Actinic Keratosis:

Psoriasis: PSORIASIS- Silvery scale, Salmon colored plaque.

Pink Papules/ Plaques/ Pinpoint bleeding (Auspitz sign)/ Physical injury (Koebner phenomenon)/ Pain.
Silver Scale/ Sharp margins
Onycholysis/ Oil spots
Rete Ridges with Regular elongation
Itching
Arthritis/ Abscess (Munro)
Stratum corneum with nuclei, neutrophils
Immunologic
Stratum granulosum absent/ Stratum Spinosum thickening.

Merylin Monro had Psoriasis. Pautrier microabscess are found in Mycosis fungoides.
Horn Cyst/Shing is found in Seborrhic Keratosis, lamellar collection of Keratin. Nuclear Atypia is found
in Actinic keratosis.
nuclear Atypia in Actinic Keratosis. Actinic/Solar keratosis are rough, Scaling papule and plaque on Sun
damaged skin. pSeudohorn in Seborrhic keratosis. Seborrhic ?Keratosis- Looks Stuck on. Sudden
appearance of Seborrhic Keratosis indicate underlying Gastric Adenocarcinoma (Leser Trelat sign).
actinic keratosiS is associated with Squamous cell carcinoma of skin. dysplastic Nevus is linked with
Malignant Melanoma.

Hypopigmentation- Cause: A PIGMENTED. Autoimmune (Vitiligo), Post inflammatory, Genetic

(Albinism