shrink and become
pyknotic, a process called as mummification
RS cells are aneuploid
Does not possess clonal chromosomal aberrations

43

False about Hodgkins lymphoma:

D; Diagnostic RS cells are usually plentiful in Lymphocyte predominant


Hodgkins lymphoma
Expl: Diagnostic RS cells are usually plentiful in Mixed cellularity type
Ref: Robbins Pg 686-690

Lacunar cells are seen in nodular sclerosis


Mononuclear RS cells are seen in Mixed cellularity and Lymphocyte rich types

44

The histologic diagnosis of Hodgkin lymphoma rests on the definitive identification of


RS cells or their variants in the appropriate background of reactive cells
Diagnostic RS cells are usually plentiful in Lymphocyte predominant Hodgkins
lymphoma
Leukemia cutis is most common in which subtype of AML:

B; M5
Ref: Robbins693

M4
M5
M6
M7

45

Megakaryocytes with single nuclear lobes or multiple separate nuclei (Pawn ball
megakaryocytes) are characteristic of:
Myelodysplastic syndrome

A; Myelodysoplastic syndrome
Ref: Robbins Pg 695

Myelofibrosis
AML M7
Polycythemia vera

46

Neutrophils withonly two nuclear lobes, the pseudo-Pelger-Huet cells are


frequently observed in:
Myelofibrosis

C; Myelodysplastic syndrome
Ref: Robbins Pg 695

AML M3
Myelodysplastic syndrome
Hodgkins lymphoma

47

Chronic myeloproliferative disorders include all except:

D; Myelodysplastic syndrome
Ref: Robbins696

CML
Polycythemia vera
Essential thrombocytosis
Myelodysplastic syndrome

48

Sea blue histiocytes which are scattered storage histiocytes with wrinkled green
blue cytoplasm are characteristically seen in:
Myelofibrosis

B; CML
Ref: Robbins698

CML
AML M5
Polycythemia vera

49

True about Reid index are all except:

C; It is decreased in Chronic bronchitis


Ref: Robbins722

It is the ratio of the thickness of the mucous gland layer to that of the wall between the
epithelium and cartilage
Normal value is around 0.4
It is decreased in Chronic bronchitis
All are true

50

Which of the following morphologic changes can be seen in advanced cases of


both obstructive and restrictive lung disease?
Marked medial thickening of pulmonary arterioles

A; Marked medial thickening of pulmonary arterioles


Ref: Robbins

Destruction of elastic tissue in the alveolar walls


Fibrosis of the alveolar walls
Hemorrhage in the alveolar lumen

51

True about Menkes disease are all except:

A; Mutations in ATP7B gene


Expl: X-linked recessive mutations in ATP7A gene causes Menkes disease;
Autosomal recessive mutations in ATP7B gene causes Wilsons disease

Mutations in ATP7B gene


Decreased blood Cu levels
IV administered Cu is normally handled by these patients
Excess Cu in intestinal mucosal cells

52

Regression of some types of lymphoproliferative disease after splenic


irradiation is called as:

Abscopal effect
Bystander effect
Both of the above
Trendelenberg effect

C; Both of the above


Expl: The Bystander Effect (or Abscopal Effect) is the phenomenon when
unirradiated cells exhibit irradiated effects from nearby radiation
treatment. Similarly, when cells are irradiated, and the medium is
transferred to unirradiated cells, these unirradiated cells undergoes
genomic instability & apoptosis. This is also attributed to the bystander
effect.

53

Yirchow's triad includes all except

D; (Intimal tear)
Three primary influences predispose to thrombus formation, the so-called
VIRCHOW'S TRIAD:
Endothelial injury (single most vital factor)
Stasis or turbulence of blood flow
Blood hypercoagulability

Vessel wall endothelial injury


Thrombus formation
Local blood stasis
Intimal tear

54

"Call-Exner bodies" are seen in

B; (Granulosa cell tumor)


GRANULOSA CELL TUMOR
Is a sex cord stromal tumor
Occurs at any age but most commonly in postmenopausal woman (2/3rd).
It is a virilizing tumor, produces estrogen, causing precocious puberty in
prepubertal girls and endometrial hyperplasia, cystic disease of breast and
endometrial carcinoma.
These are potentially malignant tumors.
The tumor cells are arranged in sheets punctuated by small follicle-like
structures filled with an acidophilic material, known as Call-Exner bodies.

Yolk sac tumor


Granulosa cell tumor
Hilus cell tumor
Brenner tumor

55

Non-caseating granulomas are seen in the following EXCEPT

D; (Metastatic lung carcinoma)


In tuberculosis, granuloma is characterized by central area of necrosis
(caseation), when classical & TNF-a plays key role.
However, non-caseating granulomas can also be seen in TB.
Non-caseating granuloma:

- Leprosy,
- Syphilis,
- Sarcoidosis,
- Berylliosis,
- Lymphogranuloma inguinale,
- Certain mycotic infections and
- Reactions of irritant lipids.
Tuberculosis
Byssinosis
Hodgkin's disease
Metastatic lung carcinoma

56

All the following cause RPGN except

D; (MPGN)
SYNDROME

ETIOLOGY

1. Acute

Streptococci

HISTOPATHOL
OGY
LM:

PATHOGEN
ESIS
Trapped

postinfectious/p
oststreptococcal
GN
2. IgA
nephropathy

Viral URI, GIT


infections, flu
like
syndrome

3. Minimal
change disease
(Nil disease,
lipoid nephrosis);
Pediatric
nephrotic
syndrome
4. Membranous
nephropathy
Streptococci

Allergy
NSAIDs

5. Focal and
segmental GN

Heroin abuse
HIV
Reflux
nephropathy
Obesity

6.
Membranoprolife
rative GN

Associated
with URI

a) Type I (Dense
deposit disease)

NHL
Carcinomas
Gold,penicilla
mine
Lupus

Mesangioprolife
rative Unknown
EM: Mesangia!
Deposits
LM: Normal IF:
No Ig
EM: Fused foot
processes/
Pseudopodes
LM: Normal IF:
No Ig
EM: Fused foot
processes/
Pseudopodes

LM: Thickened
GBM and spikes
IF: Granular IgG
& C3along the
capillary loops.
EM: Dense
subepithelial
deposits
Immune
complex
formation
LM: Focal
segmental
sclerosis
IF: IgM and C3 in
sclerotic
segment
EM: Fusion of
foot process
CgNCFlgG

LM: Mesangial
cells & matrix
IgG & IgM
EM:Dense
deposits in
subendothelium

b) Type II

7.
RPGN/crescentri
c GN

IF: C3 only.
EM: Dense
deposits in GBM

immune
complexes

Unknown
Unknown

Unknown

Activation of
alternate
complement
pathway

with
splitting of
BM (double
BM).
IF: Granular
C3, C19,
C4with
LM: Same as
type I

a) Type 1

Idiopathic,
GPS

b) Type II

Idiopathic,
SLE,
postinfectious, HSP,
SABE, mixed
cryoglobuline
mia, shunt
infection

c) Type III

Idiopathic
Wegener's
Granulomatos
is
Microscopic
PAN

LM: Crescentric
GN IF: IgG, C3
linear pattern
EM: Widening of
BM
LM: Crescentic
GN IF: IgG, C3
granular pattern
EM:
Subepithelial,
subendo- thelial
or mesangial
deposits
LM: Crescentic
GN
IF: No Ig; EM: No
deposits.

IgA nephropathy
Goodpasture's disease
Poststreptococcal infection
MPGN

57

Not a feature of constrictive pericarditis

A; (Splenomegaly)
CONSTRICTIVE PERICARDITIS
Etiology:
- Tuberculosis,
- Hemopericardium.
C/F:
- Dyspnea on exertion, orthopnea (50% cases),
- Peripheral edema,
- Rapid low-volume pulse, pulsus paradoxus,
-Elevated JVP with rapid Y-descent,
- Kussmaul's sign (rise in JVP during inspiration),
and Loud S3 or pericardial knock.
ECG:
- Low-voltage and nonspecific T wave changes
Cardiac catheterization:
- Right atrial pressure tracing: Marked Y descent
- The right and left atrial pressure pulses display an M-shaped contour,
with prominent x and y descents; the descent, which is absent or
diminished in cardiac tamponade, is the most prominent deflection in
constrictive pericarditis.
- Left and right ventricular pressure tracing: 'dip and plateau or square
root' sign.
- Equalization of end-diastolic pressures in all 4 cardiac chambers and
pulmonary artery.

CT/MRI:
- MRI and CT scanning are more accurate than echocardiography
Other features
- Prominent X and y descent
- Kussmaul's sign
- Low-voltage ECG
- Electrical alternans
- Small RV size
- Pulsus paradoxus
Treatment:
- Surgical removal of pericardium.
- Pericardial resection is the only definitive treatment of constrictive
pericarditis, but dietary sodium restriction and diuretics are useful during
preoperative preparation.
Characterist
ic

Tampon
ade

Constricti
ve
Pericardi
tis

Restrict
ive
Cardio
myopat
hy

RVMI 1

Common

Usually
absent

Rare

Rare

Prominent y
descent
Prominent x
descent
Kussmaul's
sign

Absent

Rare

Rare

Present

Rare

Absent

Usually
present
Usually
present
Present

Absent

Present

Third heart
sound
Pericardial
knock

Absent

Absent

Rare

Absent

Often
present

Absent

May be
present
Absent

Clinical
Pulsus
paradoxus
Jugular veins

Present

Electrocardiogram
Low ECG
May
voltage
be
prese
nt
Electrical
May
alternans
be
prese
nt
Echocardiography
Thickened
Absen
pericardiu
t
m

May be
present

May be
present

Absent

Absent

Absent

Absent

Present

Absent

Absent

Pericardial
calcificatio
n
Pericardial
effusion

Absen
t

Often
present

Absent

Absent

Prese
nt

Absent

Absent

Absent

RV size

Usuall
y
small
Norm
al

Usually
normal

Usually
normal

Enlarged

Normal

Usually
increase
d
Absent

Normal

Present

May be
present

Absent

Absent

Absent

Absent

Usually
absent

Absent or
present

Someti
mes

No

Myocardial
thickness

Right atrial Prese


Absent
collapse
nt
and RVDC
Increased
Absen
Present
early
t
filling,
mitral flow
velocity
Exaggerate
Prese
Present
d
nt
respiratory
variation in
flow
velocity
CT/MRI
Thickened
Absen
Present
/calcific
t
pericardiu
m
Cardiac catheterization
Equalizatio Usuall
Usually
n of
y
present
diastolic
prese
pressures
nt
Cardiac
No
No
biopsy
helpful?

Absent

Splenomegaly
Kussmaul's sign
Pulsus paradoxus
Orthopnea

58

Glycogen-containing cells is feature of

A; (Ewing's sarcoma)
EWING'S SARCOMA
Ewing's sarcoma constitutes -10-15% of all bone sarcomas.
Is common in adolescence and has a peak incidence in the second decade of
life.
It typically involves the diaphyseal region of long bones.
Also has an affinity for flat bones.
The plain radiograph may show a characteristic "onion peel"periosteal
reaction with a generous soft tissue mass, which is better demonstrated by
MRI.
The soft mass is composed of sheets of monotonous, small, round, blue cells

and can be confused with lymphoma, embryonal rhabdomyosarcoma, and


small-cell carcinoma.
The presence of p30/32, the product of the mic-2 gene (which maps to the
pseudoautosomal region of the X and Y chromosomes) is a cell-surface
marker for Ewing's sarcoma (and other members of a family of tumors called
PNETs).
Most PNETs arise in soft tissues; they include - Peripheral neuroepithelioma,
- Askin's tumor (chest wall), and
- Esthesioneuroblastoma.
It is composed of sheets of uniform small, round cells that are slightly larger
than lymphocytes, rich in glycogen with presence of Homer-Wright rosettes.
Glycogen-filled cytoplasm detected by staining with periodic acid-Schiff is
also characteristic of Ewing's sarcoma cells.
In approximately 85% of patients t (11; 22) (q24; ql2) translocation is seen.
It is very aggressive, and it is therefore considered a systemic disease.
Common sites of metastases are lung, bones, and bone marrow.
Systemic chemotherapy is the mainstay of therapy, often being used
before surgery.
Doxorubicin, cyclophosphamide or ifosfamide, etoposide, vincristine, and
dactinomycin are active drugs.
Local treatment for the primary tumor includes surgical resection, usually
with limb salvage or radiation therapy.
Patients with lesions below the elbow and below the mid-calf have a 5-year
survival rate of 80% with effective treatment.
Ewing's sarcoma is a curable tumor, even in the presence of obvious
metastatic disease, especially in children <11 years old.
It is Undifferentiatedhigh grade tumor (Ewing's is always classed G4)
Other small round cell tumors include
Tumor
1. Wilms tumor
2. Lymphoblastic lymphoma
(ALL)
3. Rhabdomyosarcoma
4. Neuroblastoma

5. Medulloblastoma
6. Retinoblastoma
7. Ependymoblastoma
8. Burkitt's lymphoma
9. Small cell carcinoma

Ewing's sarcoma
Chondromyxoid tumor

Classic cytogenetic
abnormality
11p13 deletion/mutation
t (9; 12)
t (2; 13), 11p deletion
1p deletion,
N-myc amplification,
DNA hyperploidy
17q
13q14 deletion/mutation
t (11;22)

Chondroblastoma
Osteosarcomas

59

Sago spleen is a feature of

C; (Amyloidosis)
Amyloidosis is deposition of a pathologic proteinaceous substance between
cells in various tissues of the body,
In spleen it is Characterized by splenomegaly, sagospleen (deposit largely
limited to splenic follicles, producing tapioca-like granules on gross
inspection), lardaceous spleen (2nd pattern in which amyloid appears to spare
the follicles and instead involves the wall of splenic sinuses and connective
tissue framework in red pulp, giving rise to large fused map-like areas of
amyloidosis).
Educational table:
Important Pathologic
Features
1. Lardaceous & Sago spleen

Condition

2. "Onion skin" spleen


3. Shrinking lung
4. Nutmeg liver
5. "Flea bitten" kidney

SLE
SLE
Chronic passive congestion
Local GN

6. Thyroidization of kidney

Chronic pyelonephritis

Amyloidosis

Chronic congestion of spleen


Malaria
Amyloidosis
Pneumocystis carinii

60

Red infarct is seen in

A; (Lung)
Hemorrhagic/Red
infarct

Non hemorrhagic
/pale/bland/anemic infarct

1. Ovarian torsion
2. Lung
3. Small intestine

Heart
Spleen
Kidney

Lungs
Spleen
Kidney
Heart

61

"Biphasic pattern" on histology is seen in which tumor?

B; (Synovial cell sarcoma)


The histologic hallmark of synovial sarcoma is the biphasic morphology of
tumor cells (i.e., epithelial like and spindle cells)
Architectural Pattern in Soft Tissue Tumors
Pattern
1. Biphasic

Tumor
Synovial sarcoma

2. Herring bone

Fibrosarcoma

3. Storiform

Fibrohistiocytoma

4. Palisading nuclei

Schwannoma

5. Spindle cells

6. Spider cells

Fibrous, fibrohistiocytic
smooth muscle, Schwann cell
tumor
Rhabdomyoma

7. Small round cells


8. Antoni A and B

PNET, rhabdomyosarcoma
Schwannoma

9. Triton tumors

MPNST

10. Tadpole cells

Rhabdomyosarcoma

11. R-S cells, starry sky

Hodgkin's disease

12. Sezary- Lutzner cells

Cutaneous T-cell lymphoma

Rhabdomyosarcoma
Synovial cell sarcoma
Osteosarcoma
Neurofibroma

62

Mycosis fungoides mainly affects

C; (T-cells)
MYCOSIS FUNGOIDES (CUTANEOUS T CELL LYMPHOMA
&/SEZARY SYNDROME)
It is an indolent disorder of peripheral CD4+T-cells.
Patients are usually adults with cutaneous patches, plaques, nodules or
generalized erythema.
Characteristically 3 phases are known: Premycotic plaque tumor phase.
The median age of onset is in the mid-fifties
It is more common in males and in blacks.
It is an indolent lymphoma with patients often having several years of
eczematous or dermatitic skin lesions before the diagnosis is finally
established.
The skin lesions progress from patch stage to plaque stage to cutaneous
tumors.
Early in the disease, biopsies are often difficult to interpret, and the diagnosis
may only become apparent by observing the patient over time.
In advanced stages, the lymphoma can metastasize to lymph nodes and
visceral organs.
A particular syndrome in patients with this lymphoma involves erythroderma
and circulating tumor cells. This is known as Sezary's syndrome.
Rare patients with localized early stage mycosis fungoides can be cured with
radiotherapy, often total-skin electron beam irradiation.
More advanced disease has been treated (palliative) with:
- Topical glucocorticoids,
- Topical nitrogen mustard,
- Psoralen with ultraviolet A (PUVA),
- Electron beam radiation,
- Phototherapy,
- Interferon,
- Antibodies,
- Fusion toxins, and

- Systemic cytotoxic therapy.


B-cells
Plasma cells
T cells
Macrophages

63

All are chemical carcinogens except

A; (Betacarotene)
Chemical Carcinogens
1 Direct acting

Procarcinogens

Others 1

1. -propiolactone

Benzopyrene

Thorostat

2. Dimethyl sulfate
3.Diepoxybutane
4. Anticancerous drugs
5. 1-acetyl imidazole
6. Dimethyl carbamyl
chloride

Dibenzanthracene
3-methyl cholanthrine
Aromatic amines
Amides
Azo dyes
Benzidine
p-naphthyamine
Aflatoxin B1
Griseofulvin
Betel nuts
Safrole
Cycasin

Nitrosamine
Vinyl chloride
Nickel
Chromium
Insecticides
Fungicides
Polychlorinated
biphenyls

Beta carotene
Benzene
Thorostat
Nitrates

64

True about apoptosis is all except

C; (Inflammatory process)
APOPTOSIS
Apoptosis ("Falling-off') is programmed cell death.
"Cytocrome'C'" mediates it.
It occurs in following settings:
- During development
- As homeostatic mechanism to maintain cell population
- As defence in immune reaction
- When cells are damaged by disease/noxious agents - In aging
It is characterized by 2 phases
- Initiation
- Execution
It is characterized by:
- Cell shrinkage
- Chromatin condensation
- Cytoplasmic blebs and apoptotic bodies
- In contrast to necrosis, apoptosis does not elicit inflammation.
E.g.
- Fas-Fas ligand mediated apoptosis,
- TNF- induced apoptosis,

- Cytotoxic T-lymphocyte stimulated apoptosis,


- DNA damage mediated apoptosis,
- Gene mediated bcl2 apoptosis.
Programmed cell death
Associated gene is BCL
Inflammatory process
None

65

All are prion diseases EXCEPT

D; (SSPE)
PRIONS
Pruissner was first person to describe the prion proteins (1997) & he got
Nobel Prize for the same.
Prion diseases are the transmissible spongiform encephalopathies, which
include:
- Creutzfeldt-Jakob disease
- Gerstmann-Straussler-Seheinker syndrome
- Fatal familial insomnia
- Kuru
- Mad cow disease
Prions are infectious proteins that cause degeneration of the CNS.
These infectious agents are protein in nature, devoid of DNA and RNA.
Unusually resistant to physical and chemical agents like heat, irradiation, and
formalin.
- Prion diseases are disorders of protein conformation, the most common of
which in humans is called Creutzfeldt -Jakob disease (CJD).
- CJD typically presents with dementia and myoclonus, is relentlessly
progressive, and generally causes death within a year of onset.
- Most CJD patients are between 50 and 75 years of age.
Four new concepts have emerged from studies of prions:
- Prions are the only known infectious pathogens that are devoid of nucleic
acid (No RNA or DNA).
- Prion diseases may manifest as infectious, genetic, and sporadic disorders
(no other group of illnesses with a single etiology presents with such a wide
spectrum of clinical manifestations).
- Prion diseases result from the accumulation of
- PrPSc, the conformation of which differs substantially from that of its
precursor PrPC.
- PrPSc can exist in a variety of different conformations, each of which seems
to specify a particular disease phenotype.
Glossary of prion terminology
Term
Prion

PrPSc

PrPSc

Comments
Proteinaceous /nfectious particle that lacks
nucleic acid. Prions are composed largely, if
not entirely, of PrPSc Molecules
Disease-causing isoform of the prion protein.
This protein is the only identifiable
macromolecule in purified preparations of
scrapie prions.
Cellular isoform of the prion protein. PrPC is
the precursor of PrPSc.

Prp 27-30

PRNP
Prion rod

PrP Amyloid

A fragment of PrPSc, generated by truncation


of the NH2-terminus by limited digestion
with proteinase K. PrP 27-30
retains prion infectivity and polymerizes into
amyloid.
PrP gene located on human chromosome 20.
An aggregate of prions composed largely of
PrP 27-30 molecules.
Created by detergent extraction and limited
proteolysis of PrPSc. Morphologically and
histochemically indistinguishable from many
amyloids.
Amyloid-containing PrP in the brains of
animals or humans with prion disease; often
accumulates as plaques.

Kuru
Scrapie
Creutzfeldt-Jakob
SSPE disease

66

"Crescents" on histopathologic examination of glomerulus are seen in

B; (RPGN)
RAPIDLY PROGRESSIVE (CRESCENTIC) GLOMERULONEPHRITIS
RPGN is a clinical syndrome and not a specific etiologic form of GN.
Clinically, it is characterized by rapid and progressive loss of renal
function with features of the nephritic syndrome, often with severe
oliguria and (if untreated) death from renal failure within weeks to
months.
Regardless of the cause, the histologic picture is characterized by the
presence of crescents (crescentic GN).
These are produced in part by proliferation of the parietal epithelial
cells of Bowman's capsule in response to injury and in part by infiltration
of monocytes and macrophages.
Type I (Anti-GBM Antibody)
Idiopathic
Goodpasture syndrome
Type II (Immune Complex)
Idiopathic
Postinfectious/infection related
Systemic lupus erythematosus
Henoch-Schonlein purpura/lgA nephropathy
Type III (Pauci-lmmune) ANCA associated
Idiopathic
Wegener granulomatosis
Microscopic angiitis

Minimal change disease


Rapidly proliferative GN
Membranous glomerulonephritis
MPGN

67

Fat necrosis is seen in

A; (Breast)
Fat necrosis is seen in breast, acute pancreatitis, etc. It does not denote a
specific pattern of necrosis; rather it is focal area of fat destruction, due to
release of pancreatic lipase.

Breast
Brain
Kidney
Spleen

68

Type of amyloidosis in multiple myeloma?

C; (AL)
SYSTEMIC AMYLOIDOSIS
Category

Associated
disease

Major
fibril
protein

Precurso
r
Protein

Primary

Multiple
myeloma
Chronic
inflammation

AL

l-light
chain

Hemodialysis associated

CRF

Ab2-m

Familial Mediterranean
fever

AA

Secondary

Familial amyloidotic
neuropathies
Systemic senile
amyloidosis
Localized Amyloidosis
1. Senile cerebral
2. Medullary Carcinoma
of Thyroid
3. Isolated atrial
amyloidosis

AA
SAA
2microglob
ulin
SAA

ATTR

Transthyr
etin

ATTR

Transthyr
etin

Alzheimer's
-

Ab
Acal

APP
Calcitoni
n

Type II DM

AANF

ANP

B2
AA
AL
MM

69

Thromboxane is produced by

A; (Platelets)
THROMBOXANE A2
For example, platelets contain the enzyme thromboxane synthetase, and
hence TxA2, is the major product in these cells. TXA2, a potent plateletaggregating agent and vasoconstrictor, is itself unstable and rapidly converted
to its inactive formTxB2.
TxA2 acts in cyclooxygenase pathway of inflammation.
Inflammatory actions of eicosanoids:
Metabolite

Actions

1. TxA2, LTC4, D4, E4


2. PGI2, PGE1,, PGE2, PGD2
3. LTC4, D4 and E4
4. LTB4, HETE, lipoxin
5. Chemokine eotaxin

Vasoconstriction
Vasodilatation
Increased vascular
permeability
Chemotaxis,
leukocyte adhesion
Recruitment of
eosinophils

Platelets contain the enzyme thromboxane synthetase and hence TxA2 is


major product in these cells.
Molecules Synthesized by Endothelial Cells That Play a Role in
the Regulation of Thrombosis and Fibrinolysis.
Molecule
Action
ADPase (an ectoenzyme) Nitric Degrades ADP (an aggregating
agent of platelets) to AMP + Pi
oxide (NO)
Inhibits platelet adhesion and
Heparan sulfate (a
aggregation by elevating levels
glycosaminoglycan)
Prostacyclin (PGI2, a
of cGMP Anticoagulant;
prostaglandin)
combines with antithrombin to
inhibit thrombin Inhibits
Thrombomodulin (a
glycoprotein)
platelet aggregation by
increasing levels of cAMP
Binds protein C, which is then
cleaved by thrombin to yield
activated protein C; this in
combination with protein S
degrades factors Va and Villa,
limiting their actions
Tissue plasminogen activator
Activates plasminogen to
(t-PA, a protease)
plasmin, which digests fibrin;
the action of t-PA is opposed
by plasminogen activator
inhibitor-1 (PAI-1)

Platelets
Leukocytes
Vessel wall
RBCs

70

Serotonin is produced by

C; (Platelets)
SEROTONIN (5-HT)
Serotonin (5-HT) is second preformed vasoactive mediator of inflammation.
It is present in platelets and enterochromaffin cells and in mast cells in
rodents but not humans.
Release of serotonin and histamine from platelets is stimulated when
platelets aggregate after contact with collagen, thrombin, ADP and ag-ab
complexes and platelet activating factor (PAF).

Leukocytes
RBCs
Platelets
Vessel wall

71

Rapidly proliferative glomerulonephritis is histologically characterized by


Crescent in glomerulus

A; (Crescent in glomerulus)

Diffuse glomerulosclerosis
Thickened basement membrane
Capsular drop

72

Electron microscopic feature of minimal change disease is

B; MINIMAL-CHANGE DISEASE (LIPOID NEPHROSIS)


This relatively benign disorder is the most frequent cause of the
nephrotic syndrome in children.
It is characterized by glomeruli that have a normal appearance by light
microscopy but show diffuse effacement of podocyte foot processes
when viewed with the electron microscope.
Although it may develop at any age, this condition is most common
between ages 1 and 7 years.
When the changes in the podocytes reverse (e.g., in response to
corticosteroids), the proteinuria remits.

No change seen
Loss of foot process of podocytes
Diffuse glomerulosclerosis
Thickened basement membrane

73

Acanthocy tosis is feature of which of the following?

C; (Abetalipoproteinemia)
ABETALIPOPROTEINEMIA
It is inability to synthesize apolipoprotein B.
It is transmitted by autosomal recessive (AR) inheritance.
It leads to complete absence of all lipoproteins in plasma containing
apolipoprotein B (i.e., chylomicrons, VLDL and LDL), causing further lipid
membrane abnormalities like acanthocytic erythrocytes (burr cells).
Manifests as:
- Failure to thrive,
- Steatorrhea,
- Retinitis pigmentosa.

Uremia
Liver failure
Abetalipoproteinemia
Iron deficiency anemia

74

Amoebic ulcer is:

C; For Explanation refer the Question No.31


in surgery (perforation of typhoid usually
occurs
during 3rd week).

U-shaped
Undetermined edges
Flask shaped
Everted edger

75

Longitudinal ulcers are seen in:

B; For explanation see the surgery Question


No.31 (perforation of typhoid usually occurs
during 3rd week).

Tuberculosis
Typhoid
Amoebiasis
Malaria

76

Minimal Change GN all are true except:

D; Minimal change dose (MCD) also known as Lipoid Nephrosis which is most common cause of Nephrotic syndrome in
children.
Main feature is loss of foot process, under electron microscope
It gives good response to steroids.
Note: Loss of Foot process can be seen under electron Microscope .Under
light Microscope those will be no change. M/c cause of nephritic
syndrome IgA Nephropathy (World wide). It is known as Berger's
disease. Spike & dome pattern in subepithelial-Membranous GN.

Loss of foot process


Normal Basement membrane
Lipoid Nephrosis
Poor response to steroids

77

Ovarian tumours most commonly arise from:

C; Most common ovarian tumor


egithelial cell (60%) Tumor
Most common ovarian tumor with pseudomyxoma peritonei mucinoi
cyadenoma. Most common epitheliaTcell tumor-serous cyst
adenocarcinoma. (In serous cystadenocarcinoma psammoma bodies are
seen) -In Granulosa cell Tumor ->call exner bodies Endodermal sinus
Tumor -> schiller duval bodies Hilus cell Tumors -^Reinke's Crystal.

Sex cord
Germ cell
epithelial cells
Stroma

78

HIV affects:

D; HIV infects CD4 mainly and also


macrophages, dendritic cells.
In India most common Strain of H1V-I (subtype)
Most common malignancy in AIDS patients Kaposi sarcoma
Most common Sun gal infections in AIDS patients Cryptococcus
Neoformans. Most common blindness in AIDS patients CMV retinitis
Most common space occupying lesion in AIDS- Toxoplasmosis.

CD 8
CD 4
Macrophages
B+C

79

Which of the following is not Premalignant condition:

D; Precancerous condition
1. Chronic gastritis of Pernicious Anemia.
2. Solar Keratosis of the skin.
3. Chronic ulcerative collitis.

4. Leukoplakia of the oral cavity. Vulva & Penis.


5. Crohn's disease

All these conditions are called precancerous conditions.


Note:
Malignant potential is seen in both ulcerative colitis & Crohn's
disease but ulcerative collitis is more important risk factor than
Crohn's disease. Diverticular disease and Ischemic collitis do not
predispose to cancer.
Retinitis Pigmentosa: This primary Pigmentary retinal dystrophy is a
hereditary discloser predominantly effecting the rods more than the
cones. Most common mode is Autosomal Recessive. It is not a
premalignant condition. (Reference: Robinson Page No. 287 th Edition)
Crohn's disease.
Ulcerative colitis.
Leukoplakia.
Retinitis Pigmentosa

80

Bence John's protein is:

C; Bence jones protein is seen in Multiple myeloma.. In 99% of patient of


Multiple myeloma electrophoresis reveals level of Ig in blood or
monoclonal light chains. Serum M protein & Bence Jones proteinuria are
observed in to 70% pts.
Note: Serum M Protein is not due to IgM but due to IgG immunoglobulins

Polyclonal Heavy chain


Polyclonal Light Chain
Monoclonal light chain
Monoclonal Heavy Chain

81

True about natural killer cells are all except:

D;
Nk cells are also called as large granular Lymphocytes.
Contain azeurophillic granules.
1st line defence against Neoplastic cells & virus Laden cells.
Not mediated by an Immune response & antigen - antibody
reaction.
NK cells Express CD 16 & CD 56.
1.
2.
3.
4.

Kill Virus
Large granular lymphocytes
Have azeurophilic granules
Mediates Type IV Hypersensitivity

82

Adult polycystic kidney disease is:

A; A list of Autosomal dominant disease


Adult polycystic disease Acute Intermittent porphyria
Alzheimer's disease
Alpha-1 Antitrypsin deficiency Adenomatosis Polyp
(Familial) Huntington's chorea
Marfan syndrome
Many enzyme deficiency diseases are Autosomal recessive.

Like:
Gaucher's disease. Glycogen storage disease, Flurler's & Hunier's disease,
sickle cell disease, Tay-sach's disease-phenylketonuria, Albinism,
Galactosaemia.
Autosomal dominant
Autosomal Recessive
X-Linked recessive
X-Linked dominant

83

Tuberculosis ulcer edges are:

C;
Ulcer types
Non specific ulcer

Tuberculosis ulser
Basal-cell
carcinoma (Rodent
ulcer)
Epithelioma
Syphilis

Edges
Shelving

Undermined edges
Rolled edge

Everted edge
Punched edge

What to do friends, we have to remember always the many lists.


Rolled edge.
Everted edges.
Undermined edges.
Punched out edge.

84

What type of Hypersensitivity seen in SLE?

C; Try to Remember
Type-I: Immediate Hypersensitivity (Ig E mediated)
Eg: Atopic, Asthma, Hay fever, Anaphylaxis Type-II:
Cytotoxic (Ig G /lg M Mediated) Eg: Good Pasture syndrome,Graves
disease, Myasthenia gravis, auto-immune hemolytic anemia
Erythroblastosis fetalis.
Type-Ill: Immune Complexes ( IgA/lgG)
Eg:- Arthus reaction, Serum sickness, Rheumatic fever.
Glomerulonephritis, SLE
Type-IV: Cell Mediated (delayed) (T cell / macrophages)
Eg: Tuberculosis, Contact dermatitis, Transplant rejection
(Reference: Robbins Page No. 196 16th Edition)

Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity

Type IV hypersensitivity

85

Lung carcinoma with worst prognosis:

C; Small cell Carcinoma are Highly Malignant and Blood metastasis occurs
early. Try to Remember ,
M/c variety of lung Carcinoma in IndiaSquamous cell carcinoma. .'M/c variety in worid-Adenocarcinoma
M/c variety in young patients-* Adenocarcinoma
Carcinoma which metastasis to opposite lungAdenocarcinoma ^-Histological variety that cavitates-Squamous cell
carcinoma. Lung carcinoma with worst prognosis>Small cell
carcinoma.
Variety most responsive to chemotherapy & Radiotherapy Small cell
carcinoma. M/c variety with cushing syndrome -SmalI cell carcinoma.
Variety with best prognosis>Squamous cell carcinoma.
Variety with central in location Squamous cell Carcinoma & Small cell
carcinoma. , Gynaecomastia is seen in which type of carcinoma-> Large
cell carcinoma.

Squamous cell carcinoma


Adenocarcinoma
Small cell carcinoma
Large cell carcinoma

86

Epithelioid Granuloma consists mainly of:

D; When a persistent antigen present the macrophages undergo


morphologic transformation into epithelium like cells, known as
epitheliod cells. The Epitheliod cells are surrounded by
Lymphocytes, referred as Granuloma, this pattern of inflammation TypelV Hypersensitivity.

Lymphocytes
Neutrophil Is
Histiocyte's
Macrophages

87

AH are seen in acute inflammation except:

A; Granuloma formation is seen in chronic inflammatory disease. Try to


Remember
Histamine increase the vascular permeability and the richest
source is Mast cells.
Serotonin also increase the vascular permeability. The sources
are platelet and Enterochromaffin cells.
Bradykinin is the potent agents, which increases the vascular
permeability.
C3a, C5a and leukotriene C4, D4, E4 Increases the vascular permeability.

Granuloma
Increased vascular permeability
Vasodilation
Neutrophil migration

88

About Hemolytic anemia all are true except'.

A; There is decreased level of I laptoglobins in Hemolytic Anemia.

Haptoglobin is a globulin produced by the liver, which binds free


Haemoglobin to form a complex not to be excreted by the kidney. Other
feature of Haemolysis
1. Increased Bilirubin
2. Increased I.DH (Due to Red cell destruction)
3. Increased Reticulocytes.
+ ve urinary Haemosidcrin.
Increased Haptoglobin
Reticulocytosis
Spherocytcs are seen
Increased unconjugated bilirubin

89

Invasive Carcinoma differs from Carcinoma in situ by:

B; Any Carcinomas that have not invaded through the basement


membrane of the dermo epidermal junction known as carcinoma in situ.
Example: Basal cell carcinoma, Paget's disease.

Pleomorphism.
Basement membrane Involvement
Both
None

90

Morphology Report says few neutrophil, with heavy, boggy, red lung. What is the
stage of lobar pneumonia?

A; In lobar Pneumonia, 4 stages of inflammatory Response.


Congestion predominates in the first 24 hours. Morphology
Report says few neutrophil, with heavy, boggy, red lung.
Red Hepatization i.e.Massive confluent Exudation with Red
cells & Neutrophils:
Gray Hepatization i.eFibrino-supprative exudates.
Resolution i.econsolidated exudates.

Congestion
Red hepatization
Gray hepatization
Resolution

91

Major Histocompatibility Complex (MHC. have all the characters except-.

D; MHC also known as HLA (Human Leukocyte antigen).


Genes codes for Histocompatibility is located short arm of 6th
Chromosome.
There are 3 type of HLA
HLAclass I->for all nucleated cells and platelets. (HLA -A, HLA-B,
HLA-C), For CD8 HLAClass-II expression on Macrophages B
cells, T-cells. [HLA-D], For CD4
HLAClass -III-*Complement, TNF TNF

Located at short ARM 6th chromosomes.


Responsible for graft rejection
Have genes of complements.
Class II for all nucleated cells.

92

Transplant hyper acute rejection is takes place at most is:

A;

Hyper acute Rejection occurs when performed Antidonar


antibodies are present in the circulation of recipient.

It presents within minutes or hours after transplantation.

Some times may be recognized. By Surgeon as it rapidly


becomes cyanotic mottled and flaccid and may excrete few drops
of bloody urine.
It is a type II hypersensitivity reaction. Acute rejection: Appears within
days. Both Cellular and humoral immunity Play role. Acute cellular
rejection: is most commonly seen within initial months after
transplantation.
Within Few Minutes to hour
1 -2 weeks later operation
6 Months later operation
After several years

93

MHC is important in pathogeneses of:

B; Class-I Antigen
Are expressed on all nucleated cells and platelets.
Encode cell surface glycoprotein.
They are encoded by three closely relate LOCl HLA-A, HLA-B,
HLA-C.

CD8+ T cells widely express Class-I HLA antigen.


Class-II Antigen
Are expressed on macrophages, B cells and T cells.
Encode cell surface Glycoproteins.
Class-Ill Antigen
These encodes complements of the Complement system.
MCH is important in pathogenesis of Autoimmunity. E.g. Strong

association has been found between ankylosing spondylitis and HLA


B.27, Rheumatoid arthritis and HLA DR4 and many auto-immune
condition with HLA-DR3.
Important: Several gene code for MHC, the most important one is
Chromosome 6.
Immuno deficiency disease
Auto-immune disease
Genetic disorder
None of the above

94

Which of the following is not seen in glomerulonephritis?

C; (Hypotension): Hypotension is not seen in glomerulonephritis.

Acute Glomerulonephritis
This group of glomerular disease is
Characterized anatomically by inflammatory
alterations in the glomeruli and clinically by the

syndrome of acute nephritis.


The nephritic patients usually presents with
Hematuria, red cell casts in the urine, azotemia,
oliguria, and mild to moderate hypertension.

Hypertension
Hematuria
Hypotension
Proteinuria

95

No. of domains in MHC-I:

C; (Three): No. of domains in MHC I is three.


Major Histocompatibility Complex I (MHC I)
Class I MHC molecules are expressed on all
nucleated cells and plateletsQ.
They are encoded by three closely linked loci,
designated HLA-A, HLA-B, HLA-C.
Each of these molecule is a heterodimer,
consisting of polymorphic a, or heavy chain
linked non-covalently to a smaller
nonpolymorphic peptide called p2 microglobulin,
which is not encoded within the MHC.
The Extracellular region of heavy chain is
divided into three domainsQ.
In general, class I MHC molecules bind and
display peptides that are derived from proteins,
such as viral antigens, synthesized within the
cellQ.

One
Two
Three
Four

96

Duchenne muscular dystrophy is:

D; (X-linked recessive): Duchenne muscular dystrophy is X-linked


recessive. See Q. no. 46 DPG 2006.

Autosomal dominant
Autosomal recessive
X linked dominant
X linked recessive

97

Causes of megaloblastic anemia are all except:

B; (Hookworm): Hookworm doesn't cause megaloblastic anemia, causes


iron deficiency anemia.

Alcoholism
Hookworm
B12 deficiency
Folic acid deficiency

98

Which of the following is Autosomal recessive?

B; (|3 thallesemia): (3 thallesemia is Autosomal recessive.

Hereditary spherocytosis
Thalassemia
Turners syndrome
Hemophilia

99

Scarring is seen grossly and diffusely in:

A; (Chronic glomerulonephritis): Scarring is seen grossly and diffusely in


chronic glomerulonephritis.

The Characteristic changes of chronic


Pyelonephritis: The kidneys usually are
irregularly scarred; if bilateral, the
involvement is asymmetric.
This contrasts with chronic
glomerulonephritis, in which the kidneys are
diffusely and symmetrically scarred.
The hallmark of chronic Pyelonephritis is the
coarse, discrete, corticomedullary scar overlying
a dilated, blunted, or deformed calyx.
The scars can vary several in number and my
affect one or both kidneys. Most are in the
upper or in lower poles, consistent with the
frequency of reflux in these sites.

Chronic glomerulonephritis
Pyelonephritis
Hypertension
D.M.

100

Chronic liver disease is caused by all except:

A; (Hepatitis A): Hepatitis A doesn't cause chronic liver disease.


Chronic Viral Hepatitis
Both the enterically transmitted forms of viral
hepatitis, hepatitis A and E, are self-limited and
do not cause chronic hepatitis9.
In contrast, the entire clinicopathologic
spectrum of chronic hepatitis occurs in
patients with chronic viral hepatitis B and CQ
as well as in patients with chronic hepatitis D
superimposed on chronic hepatitis BQ.

Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D

101

In nephrotic syndrome following would be seen:

D; (All of the above): All options are correct.


Nephrotic Syndrome
The manifestation of nephrotic syndrome include

1.Massive proteinuria, with the daily loss of 3.5 gm or


more of protein
2.Hypoalbuminemia, with plasma albumin levels less
than 3 gm/dL
3.Generalized edema
4.Hyperlipidemia and lipiduria
Most important facts about Nephrotic syndrome:
The lipid appears in the urine either as free fat or
as oval fat bodies, representing lipoprotein
resorbed by tubular epithelial cells and then
shed along with the degenerated cells.
Most proteins are decreased in nephrotic
syndrome except Fibrinogen and lipoproteins,
due to increased synthesis.
Renal vein thrombosis is particularly common
(upto 40%) in patients with nephrotic syndrome
due to membranous glomerulopathy,
memranoproliferative glomerulonephritis, and
Amyloidosis
Spontaneous bacterial peritonitis
Loss of clotting factors
Thrombosis
All of the above

102

The blast cells of acute lymphoblastic leukemia in childhood contain:

B; (CALLA Ag):
The blast cells of acute lymphoblastic leukemia in childhood contain
CALLA Ag.
Causes of Thrombocytosis
Iron deficiency anemia
Hyposplenism

Idiopathic
Myelofibrosis
Essential
Thrombocytosis

Postsplenectomy
Malignancy
Collagen vascular
disease

CML
Myelodysplasia
Post surgery

Inflammatory bowel
disease

Rebound (cessation
of ethanol intake,

Infection

correction of vitamin
B12, folate

Polycythemia vera
Hemolysis
Hemorrhage

deficiency)

Surface antigen
CALLA Ag
Antibodies to WBC
Thrombocytosis

103

Most important histopathological indicator of malignancy in


pheochromocytoma:

D; (None of the above):


Criteril for malignancy is based exclusively on persent of meteastases,as
even capsular or vascular invasion can be present in beni tumors.
Pheochromocytoma
Most important points
Histologically tumor composed of polygonal
to spindle Chromaffin cells clustered into
small nests or alveoli (Zelballen) by a rich
vascular network. Nuclei are round with
"salt and pepper" chromatin.
Extra-adrenal pheochromocytoma (10%
cases) occur in organ of zuckerandt (MC site)
and the carotid body.
Criteria for malignancy is based exclusively
on presence of metastases, as even capsular
or vascular invasion can be present in benign
tumors.
Tumors are not innervated so catecholamine
release doesn't result from neural'
stimulation.
Most pheochromocytoma produce both NA
and Adr, with NA>Adr.
Extra-adrenal pheochromocytoma /
paraganglioma secrete NA exclusively.
Those associated with MEN may secrete
Adr alone.
Increased production of dopamine and
homovanillic acid is usually seen with
malignant lesions.
MC symptom is headache, and MC
manifestation is hypertension.
MRI is IOC for extra-adrenal
pheochromocytoma.
(Harrison 16th2151: MIBG scanning may be useful in
characterizing lesions discovered by CT when
biochemical confirmation is indeterminate, but is less
useful at localizing
extra-adrenal pheochromocytoma, than MRI or PET.
Features s/o Aggressive behavior (but not metastases)
Confluent tumor necrosis

Number of metastases
Spindle cell morphology

Pleomorphism
High mitotic activity
Vascular invasion
None of the above

104

104. Predominant constituent of hyaline membrane is:

C; (Fibrin rich exudates): Predominant constituent of hyaline membrane


is fibrin rich exudates.
Hyaline membrane disease
The hyaline membrane are largely
made up of fibrinogen and fibrin
admixed with cell debris derived
chiefly from necrotic type II
pneumocytes.

Albumin
Anthracotic pigment
Fibrin rich exudates
None of the above

105

Duchenne muscular dystrophy is a:

A; (X-linked recessive disease): Duchenne muscular dystrophy is X-linked


recessive disease.
Autosomal
dominant
disorders
- Familial
hypercholesterole
mia
- Hereditary
nonpolyposis
colon cancer
- Polyposis of the
colon

Autosomal
recessive
disorders
- Deafness

X-Linked
disorders

- Albinism

- BRCA1 and
BRCA2 breast
cancer
- Hereditary
hemorrhagic
telengiectasia
- Marfan's
syndrome
- Hereditary
spherocytosis

Hemochromatos
is
- Sickle cell
anemia

- G6PD
deficiency
(recessive)
Ducchene/Becke
r muscular
dystrophy
(recessive)
- Fabry's disease

- Adult polycystic
kidney disease

- Hereditary
emphysema(
antitrypsin
deficiency)
-

- Huntington's

- Wilson's
disease

- beta
thalassemia
- Cystic fibrosis

- Hemophilia A
(recessive)

- Ocular albinism

- Testicular
feminization
- Chronic
granulomatous
disease
Hypophosphate
mic rickets
(dominant)
- Fragile-X

chorea

Homocystinuria

- Acute
intermittent
porphyria
- Osteogenesis
imperfecta
- von
Willebrand's
disease
- Myotonic
dystrophy
- Familial
hypertrophic
cardiomyopathy
Neurofibromatos
is
- Tuberous
sclerosis
- Otospongiosis
- Achondroplasia

- Freidrich's
ataxia

syndrome
(recessive)
- Color blindness

Phenylketonuria
- Fanconi's
Syndrome
- Gaucher's
Disease

X-linked recessive disease


Autosomal dominant disease
Autosomal recessive disease
X-linked dominant disease

106

Nerurofibromatosis is a:

B; (Autosomal dominant disease): Neurofibromatosis is Autosomal


dominant disease.

X-linked recessive disease


Autosomal dominant disease
Autosomal recessive disease
X-linked dominant disease

107

Characteristic cell seen in Malacoplakia is

A; (Foam cell): Characteristic cell seen in malakoplakia is foam cell.


Malakoplakia
Its a variant of cystitis, related to chronic bacterial infection mostly by
E. coli or occasionally by proteus species.
It is characterized by unusual appearing macrophages and giant
phagosomes.
It points to defect in phagocytic or degradative function of macrophage.
Histologically it is characterized by infiltration with large foamy
macrophages.
The macrophages have an abundant granular cytoplasm and the
granularity is PAS positive.
In addition to these histological changes, malakoplakia is also
characterized by Michaelis Guttman bodies.
Michelis Guttman bodies are Laminated mineralized concretions
resulting from deposition of calcium in enlarged lysosomes.

Foam cell
Melanocyte
Keratinocyte
None of the above

108

Which of the following is true about Wilm's tumor?

C; (Associated with WAGR syndrome in 40% cases): Wilm's tumor is


associated with WAGR syndrome in 40% cases.
Wilm's Tumor
Wilm's tumor is the most common primary renal
tumor of childhood (2-5 years).
Arise from kidney and is usually composed of
three elements- blastema, epithelium and
stroma.
MC presenting feature is asymptomatic
abdominal mass or swelling.
Characterized by triad of abdominal mass, fever
and microscopic hematuria.
Associated malformations
1. WAGR Syndrome: It consists of
Aniridia
Genital anomalies
Mental retardation
The risk of Wilm's tumor is increased by 33% in
this syndrome.
2. Denys-Drash Syndrome: It consists of
Gonadal dysgenesis (Male
pseudohermaphroditism)
Nephropathy leading to renal failure
Majority of patients with this syndrome have renal
failure.
3. Beckwith-Wiedmann Syndrome: It consists
of
Enlargement of body organs
Hemi-hypertrophy
Renal medullary cysts
Abnormal large cells in adrenal cortex
Diagnosis:
USG (most important investigation) or CT
abdomen
Calcification tends to be more crescent
shaped, discrete and peripheral in comparison
of finely stippled calcification of neuroblastoma.

Treatment:
Surgical excision is treatment of choice.
In unfavourable histology, Radiation therapy
should be begin within 10 days after surgery,
Chemotherapy should be started 5 days after
surgery
Remember: The histology of wilms tumor is
identified as most important determinant of
prognosis.
Most commonly presents with hematuria
Arises from tubular epithelium
Associated with WAGR syndrome in 40% cases
Poor prognosis

109

Fibrolamellar carcinoma is characterized pathologically by:

A; (Localized single hard nodule):


Fibrolamellar carcinoma, is characterized pathologically by localized
single hard nodule.
Fibrolamellar carcinoma of liver
It occurs in young male and female adults (20-40 years of age)
Equal incidence in males and females
It presents as a single, large, hard schirrhous tumor with fibrous bands
coursing through it.
It has no association with HBV or underlying cirrhosis.
It has good prognosis as compared to hepatocellular carcinoma.
Surgical resection results in 5-year survival of >50%.
Serum AFP levels are not increased.

Localised single hard nodule


Multiple nodules in a background of cirrhosis
Poorly differentiated carcinoma
Minimal connective tissue

110

Most carcinoma of stomach metastasize to:

D; (Celiac lymph nodes)


Most carcinoma of stomach metastasizes to celiac lymph node.

Aortic lymph node


Hepatic lymph node
Left gastric lymph node
Celiac lymph node

111

Free radical injury is involved in all except:

C; (Meiosis): Free radical injury is not involved in meiosis.


Ischemia-Reperfusion injury: New damage may be initiated during
reoxygenation by increased generation of oxygen free radicals from
parenchymal and endothelial cells and from infiltrating leucocytes.
Oxygen derived free radicals: Implicated in following responses
Lipid peroxidation of membranes
Oxidative modifications of proteins
Lesions in DNA (cell ageing & malignant transformation)

Reperfusion injury
Carcinogenesis
Meiosis
Phagocytosis.

112

Reversible injury is due to:

A; (Damage to Na+-K+ ATPase): Reversible injury is due to damage to


Na+-K+ ATPase.
Cell Injury
Reversible injury: Occurs due to widespread effects of depletion of ATP
(decreased activity of Na+-K+ ATPase), which occurs as a result of
hypoxia5. Features of reversible injury include:
1. Cellular swelling
2. Loss of microvilli
3. Bleb formation
4. ER swelling: Detachment of ribosomes
5. Myelin figures
6. Nuclear: Clumping of nuclear chromatin
Irreversible injury: Membrane damage is a central factor in
pathogenesis of irreversible injury.
Features of irreversible injury include:
A. Severe swelling of mitochondria: Large, flocculant, amorphous
densities develop in mitochondrial matrix (Increased Ca2+ influx)
B. Severe swelling of lysosomes: Injury to lysosomal membrane follows;
various enzymes are released leading to:
1. Decreased basophilia
2. Nuclear changes (Pyknosis, karyolysis, Karyorrhexis)
3. Protein Digestion
C. Serve damage to plasma membrane

Damage to Na+-K+ ATPase


Formation of free radicals
Clumping of nuclear chromatin
Cytoskeletal damage

113

Equivalent of Heymann's nephritis:

B; (Membranous nephritis): Membranous nephritis is equivalent to


Heymann's nephritis.
The Heymann model of rat glomerulonephritis is induced by
immunizing animals with an antigen contained within preparations of
proximal tubular brush border. The rats develop antibodies to this
antigen, and a membranous glomerulopathy, resembling human
membranous glomerulopathy, develops.

Anti-GBM nephritis
Memberanous nephritis

Good Pastures Nephritis


RPGN

114

Brownish staining of liver is seen in:

A; (Melanosis of liver)
Brownish staining of liver is seen in melanosis of liver.
I searched Robbin's, Harshmohan, Harrison and internet but couldn't get
direct answer that brownish staining of liver is seen in melanosis of liver,
internet says that brownish colouration is seen in melanosis in sheeps. No
references were available for melanosis of liver in human beings. But trust
me, this is the most appropriate answer as suggested by SR pathology,
MAMC.

Melanosis of liver
Dubin-Johnson syndrome
Rotors syndrome
Gilbert's syndrome

115

Curschmann's spiralis indicate:

C; (Asthma): Curschmann's spiralis indicate asthma.


Asthma: Morphology
Grossly, the lungs are overdistended because of overinflation.
The most striking macroscopic finding is occlusion of bronchi and
bronchioles by thick, tenacious mucus plugs.
Histologically, the mucus plugs contain whorls of shed epithelium, which
give rise to the well-known Curschmann spiralis.

COPD
Idiopathic pulmonary fibrosis
Asthma
Chronic bronchitis

116

Cryoprecipitate contains:

C; (Factor VIII): Cryoprecipitate contains factor VIII.


Cryoprecipitate
Cryoprecipitate is a source of fibrinogen, factor VIII and von
Willebrand factor (vWF).
It is ideal for supplying fibrinogen to the volume-sensitive patient.
1 unit of cryoprecipitate contains 80-145 units of Factor VIII and 250 mg
of fibrinogen.
Cryoprecipitate is pooled from many donors, so there are maximum
chances of disease transmission among all blood products.

All coagulation factors


Plasma proteins
Factor VIII
Platelet and plasma proteins

117

Which of the following is true about Warthin's tumor?

C; (Bilayered Epithelial cell on lymphoid base): Bilayered Epithelial cell on


lymphoid base is seen in Warthin's tumor.
Warthin's Tumor (Papillary cystadenoma lymphomatosum)
Is the second most common benign tumor of the parotid gland (1st is

pleomorphic adenoma)
It consists of both epithelial and lymphoid elements thus known as
adenolymphoma (probably arises from remnants of parotid tissue
trapped in iymphnodes within the parotid gland)
The tumor arises only in the parotid gland.
Almost always arises in the lower portion of the parotid gland overlying
the angle of mandible.
Conamon in males. Age: 5th to 7th decade.
Association is seen with smoking.
Bilaterality is seen in 10% cases.
A peculiar feature of Warthin's tumor is that it shows 'hot' spot in 99m
Tc- pertechnate scan. Other tumors of the parotid show 'cold' spot.
Morphology:
Its well encapsulated, extremely slow growing tumor, never turns
malignant.
On microscopic examination, these spaces are lined by a double layer
of neoplastic epithelial cells resting on a dense lymphoid stroma
sometimes bearing germinal centres.
The double layer of lining cells distinctive, with a surface palisade of
columnar cells resting on a layer of cuboidal to polygonal cells
Uncommon in parotid
Serous and acinar hyperplasia
Bilayered Epithelial cell on lymphoid base
More common in females

118

True about Nephronopthisis is all except:

B; (Cortical tubular hypertrophy) cortical tubular hypertrophy is not seen


in nephronopthisis.
Nephronophthisis
The common characteristic is presence of a variable number of cysts
in the medulla, usually concentrated at the corticomedullary
junction.
Although the presence of medullary cysts is important, the cortical
tubulointerstitial damage is the cause of the eventual renal
insufficiency.
20% cases are non-familial or sporadic
Affected children presents first with polyuria and polydipsia, which
reflect a marked defect in the concentrating ability of renal tubules.
Sodium wasting and tubular acidosis are also prominent.
Morphology:
In the cortex, there is widespread atrophy and thickening of the
basement membranes of proximal and distal tubules, together with
interstitial fibrosis.

Cysts in the medulla


Cortical tubular hypertrophy
Interstitial fibrosis

20% cases are nonfamilial

119

Asbestos exposure can cause all except:

D; (Arthralgia): Asbestos exposure doesn't cause arthralgia.

Bronchogenic carcinoma
Mesothelioma
Carcinoma larynx
Arthralgia

120

In Wilson disease, deposition of_ occurs

A; (Cu):
WILSON DISEASE - Autosomal recessive disorders marked by the
accumulations of toxic levels of copper in many tissues and organs
principally the liver, brain and eye.
The gene for Wilson disease, designated ATP 7B, is on chromosome
13.
Biochemical diagnosis of Wilson disease is based on a decrease in serum
ceruloplasmin, an increase in hepatic copper content, and increased
urinary excretion of copper. Serum copper levels are of no diagnostic
values, since they may be low, normal or elevated.

Cu
Fe
Se
Mn

121

Cerebral amyloid angiopathy presents as

A; (Dementia):
Cerebral amyloid angiopathy (CCA) is an almost invariable
accompaniment of Alzheimer disease, however it can also be found in
brains of individuals without Alzheimer disease. Vascular amyloid is
predominantly A ~40 as is also true when CCA occurs without AD.
Principal clinical manifestation is dementia, that is progressive loss of
cognitive function independent of the state of attention.

Dementia
Lobar infarct
Haemorrhage
Lacunar infarct

122

LAP (Leucocyte alkaline phosphate) is increasd in all except

A; (CML):
Leucocyte alkaline phos
hate increased in:
Polycythemia vera
Hodgkin's disease
Myeloid leukaemoid
reaction
Hairy cell leukemia
Aplastic anemia

Leucocyte alkaline
phosphate decreased
in:
Chronic myeloid
leukemia (CML)
Paroxysmal nocturnal
haemoglobinuria (PNH)

Leukamoid reaction - is defined as a reactive excessive leucocytosis in the


peripheral blood resembling that of leukemia in a subject who does not

have leukemia.
CML
ALL
PNH
Leukemoid reaction

123

Apoptosis is

B; (Programmed cell death):


APOPTOSIS is morphologic event, which may not always underlie the
functionally defined "programmed cell death" of embryologists the terms
are currently used synonymously by most workers.
Contrastin features of Apoptosis and Necrosis
Features
1. Definition

APOPTOSIS
Programmed
and
coordinated
cell death

2. Causative
agents

Physiologic and
pathologic
process
No
inflammatory
reactions
Death of
single cells
Cell shrinkage
Cytoplasmic
blebs on
membrane
Apoptotic
bodies
Chromatin
condensation
Phagocytosis
of apoptic
bodies by
macrophages

3. Morphology

4. Molecular
changes

Lysosomes
and other
organells intact
Genetic
activation by
protooncogenes and

NECROSIS
Cell death along
with
degradation of
tissue by
hydrolytic
enzyme
Hypoxia and
toxis
Inflammatory
reactions
always present
Death of many
adjacent cells.
Cell swelling
initially
Damaged
organells
Nuclear
disruption
Phagocytosis
of cell debris by
macrophages

Lysosomal
breakdown
with liberation
of hydrolytic
enzymes
Cell death by
A TP depletion,

onco
suppressor
genes and
cytotoxic, T-cell
mediated target
cell killing

membrane
damage, free
radical injury.

Regulators of apoptosis
Inhibit Promote
Bcl-2 BaX
Bcl-XL Bad
Others Others
Cell reproduction
Programmed cell death
Ptosis associated with chemical injury
Thyroid ophthalmopathy

124

Amyloidosis of kidney presents as

A; (Proteinuria):
Clinical correlation of Amyloidosis
Nonspecific - weakness, weight loss, lightheadedness, or syncope
Specific-Renal- give rise to proteinuria and is an important cause of
the nephrotic syndrome, progressive obliteration of glomeruli in
advanced cases ultimately leads to renal failure and uremia
Cardiac- insidious CHF, conduction disturbances and arrythmias,
restrictive pattern of cardiomyopathy and masquerades as chronic
constrictive pericarditis.
Gastrointestinal- tongue enlargement and hamper speech and
swallowing, malabsorption, diarrhoea and disturbances in digestion.

Proteinuria
Hypertension
Vascular necrosis
Haematuria

125

Immunofluroscent immune complex deposition occurs in all except

C; (RPGN I, 1II):
Immunologic Mechanisms of Glomerular Disease
A.
Antibody-mediated
glomerular injury
1. Immune complex
Immune complex
disease
mediated GN (Acute
diffuse proliferative
GN, membranous GN,
membranoproliferative GN, IgA
nephropathy;
secondary glomerular
disease in SLE,
malaria etc)
2. Anti-glomerular
Good pasture's

3.

basement
membrane (AntiGBM) disease
Alternate
pathway disease

Other
mechanisms (anti
neutrophil
cytoplasmic
antibodies ANCA,
anti endothelial
cell antibodies
AECA)
Cell mediated
glomerular injury
Secondary
pathogenetic
mechanisms

4.

B.
C.

disease
Membranoproliferative GN type
II
Focal segmental GS

Pauci-immune GN
(type III RPGN)
Mediate glomerular
injury in various
primary and
secondary glomerular
diseases

Type I RPGN (Anti-GBM disease) - Linear Ig and C3


Type II RPGN (Immune complex disease) - Granular Ig and C3 Type III
RPGN (Pauci-immune GN) - Sparse or absent Ig and C3
Acute tubular necrosis
RPGN II
RPGN I, III
Acute glomerulonephritis

126

Mixed connective tissue disease, deposition of _ occurs

C; (Anti-RNP):
MIXED CONNECTIVE TISSUE DISEASE - describe the disease seen in a
group of patients who are identified clinically by the co-existence
offeatures suggestive of SLE, polymyositis, rheumatoid arthritis, and
systemic sclerosis, and serologically by high titers of antibodies to
RNP particle-containing U1-RNP
Two other factors have been considered important in lending
distinctiveness to mixed connective tissue disease-the paucity of renal
disease and an extremely good response to corticosteroids both of which
could be considered indicative of a good long term prognosis.

Anti smooth muscle


Anti DNA
Anti RNP
Anti nuclear

127

Congenital disease are/is

B; (Infantile polycystic kidney):


Renal cystic diseases

Adult
polycysti

Inherita
nce

Pathologic
features

Autosom
al

Large
multicystic

Clinical
features or
complicati
ons
Hematuria,
flank pain,

Typical
outcome

CRF
beginning

c kidney
disease

dominan
t

kidneys, liver,
cysts, berry
aneurysms

UTI, renal
stone,
hypertensi
on
Hepatic
fibrosis

at age 4060 years

Childhoo
d
polycysti
c kidney
disease

Autosom
al
recessiv
e

Enlarged
cystic kidneys
at birth

Medullar
y sponge
kidney

None

Medullary
cysts on
excretory
urography

Hematuria,
UTI,
Recurrent
renal
stones

Benign

Adultonset
medullar
y cystic
disease
Acquired
renal
cystic
disease

Autosom
al
dominan
t

Corticomedull
ary cysts,
shrunken
kidneys

Salt
wasting,
polyuria

None

Cystic
degeneration
in end-stage
kidney
disease

Hemorrha
ge,
erythrocyt
osis
neoplasia

CRF
beginning
in
adulthoo
d
Depende
nce on
dialysis

Variable
death in
infancy
or
childhoo
d

Childhood polycystic kidney disease is subcategories into Perinatal,


neonatal, infantile, and juvenile.
Medulalry sponge kidney
Infantile polycystic kidney
Adult polycystic kidney
Medullary cystic kidney

128

Most common change in atherosclerotic vessel is

A; (Dystrophic calcification):

Dystrophic calcification
Superimposed thrombosis
Aneurysm thrombosis
Haemorrhage

129

Liquification necrosis is seen in

D; (Brain):
Hyaline degeneration of voluntary muscle, also calIed Zenker's
degeneration, occurs in rectus abdominalis muscle in typhoid fever.
The muscle loses its fibrilIar staining and becomes glassy and hyaline.
NECROSIS
LIQUEFACTION
(Colliquative)
Most common
Commonly due to
type
ischaemic injury
and bacterial or
Sudden cessation
fungal infections
of blood flow
Examples - Brain
(ischemia) and is
exemplified well in
infarcts and
a infarcts of solid
Abscesses
COAGULATIVE

GASEOUS
Combines features
of both coagulative
and liquefactive
necrosis
"Cream-cheesy
appearances" of
necrosis

organs e.g. Heart,


spleen and kidneys
*Myocardial
infarction is an
excelIent examples

examples Tuberculosis

Pancreatic tissue
Tuberculous lesion
Cardiac tissue
Brain

130

Primary achalasia cardia, defect lies in

D; (One or multineuraI defect):


ACHALASIA means "failure to relax". It is characterized by
1. Aperistalsis
2. Partial or incomplete relaxation of the LES with swalIowing
3. Increased resting tone of the LES
It is thought to involve dysfunction of inhibitory neurons containing
nitric oxide and vasoactive intestinal polypeptide in the distal
esophagus
Morphology - In primary achalasia there is progressive dilation of the
esophagus above the level of the LESThe wall of the esophagus may be of
normal thickness, thicker than normal owing to hypertrophy of the
muscularis, or markedly thinned by dilation. The myenteric ganglia are
usually absent from the body of the esophagus, but may or may not be
reduced in number in the region of the LES. The mucosal lining may be
unaffected, but sometimes inflammation, ulceration or fibrotic thickening
may be evident just above the LES.

Crus of diaphragm is tight


Kinking of oesophagus
Mediastinal fibrosis
One or multineural defect

131

Myenteric plexus is absent in/very much sed.

C; (Achalasia cardia):
ACHALASIA (Cardiospasm) is a neuromuscular dysfunction due to which
the cardiac sphincter fails to relax during swalIowing and results in
progressive dysphagia and dilatation of the esophagus (megaoesophagus)

Globus pharyngeus
Pharayngealpouch
Achalasia cardia
Megacolon

132

Atherosclerosis, LDL is present in the

D; (LDL-monocytes):
Atherosclerosis to be a chronic inflammatory response of the
arterial wall initiated by injury to the endothelium. Moreover,
lesions progression is sustained by interaction between modified
lipoproteins, monocyte-derived macrophages, T-lymphocytes and
the normal cellular constituents of the arterial wall.
Accumulation of lipoproteins, mainly LDL, with its high cholesterol

content, in the vessel wall. Oxidized modified LDL - Is ingested by


macrophages through the scavenger receptor, distinct from LDL
receptor, thus forming foam cells.
- Increases monocyte accumulation in lesions
- Stimulates release of growth factors and cytokines
Is cytotoxic to endothelial cells and smooth muscle cells
HDL epithelium
LDL reduction
LDL endothelium
LDL monocytes

133

True statement regarding Libman Sach's endocarditis is

D; (All of the above):


Endocarditis of SLE (Libman-Sacks Disease)
In SLE, mitral and tricuspid valvulitis with small, sterile
vegetations, called Libman-Sacks endocarditis.
The lesions are small single or multiple, granular pink vegetations
ranging from I to 4 mm in diameter. The lesions may be located on
the undersurfaces of the A V valves on the valvular endocardium,
on the cords, or on the mural endocardium of atria or ventricles.
Rheumatic-endocarditis - Vegetations are small, multiple warty,
grey brown, translucent, firmly attached, sterile generally
produced permanent valvular deformity.
Lesions occurs along the line of closure, atrial surface of A. V. valve and
ventricular surface of semilunar valves.

Because of SLE
Vegetations are sterile
Both side valve defect
All of the above

134

True about Hepatitis E is all except

D; (None):
Hepatitis-E
HEV is an enterically
transmitted water born
infections that occurs
primarily in young to
middle-aged adults
High mortality rate
among pregnant women,
approaching 20%
Single stranded RNA
virus that is structurally
similar to calciviridae
HEV is not associated
with chronic liver or
persistent viremia

Hepatitis-G
The HGV, single
stranded RNA virus
HGV is transmitted by
contaminated blood or
blood products and
possibly via sexual route
The site of HG V
replication is most likely
in mononuclear cells
hence HG V is
inappropriately named.
as it is not hepatotropic
and does not cause
elevation of serum
amino transferases.
Extensive data do not
indicate any pathologic
effects of HGV, and the
blood supply does not

appear to need
screeningfor HGV RNA.
This virus commonly coinfects patients with
H1V, and curiously this
dual infection is
somewhat protective
against H1V disease.
Transmitted by faecooral route
It is unenveloped single stranded RNA virus
Belongs to calici virus
None of the above

135

All are true about Leucoerythroblastosis EXCEPT

D; (None):
LEUKOERYTHROBLASTOSIS - The presence of erythroid and
granulocytic precursors in the peripheral blood is termed
leukoerythroblastosis.
Development of severe anemia may result from infiltration of the
marrow termed as myelophthisic anemia (normocytic, normochronic with some fragmented red cells, basophilic stippling and
normoblast in PBS)
Thrombocytopenia is usually present but the leucocyte count is
increased with slight shift to left of myeloid cells.
Causes of bone marrow infiltrations include
Haematologic malignancies e.g. leukaemia, lymphoma, myeloma
Metastatic deposits from non-haernotologic malignancies (e.g. cancerbreast, stomach, prostate, lung, thyroid)
Advanced tuberculosis
Primary lipid storage disease (Gaucher's and Niemann-Pick's disease)
Osteopetrosis and myelofibrosis (rarely)

Is characteristics of myelophthistic anemia


A variety of misshappen erythrocytes along with WBC seen
There is infiltration of bone marrow with tumour, fibrosis, or granulomas
None of the above

136

Decreased Ferritin is seen in

A; (Iron deficiency anemia):


Test
Iron
Chronic
deficien disorde
cy
rs
1. MCV,
Low

MCH,
normal
MCHC
to
reduced

2. S.

Thallass
aemia
Very

Normal

Siderobl
astic
anaemia
(excep
t MCV
raised
in
acquire
d type)

iron
3. TIBC
4. S.
ferritin

5.
Marrow
-iron
stores
6. Iron
in
normob
last
7. Hb
electrophoresi
s

Normal
Normal

Absent

Present

Present

Absent

Absent

Present

Normal

Normal

Normal

Abnorm
al

Normal

Normal

(comple
te
saturati
on)
Present
Ring
siderobl
asts

Iron deficiency anemia


Anaemia of chronic infection
-thalessenmia trait
Sideroblastic anemia

137

Sideroblastic anaemia, TRUE is

A; (X-linked disorders):
HEREDIT ARY SIDEROBLASTIC ANAEMIA - rare X-linked disorder
associated with defective enzyme activity of aminolevulinic acid (ALA)
synthetase required for haem synthesis. The affected males have
moderate to marked anaemia while the females are carriers of the
disorders and do not develop anaemia. The conditions manifests in
childhood or in early adult life.

X-linked disorder
Autosomal dominant
Autosomal recessive
Y-linked disorder

138

All are true about Papillary carcinoma, EXCEPT

B; (Invades blood vessels early):


Papillary carcinoma of thyroid - slow growing malignant tumour.
Involvement of the regional lymph nodes is common but distant
metastasis to the organs are rare
In minority of patients hematogenous metastasis are present at the
time of diagnosis, most commonly in the lung.
Contrasting Features of Main Histologic Types of Thyroid Carcinoma
Features
Papillar
Follicul Medull Anapla
y
ar
ary
stic
carcino
carcino carcino carcino

1. I.
Frequency
2. Age

3.
Female/m
ale ratio
4. Cell of
origin
5. Gross

6.
Pathogno
monic
microscop
y

7. Regional
metastasis
8. Distant
metastasis
9. 10-year
survivals

ma
75-80%
(MC)
All ages

3:1

Follicula
r
Small,
multi
focal

Nuclear
features,
papillar
y
pattern
Psammo
ma
bodies
Commo
n
Rare
80-95%
(Goodprognos
is)

ma
1020%
Middle
to old
age
2.5:1

ma
5%

ma
5%

Middle
to old
age
Familia
l to 1:1

Old age

Follicul
ar
Moder
ate
size,
nodula
r
Vascul
ar and
capsul
ar
invasio
n

Parafol
licular
Moder
ate
size

Follicul
ar
Invasiv
e
growth

Solid
nests,
amyloi
d
stroma

Undiffe
rentiat
ed,
spindle
shaped
, giant
cells

Rare

Comm
on
Rare

Comm
on
Comm
on
5-10%
(media
n
surviva
l about
2
months
)

Comm
on
5070%

6070%

1.5: 1

Multicentric
Invades blood vessels early
M.C. malignancy after radiation
Good prognosis

139

Found in Wiscot-aldrich syndrome are A/E

D; (Autosomal disorder):
WISKOTT-ALDRICH-SYNDROME - It is an X-linked recessive disease
characterized by thrombocytopenia, eczema and a marked vulnerability
to recurrent infections, ending in early death.
Patients do not make antibodies to polysaccharide antigens and
the response to protein antigen is usually poor.

IgM levels in the serum are low, but the levels of IgG are usually
normal. Paradoxically the levels of IgA and IgE are often elevated.
Patients are prone to developing malignant lymphomas.
The Wiskott-Aldrich syndrome maps to Xp 11-23 where the
gene encoding Wiskott-Aldrich syndrome protein (WASP) is
located
The only treatment is bone marrow transplantation.
Thrombocytopenia
Eczema
Bone marrow transplantation is curative
Autosomal disorder

140

In MEN II B, included are A/E

A; (Hyperparathyroidism):

Hyperparathyroidism
Marfanoid feature
Medullary thyroid carcinoma
Pheochromocytoma

141

Most common type of pathological changes seen in Rabies

D; (Brain stem encephalitis):


Rabies is a severe encephalitis transmitted to humans by the bite of a rabid
animals
Morphology - M/E examination the brain shows intense edema and vascular
congestion
There is wide spread neuronal degeneration and an
inflammatory reaction that is most severe in the
rhombencephalon (midbrain, and floor of the fourth ventricles
particularly in the medulla)
*Negri bodies the pathognomic microscopic finding are cytoplasmic round to
oval, eosinophilic inclusions that can be found in pyramidal neurons of the
hippocampus and Purkinje cells of the cerebellum, sites usually devoid of
inflammation.

Meningitis
Cranial arteritis
Ventriculitis
Brain stem encephalitis

142

Serum vitamin B12 level increased in all EXCEPT

D; (Cholestatic jaundice):
The major source of vitam en BIZ loss is via bile and shedding of intestinal
epithelial cells.
Vitamen B12 deficiency
Decreased intake - Inadequate diet vegetarianism
Impaired absorption
Intrinsic factor deficiency
Pernicious anaemia
Gastrectomy
Malabsorption states
Diffuse intestinal disease eg lymphoma,

systemic sclerosis, ileal resection, i1eatis


Competitive parasitic uptake Fish
tapeworm infestations
Bacterial overgrowth in blind loops and
diverticula of bowel
Increased requirement - Pregnancy, hyperthyroidism, disseminated cancer

Hepatitis
Cirrhosis of liver
Hepatocellular carcinoma
Cholestatic jaundice

143

Normal platelet count is found in

B; (H. S. purpura):
HENOCH-SCHONLEIN PURPURA
- (Anaphylactoid purpura)
Most common systemic vasculitis in children
Typical features are - Palpable purpura, abdominal pain, arthritis,
and hematuria
Pathological features include -leukocytoclastic vasculitis with IgA
deposition
Biopsy of the kidney reveals segmental glomerulonephritis with
cresent and mesangial depositional IgA
** All coagulation tests are normal
Causes of Thrombocytopenia
[A]BM-disorder - Aplastic anemia, Hematologic malignances, Myelodysplasia,
Megaloblastic anemia, chronic alcoholism
[B] Nonmarrow disorders - Immune disorders-Idiopathic thrombocytopenic
purpura Drug induced, secondary (CLL, SLE) Post transfusion purpura
Hypersplenism, DIC, Thrombotic thrombocytopenic purpura. Hemolytic
uraemic syndrome, Sepsis, Hemangioma, Viral infections, AIDS, Liver failure

Wiskott-aldrich syndrome
H. S. purpura
Immune thrombocytopenia
Mayer-Rokitansky - K.H. syndrome

144

Anemia of chronic disease is characterised by all EXCEPT

C; (Decreased serum ferritin levels):


Test
Iron

Anemia
deficien
of
Thalasse
cy
mia trait chronic
disease
Serum

iron

TIBC

Serum
ferritin

Red cell

Siderobl
astic
anemia

protopo
rphyrin

N
N

HbAz
Common causes includes - Chronic infections or inflammation cancer
and liver disease

Serum iron level


TIBC
Serum ferritin level
Increased macrophages iron in marrow

145

Amyloid is

C; (Glycoprotein):
AMYLOID - chemical analysis reveals the complex nature of amyloid
(heterogenous) 2 main types of complex proteins
1. Fibril proteins comprise about 95% of amyloid
2. Non-fibrillar components which include P-Component
These are mainly glycoproteins

Mucopolysaccharide
Lipoprotein
Glycoprotein
Intermediate filament

146

Irreversible injury in cell is

A; (Deposition of Ca++ in mitochondria):


Reversible cell Injury
1. Endoplasmic reticulum distension of cisternae by
fluid and detachment of
membrane bound
polyribosomes from
surface of RER
2. Mitochondria mitochondrial swelling and
phospholipid rich
amorphous densities
3. Plasma membrane - Loss of
microvilli and focal
projections of the
cytoplasm (blebs)
4. Myelin figures
5. Nucleolus - There is
segragation of granular
and fibrillar components of
nucleolus and reduced
synthesis of ribosomal
RNA clumped nuclear
membrane

Deposition of Ca ++ in mitochondria
Swelling
Mitotic figure

Irreversible cell injury


1. Lysed ER

2. Mitochondrial dysfunction
- mitochondrial swelling
& calcifications (large
cytosolic influx of Ca++
ion occurs)
3. Membrane damageliberation of the
intracellular enzyme
(Important factor)
4. Nuclear changes (Pyknosis,
Karyolysis, Karyorrhexis)
5. Damage to lysosomal

membrane is followed
by liberation of
hydrolytic enzymes
6. Basophilia ( RNP) and
protein digestion

Ribosomes detachment

147

Commonest site of varices in portal hypertension is

A; (Oesophagus): Oesophageal varices are tortuous, dilated and engorged,


oesophageal veins seen along the longitudinal axis of oesophagus. They occur as a
result of elevated pressure in the portal venous system, most commonly in
cirrhosis of the liver. Less common causes are portal vein thrombosis, hepatic vein
thrombosis (Budd-Chiary syndrome) and pylephlebitis
The increased venous pressure in the superficial veins of the oesophagus may
result in ulceration and massive bleeding

Oesophagus
Anal canal
Periurnblical
Liver

148

Salt losing nephritis is due to

C; (Interstitial nephritis):
Interstitial nephritis - 'Essential of Diagnosis'
Fever
Transient maculopapular rash
Pyuria (including eosinophiluria) white blood cells casts and hematuria.
Acute interstitial nephritis accounts for 10-15% of cases of intrinsic renal failure.
Although drugs account for over 70% of cases it also occurs in infections diseases,
immunological disorders or as an idiopathic conditions.

Lupus nephritis
Streptococcal infection
Interstitial nephritis
G.P. syndrome

149

According to WHO class II lupus are

C; (Hematuria):
LUPUS-NEPHRITIS - The two cardinal manifestations are proteinuria & hematuria.
In additions hypertension and casts of different types such as RBC, fatty casts and
leucocytes cast in the urinary segments are found. WHO classified lupus nephritis
as
Class I (no-histologic changes)
Class II (Proliferative changes confined to mesangium)
Class III (Proliferative changes in tufts of 10 to 50% of
glomeruli higher proportions of glomeruli
affected suggest worse prognosis)
Class IV
[Diffuse proliferative glomerulonephritis
(DPGN) affecting> 50% of glomeruli]
Class V
[Predominantly membranous changes with
various degrees of proliferation]
Class VI
[End stage, scarred glomeruli]

Transient protenuria
Massive protenuria
Hematuria
RBC-cast

150

Centrilobular necrosis occur in

(CCI4):
DRUG & TOXIN-INDUCED HEPATIC INJURY

Hepatocellular damage
1. Microvesicular fatty
change
2. Macrovesicular fatty
changes
3. Centrilobular necrosis

4. Diffuse or massive
necrosis

5. Hepatitis-cirrhosis

6. Fibrosis-cirrhosis

7. Granuloma formation

8. Cholestasis (with or
without hepato cellular
injury)

Examples
Tetracyclines, salic lates,
ellow has horus ethanol
Ethanol, methotrexate,
amiodarone
Bromobenzene, CCI4,
acetaminophen, Halothane,
rifampin
Halothane, isoniazid,
acetaminophen,
methyldopa,
trinitrotoluene, Amanita
phulloides (mushroom)
toxin
Methyldopa, isoniazid,
nitrofurantoin, phenytoin,
ox henisatin
Ethanol, methotrexate,
amiodarone, most drugs
that causes chronic he atitis
Sulfonamides,
methyldopa, quinidine, hen
lbutazone, hydralazine,
allopurinol
Chlorpromazine, anabolic
steroids, erythromycin

Phosphorous
Phenol
Arsenic
Mercury

151

Secondary granules found in neutrophil is

D; (Lactoferin):
The specific or secondary granules contain unique constituents such as
1. Lactoferrin
2. Vitamin B12 - binding protein
3. Membrane components of NADPH oxidase
Histaminase

Catalase
Gangliosidase
Proteolytic enzyme
Lactoferin

152

All are malignant in nature EXCEPT

A; (Juvenile polyp):
Polyps and Tumours of the Large Intestine

I Colorectal polyps
A. Non-neoplastic polyps
1. Hyperplastic (metaplastic) polyps
2. Hamartomatous polyps
i. Peutz Jeghers polyps and polyposis
ii. Juvenile (Retension) polyps and polyposis

3. Inflammatory polyps (Pseudopolyps)


4. Lymphoid polyps
B. Neoplastic polyps
1. Adenoma
i. Tubular adenoma (Adenomatous polyp)
ii. Villous adenoma (villous papilloma)
iii. Tubovillious adenoma (Papillary adenoma, villoglandular adenoma)
2. Polypoid carcinoma
C. Familial polyposis syndrome
1. Familial polyposis coli (Adenomatosis)
2. Gardner's syndrome
3. Turcot's syndrome
4. Juvenile polyposis syndrome
II Other benign colorectal tumours
(Leiomyomas, leimyoblastoma, neurilemmoma, lipoma and vascular
tumours) rn Malignant colorectal Tumours
A. Carcinoma
1. Adenocarcinoma
2. Other carcinoma (Mucinous adenocarcinoma signet ring cell CA,
Adenosquamous CA, undifferentiated CA)
B. Other malignant tumours
(Leiomyosarcoma, malignant lymphoma, Carcinoid tumours*)

Juvenile polyp
Familial polyp
Carcinoid tumour
Villous adenoma

153

Normocytic normochromic anemia is seen in all EXCEPT

D; (Thalassemia):
MORPHOLOGIC CLASSIFICATIONS
MICROCYTIC
HYPOCHROMIC
MCV, MCH, MCHC
are all reduced
Causes
Iron deficiency
Sideroblastic
anaemia
Thalassaemia
Pyridoxin
responsive
anaemia
Lead poisoning

NORMOCYTIC
NORMOCHROMIC
MCV, MCH, MCHC,
are all normal
Causes
Acute blood loss /
hemolysis
Haemolytic
anaemias
- Pure red cell
aplasia
- Aplastic anemia
Chronic renal or

MACROCYTIC
NORMOCHROMIC
MCV is raised

Causes
Vitamin BI2 or folic
acid deficiency

Copper deficiency
HbE disease
Anaemia of
chronic disorders

liver disease
Bone marrow
failure
Physiological
anemia of infancy
Hypothyroidism
Myeloproliferative
disorders

Aplastic anemia
Chronic renal disease
Pure red cell aplasia
Thalassemia

154

Most specific and sensitive marker of ANCA is seen in

A; (Idiopathic cresentric glomerulonephritis):


Rapidly Progressive Glomerulonephritis (RPGN)
Type I RPGN
Type II
Type III RPGN
(Anti GBM
RPGN (Immune
(Pauci-Immune)
antibody)
comlex)
Idiopathic
Idiopathic
ANCA
associated
Good pasture
Post infections
syndrome
Idiopathic
SLE
Wegner's
Henochgranulomatosis
Schonlein
purpura (IgA)
Microscopic
polyarteritis
Others
nodosa
(microscopic
poly angiitis)

In many cases, however, pauci-immune cresenteric glomerulonephritis is


isolated and hence idiopathic. More than 90% of such idiopathic cases have
cANCA or pANCA in the sera.
The presence of circulating ANCAs in both idiopathic RPGN and cases of RPGN that
occurs as a component of systemic vasculitis

Idiopathic cresenteric GN
Post streptococcal GN
Membranoproliferative GN
Focal segmental glomerulosclerosis

155

Most common cause of renal papillary necrosis is

C; (Diabetes-mellitus):
RENAL-PAPILLARY NECROSIS - When infections of the renal pyramids
develops in association with vascular disease of the kidney or with urinary
tract obstruction, renal papillary necrosis is likely to result

Patients with Diabetes, sickle cell disease, chronic alcoholism, and vascular

disease seem peculiarly susceptible to this complications


Hematuria, pain in the flank or abdomen and chills and fever are the most
presenting symptoms (1720-H) Analgesic nephropathy is a chronic renal disease
caused by excessive intake of analgesic mixtures (Aspirin & phenacetin) and
characterised morphologically by chronic tubulointerstitial nephritis with renal

papillary necrosis (1003-R)

Analgesic nephropathy
Sickle cell disease
Diabetes mellitusC
Chronic pyelonephritis

156

A 76 year old male presented with anemia with splenomegaly. PBS shows tear
drop shaped cells, bone marrow examination reveals normal. The diagnosis

A; (Myelofibrosis):
Myelofibrosis with myeloid metaplasia also known as agnogenic (of
unknown origin) myeloid metaplasia primary myelofibrosis and
myelosclerosis is characterized by proliferation of neoplastic stem cells at
multiple sites outside the bone marrow (i.e. extramedullary haematopoiesis)
especially in the liver and spleen
Essentials of Diagnosis
Striking splenomegaly
Tear drop poikilocytosis
on PBS
Leukoerythroblastic
blood picture giant
abnormal platelets
Hypercellular bone
marrow with reticulin on
collagen fibrosis

PBS - bizarre red cell shapes,


tear drop poikilocytes,
basophilic stippling,
nucleated red cells
immature leukocytes (i.e.
leukoerythroblastic
reaction) basophilia and
giant platelet forms
BM-aspiration - is generally
unsuccessful and yield "dry
tap"

Biopsy - shows focal areas of hypercellularity and increased network and variable
amount of collagen in which clusters of megakaryocytes

Myelofibrosis
Iron deficiency anemia
Folic acid deficiency
CML

157

ANCA antibody with peripheral rim distribution is seen in

C; (Anti double stranded DNA):


Four basic pattern of nuclear fluorescence suggests the type of antibody present
in the patients serum of SLE

Homogeneous or diffuse nuclear staining - usually reflects


antibodies to chromatin, histones and occasionally, doublestranded DNA
Rim or peripheral staining patterns are most commonly indicative of
antibodies to double-stranded DNA

Speckled pattern refers to the presence of uniform or variable sized


speckles. This is one of the most commonly observed patterns of
fluorescence and therefore the least specific. It reflects the presence of
antibodies to non-DNA nuclear constituents. Example include Sm
Antigen, ribonucleo protein and SS-A and SS-B reactive antigens
Nuclear pattern refers to the presence of a few discrete spots of fluorescence
within the nucleus and represents antibodies to nucleolar RNA. This pattern is

reported most often in patients with systemic sclerosis

Antihistone antibody
Anti smith antibody
Anti double stranded DNA
Anti double stranded RNA

158

Which of the following is an evidence of hematuria of glomerular origin

B; (Dysmorphic RBC):
Dysmorphic (irregularly shaped) cells have an uneven distribution of hemoglobin
and cytoplasm and usually indicate glomerular origin

Haemoglobinuria
Dysmorphic RBC
Bright RBC
Fine RBC

159

Most common vascular tumour in AIDS

A; (Kaposi's sarcoma):
Patients with AIDS have a high incidence of certain tumours especially
Kaposi sarcoma (KS), non-Hodgkin B cells lymphoma, cervical cancer in
women and anal cancer in men.
KS is a vascular tumour that is otherwise rare in US is the most common
neoplasm in patients with AIDS.
The lesion of KS are characterised by the proliferation of spindle shaped cells that
express markers of both endothelial (vascular or lymphatic) and smooth muscle
lineages. There is also a profusion of slit-like vascular spaces, suggests that the
lesions may arise from primitive mesenchymal precursors of vascular channels.

Kaposi-sarcoma
Angio sarcoma
Lymphangioina
Lymphoma

160

Charateristics microscopic features of Osteogenic sarcoma is

B; (Osteoid formation by mesenchymal cells with pleomorphism):


Osteosarcoma is defined as a malignant mesenchymal tumour in which the
cancerous cells produce bone matrix
It is the most common primary malignant tumour of bone, exclusive of
myeloma and lymphoma and account for approximately 20% of primary bone
cancers.
Most common subtype is osteosarcoma that arises in the metaphysis of
long bones; is primarily solitary, intramedullary and poorly
differentiated; and produces a predominantly bony matrix
The formation of bone by the tumour cells is characteristic of osteosarcoma. The
neoplastic bone has a coarse, lacelike architecture but is also deposited in broad
sheets or as primitive trabeculae other matrices, including cartilage or fibrous
tissues may be present in varying amounts.

Osteoid formation
Osteoid formation by mesenchymal cells with pleomorhism
Codman's triangle
Predominant osteoclast

161

Thyrotoxicosis with a low uptake of iodine in the thyroid bed but uptake in the

D; Ovarian teratomas can contain thyroid tissue (struma ovarii) and

pelvis can be seen with which of the following?

rarely cause thyrotoxicosis with excess thyroid hormone produced by the


teratoma rather than the thyroid.

Graves' disease
Jod-Basedow phenomenon
Choriocarcinoma
Struma ovarii

162

A low TSH, high T4, and high T3 suggests which of the following diagnosis

A; Low TSH with high T4 and T3 or T3 alone (T3 toxicosis) reflects


hyperthyroidism.

Hyperthyroidism
Nonthyroidal illness (sick euthyroidism)
Estrogen therapy
Subclinical hypothyroidism

163

A patient with thyroid cancer is told that he has a life expectancy of less than 6
months from diagnosis. The variety of thyroid cancer with this prognosis is
which of the following?
Thyroid lymphoma

D; The prognosis of anaplastic cancers, which likely represent


dedifferentiation of better differentiated papillary or follicular
carcinomas, is very poor with average survival less than 6 months.

Medullary thyroid carcinoma


Papillary thyroid carcinoma
Anaplastic thyroid carcinoma

164

On the basis of physical findings, you suspect a 48-year-old woman has


acromegaly. The definitive diagnostic test for acromegaly is measurement of
growth hormone in which of the following settings
Random

D;

TRH stimulation test


Insulin tolerance test
Oral glucose tolerance test

165

You confirm acromegaly in a 58-year-old woman, and a MRI of the pituitary


shows a microadenoma. Which of the following is the best choice for treatment?

A; Transsphenoidal surgery has the advantages of potential cure with


rapid therapeutic response. If the tumor is completely resected, the
patient may experience a complete cure. Medical therapy with
somatostatin agonist or bromocriptine is helpful, but the patient is
dependent on medical therapy indefinitely. Irradiation takes years for full
effectiveness and the patient may develop hypopituitarism. Transfrontal
surgery is rarely used now.

Transsphenoidal surgery
Medical therapy with somatostatin agonist
Irradiation
Medical therapy with bromocriptine

166

A 47-year-old man presents with headache, impotence, and galactorrhea for the
past 2 months. Which of the following is a likely hormonal profile on this
patient?

D; Men frequently present with marked hyperprolactinemia from a


macroadenoma. Presenting manifestations typically are sexual
dysfunction and decreased libido. The prolactin causes decrease in LH and
concomitant decrease in testosterone. Thus, the patient will have a high
prolactin associated with a low LH and low testosterone. The pattern of

low testosterone, high LH, and low prolactin is typical of primary


hypergonadism.
Low testosterone, high LH, and low prolactin
Low testosterone, low LH, and low prolactin
Low testosterone, high LH, and high prolactin
Low testosterone, low LH, and high prolactin

167

A 26-year-old woman has been amenorrheic for 2.5 months. Which of the
following is the most appropriate first choice for diagnostic evaluation

A; The first choice in testing in this patient is a pregnancy test. If her


prolactin level was measured without a pregnancy test, an elevation of
prolactin could be wrongly considered primary rather than due to
pregnancy. The other tests of LH, estradiol, progesterone are not first
choices in the evaluation of amenorrhea.

Hcg
LH
Estradiol
Prolactin

168

A 40-year-old man has erectile dysfunction. He is noted to have


hyperprolactinemia (prolactin of 400 g/L). On MRI a macroadenoma with
supersellar extension is found. Which of the following is the best course of
therapy for the patient

A; Established therapy of hyperprolactinemia from a pituitary adenoma is


treatment with a do-pamine agonist such as bromocriptine. Surgical
therapy usually does not result in a cure in a macroadenoma and is
reserved for those patients who are intolerant to dopamine agonist.
Transfrontal surgery is rarely used. Somatostatin agonist and thyroxine
have little effects on hyperprolactinemia.

Medical therapy with bromocriptine


Transsphenoidal surgery
Transfrontal surgery
Medical therapy with somatostatin agonist

169

A 35-year-old man has a prolactinoma and a history of severe peptic ulcer


disease. There is a family history of pituitary tumors. The findings of what other
diagnostic test at this time may be abnormal and potentially useful in diagnosis

B; This patient may have multiple endocrine neoplasia syndrome-1, which


presents with pituitary tumors, pancreatic tumors, and
hyperparathyroidism. With the history of severe peptic ulcer disease
(possible Zollinger-Ellison syndrome) and family history of pituitary
tumors, one must suspect MEN-1. A serum calcium will be useful in
diagnosing potential hyperparathyroidism. Calcitonin and urinary
metanephrines are elevated and characteristic of MEN-2. Serum ferritin
and fasting blood sugar would be elevated in hemochromatosis.

Fasting blood sugar


Serum calcium
Serum calcitonin
Urinary metanephrine

170

A 65-year-old man with a lung mass has increasing skin pigmentation and
significant muscle weakness and wasting. Urinary free cortisol is 690 g/24 h (10
to 80) and is nonsuppressible. Which of the following tests would probably be
most diagnostic
ACTH stimulation test
MRI of the pituitary

D; This patient's presentation suggests ectopic ACTH secretion and ACTH


will likely be elevated above 300. A MRI of the pituitary and CT of the
abdomen are not useful, because the source of ACTH is from the small cell
carcinoma in the lung mass.

CT of the abdomen
Plasma ACTH

171

A 23-year-old woman presents with weakness and amenorrhea. She is clinically


hypothyroid. A CT scan of the pituitary shows an expanded sella with a large
cystic component with calcifications. Which of the following is the most likely
diagnosis

C; This is the common CT finding and clinical presentation for


craniopharyngioma. Empty sella does not usually cause marked
enlargement of the sella, and there is no cystic structure with calcification.
Pituitary macroadenomas can expand the sella but are not commonly
cystic and calcified. Optic glioma and hypothalamic hamartoma are rarely
cystic

Pituitary macroadenoma
Empty sella syndrome
Craniopharyngioma
Optic glioma

172

A 45-year-old man has decreased libido and erectile dysfunction. He has noted
increasing pigmentation. He has developed liver disease and arthropathy
recently. Which of the following is the best diagnostic test

D; The patient has classic manifestations of hemochromatosis that


impairs hypothalamic pituitary function. Serum ferritin is potentially
diagnostic in this patient. All the other tests are not diagnostic for
hemochromatosis.

Serum TSH
Serum calcium
Serum prolactin
Serum ferritin

173

A patient has an excess of 17 -hydroxyprogesterone and 17 hydroxypregnenolone in the urine, and no androgens. Which of the following
enzymes is deficient

D; 20,22-Desmolase changes cholesterol to pregnenolone. 3 hydroxysteroid dehydrogenase changes pregnenolone to progesterone


and 17 -hydroxypregnenolone into 17 -hydroxyprogesterone. 17Hydroxylase changes pregnenolone and progesterone into 17 hydroxypregnenolone and 17 -hydroxyprogesterone, respectively. 17,20Desmolase changes 17 -hydroxypregnenolone into
dehydroepiandrosterone (a weak androgen) and 17 hydroxyprogesterone into androstenedione (a weak androgen). 17ketoreductase changes dehydroepiandrosterone and androstenedione to
androstenediol and testosterone, respectively.

20,22-Desmolase
3 -Hydroxysteroid dehydrogenase
17-Hydroxylase
17,20-Desmolase (17,20 lyase)

174

A 28-year-old woman presents to the office with 2 days of abdominal pain and a
positive pregnancy test. Her last menstrual period was 9 weeks ago. She reports
no dysuria. She reports a history of two episodes of pelvic inflammatory disease.
Which of the following is the most likely cause of the abdominal pain

Endometriosis
Urinary tract infection

C; Pelvic inflammatory disease is a cause of tubal scarring, setting the


stage for an ectopic (tubal) pregnancy. As the pregnancy grows, the tube
is stretched, causing pain. Endometriosis causes pain with each menstrual
cycle, which is not the case here. Urinary tract infection can cause pain,
but she would be expected to have dysuria. Placental abruption occurs
only after 20 weeks of pregnancy. She is clearly not premenstrual,
because she is pregnant.

Ectopic pregnancy
Placental abruption

175

A 38-year-old woman comes into the office with complaints of amenorrhea for 6
months, with increased cold intolerance, loss of energy, and hair loss. Her
menses were normal until this episode started, and she has also gained 22
pounds over these 6 months. Her pregnancy test is negative. Which of the
following tests should you now order
FSH and LH

D; Hypothyroidism is the cause of this patient's amenorrhea. Classic


findings of hypothyroidism presented here are increased cold intolerance,
loss of energy, hair loss, and weight gain. TSH is the best test for this
disorder, and it would be increased in the hypothyroid patient

Estrogen levels
Testosterone level
TSH

176

A 19-year-old woman comes to the office complaining of galactorrhea. She has


never been pregnant. Which of the following hormones is most likely to be
responsible for this situation

A; Prolactin is the major stimulator of breast milk production.


Overproduction of prolactin leads to galactorrhea. Estrogen,
progesterone, thyroxine, and cortisol are all needed for proper breast
development but play no role in actual milk production

Prolactin
Estrogen
Progesterone
Thyroxine

177

A 15-year-old male comes into the office complaining about a lack of pubic hair
growth. He also informs you that his voice has not yet deepened, and he has no
interest in sexual activity. He is an only child. Blood drawn reveals a very high
testosterone level. Which of the following is the most likely problem

C; Androgen insensitivity can present as an inability for a male child to go


into puberty. Low FSH and LH are expected to yield low testosterone
levels. High FSH and LH are usually markers of end organ damage and
lack of feedback of testosterone on the pituitary due to low levels. Puberty
can be delayed by hypothyroidism, with FSH and LH usually appropriate
to the testosterone level. XXY karyotype (Klinefelter's) often has no effect
on testosterone level

Low FSH and LH


High FSH and LH
Androgen insensitivity
Hyperthyroidism

178

A 31-year-old male presents to the office due to infertility. On history, it is


revealed that he has Kartagener's syndrome. Which of the following is the most
likely cause of his infertility

B;
Kartagener's syndrome is also known as the immotile cilia syndrome.
Asthenospermia or poor sperm motility is due to missing dynein arms, the
basic defect of Kartagener's syndrome. Kartagener's syndrome has no
effect on either sperm count or basic anatomy of the male reproductive
tract

Oligospermia
Asthenospermia
Absence of the vas deferens
Epididymal obstruction

179

In which ovarian compartment is plasminogen activator produced

A; Plasminogen activator is produced in the granulosa. Other endocrine


and paracrine products of the granulosa include Mllerian-inhibiting

substance, activin, inhibin, follicle regulatory protein, insulin-like growth


factor-1, epidermal growth factor-like, platelet-derived growth factor,
proopiomelanocortin, and gonadotropin surge-inhibiting factor. Some of
these are produced also in other ovarian compartments, such as inhibin in
the theca and corpus luteum, follicle regulatory protein in the follicular
fluid and theca, and epidermal growth factor-like in the theca
Granulosa
Theca
Follicular fluid
Follicles

180

In which ovarian compartment is basic fibroblast growth factor produced

D; Basic fibroblast growth factor is produced in the corpus luteum. Other


endocrine and paracrine products of the ovarian compartments include
the following: from the granulosa: Mllerian-inhibiting substance, activin,
inhibin, follicle regulatory protein, insulin-like growth factor-1, epidermal
growth factor-like, platelet-derived growth factor, proopiomelanocortin,
and gonadotropin surge-inhibiting factor; from the theca: transforming
growth factor- and transforming growth factor- , renin, inhibin, and
relaxin; and from the follicular fluid: luteinizing inhibitor and luteinizing
stimulator, oocyte meiosis inhibitor, follicle regulatory protein, and
rennin

Granulosa
Theca
Follicular fluid
Corpus luteum

181

A 31-year-old man whom you treated for alcoholic intoxication at the emergency
room 2 days ago comes to your office because he wants another opinion about
his infertility. He has seen other physicians for this condition. Considering his
excessive alcoholic intake for the past decade. Which of the following is the likely
site of his infertility

B; Testicular causes are those with a direct effect on the testicles. Alcohol
directly affects the testicles causing atrophy with inadequate sperm
production. It also causes decreased plasma testosterone. Posttesticular
causes are those that affect sperm transport, and pretesticular causes are
those that affect the hormones that stimulate the testicles. Idiopathic
causes represent those causes that are likely genetic and not elsewhere
classified

Pretesticular
Testicular
Posttesticular
Idiopathic

182

Cancer cachexia ia attributed to the action of:

C;

IL 2
IL 4
TNF-a
TNF-

183

While in the ICU, you are called to your patient's bedside because of the
development of seizure activity in a ventilator patient with nosocomial

D; -Lactam antibiotics, in particular high-dose penicillin G and imipenin,


are known to induce seizures especially in the face of renal dysfunction.

pneumonia. You review the situation including the medication record. The
patient is currently receiving dopamine, one-half normal saline, imipenem/
cilastatin, tobramycin, lisinopril, clonidine patch, and famotidine. The
laboratory test results from this morning show normal electrolytes, except for a
mildly elevated creatinine of 2.4 that is chronic, and CBC shows an improving
white blood count of 15,000. After stopping the acute seizure event, which of the
following is the most appropriate next step in preventing further seizures
Stop dopamine

Acute treatment of the seizure would be the same as for any other source
of seizure. Other medications could contribute to lowering seizure
threshold via lowering the magnesium level (such as diuretics). The use of
phenytoin should not be necessary unless recurrent events occur. The CT
of the head is reasonable; however, the discontinuation of the -lactam
would be the first step.

Stop clonidine
Intravenous phenytoin
Change antibiotic coverage

184

A 64-year-old man complains of a resting tremor that lessens with intentional


movement and that causes him substantial embarrassment. Which of the
following is the likely cause

A; The tremor of Parkinson's disease is a coarse resting tremor that


decreases with intentional movement. Cogwheel rigidity occurs in
Parkinsonism. By contrast, the tremor of hyperthyroidism is very high
frequency and fine, and it does not depend on rest or movement. In
hepatic encephalopathy, the "flapping" tremor of asterixis is seen. Drugrelated tremors are usually seen with -2 agonists and methylxanthines.
These are frequently of abrupt onset and time related to the usage or
dosage adjustment with these medications.

Parkinson's disease
Essential tremor
Asterixis
Hyperthyroidism

185

A 45-year-old man who has consumed excess alcohol for at least 20 years is seen
for evaluation of progressive difficulty in walking. He has an ataxic gait and his
muscles are generally hypotonic. He has an intention tremor in his arms and legs
and he also demonstrates "past pointing." His primary brain pathology will be
found in which part of the brain
Occipital cortex

C; The cerebellum functions as a coordinating center for the maintenance


of muscle tone and the regulation of motor tasks. It does not supply nerve
impulses to directly cause muscles to contract

Temporal lobe
Cerebellum
Brainstem

186

A patient who has been diabetic for 15 years comes to your office complaining of
a burning or tingling sensation in both of his feet and the lower aspects of both
legs, which bothers him especially at night. Which of the following is the most
likely diagnosis

C; Numerous localized disorders and many systemic diseases can damage


the spinal cord or the peripheral nerves. The pattern of pain, sensory loss,
and sometimes weakness can help classify the disorder. A
mononeuropathy involves pain/temperature and vibratory/joint position
abnormalities, along the precise path of an individual nerve with
associated weakness and pain. Mononeuropathy multiplex involves
multiple noncontiguous peripheral nerves in a sequential fashion taking
place over days to years. A radiculopathy involves a nerve root with
dermatome distribution of both pain/temperature and vibratory/joint
position abnormalities and weakness of the innervated muscles. BrownSquard's syndrome also involves pain/temperature and vibratory/joint
position abnormalities; however, the distribution is ipsilateral
pain/temperature and contralateral vibratory/joint position

abnormalities with an ipsilateral motor deficit. A polyneuropathy


similarly involves pain/temperature and vibratory/joint position
abnormalities with a stocking-glove distribution and painful
paraesthesias.
Mononeuropathy
Brown-Squard's syndrome
Polyneuropathy
Mononeuropathy multiplex

187

A 2-year-old boy is brought to your office by his parents who believe he may not
have normal hearing. You determine that he has congenital damage to the left
cochlea. This is classified as which of the following

B; Sounds must be conducted through the middle ear and sensed by the
cochlea and CN VIII; then they are processed by the cochlear nuclei and
CNS pathways. Conductive deafness is hearing loss due to external
auditory canal or middle ear disease. Sensineural deafness is a perceptive
loss of hearing due to disease of the inner ear or eighth nerve. In
conductive deafness, bone conduction is better than air conduction, and
the reverse is the case for sensineural deafness. Central deafness is caused
by disease affecting the central auditory pathways. Tinnitus an annoying
noise in the ear that is usually benign, often is caused by cochlear or
eighth nerve disorders. Hearing may be diminished, but the patient is not
rendered fully deaf. Presbyacusis is hearing loss due to advanced age.

Conductive deafness
Sensorineural deafness
Central deafness
Tinnitus

188

Which cerebral artery is blocked in an ischemic stroke that presents with


aphasia, right hemiparesis, and right arm numbness

D; An infarction of the left hemisphere causes weakness or paralysis and


sensory loss on the right. Most right-handed patients have their dominant
speech center on the left, and it is supplied by the middle cerebral artery,
as is the somatic motor area.

Right anterior cerebral


Right middle cerebral
Right proximal posterior cerebral
Left middle cerebral

189

Growth retardation, hypophosphatemia, and glycosuria may be associated with


which of the following

B; Type 1 RTA is a distal nephron disorder of acid excretion; nongap


metabolic acidosis and hypokalemia ensues. Common causes include
Sjgren's syndrome and hypergammaglobulinemia. Type 2 RTA is a
proximal disorder of bicarbonate reclamation; it may be associated with
Fanconi's syndrome (phosphate, amino acid, and glucose loss in the
urine). Type 4 RTA presents with hyperkalemia and is caused by diabetes
and tubulointerstitial nephropathy

Type 1 RTA
Type 2 RTA
Type 4 RTA
Diabetic nephropathy

190

A pancreatic nodular rest in small intestinal mucosa is called as:

C;

Hamartoma
Chloroma
Choristoma
Chordoma

191

Reversible loss of 'polarity with abnormality in size & shape is:

D;

Metaplasia
Hyperplasia
Anaplasia
Dysplasia

192

Benign neoplasm which is never encapsulated is:

A;

Hemangioma
Lipoma
Rhabdomyoma
Fibrous histiocytoma

193

Which of the malignant tumour rarely metastasize:

C;

Medulloblastomas
Nasopharyngeal carcinoma
Gliomas
Renal cell carcinoma

194

The characteristic nuclear feature for malignancy is:

C;

Nuclear hyperchromasia
Nuclear pleomorphism
Atypical mitosis
Bizarre tumour giant cells

195

Differentiation' between carcinoma in situ & invasive carcinoma is done by:

B;

Number of mitoses
Penetration of basement membrane
Necrosis
Anaplasia

196

Grading ofturnourls based on:

B;

Metastasis
Cellular anaplasia
Size of tumour
Extent of the tumour

197

The important factor in prognosis of malignant tumours is :


Grade of tumour
Stage of tumour

B;

Histologic type
Site of tumour

198

Carcinoma frequently metastasizing through hematogenous route is:

B;

Papillary carconima thyroid


Renal cell carcinoma
Basal cell carcinoma
Colorectal adenocarcinoma

199

Earliest site for lymph node metastases is:

D;

Sinuses
Lymphoid follicle
Medulla
Paracortex

200

Criteria for malignancy, in malignant endocrine tumours is:


Mitoses
Capsular invasion
Necrosis
Bizarre tumour giant cells

B;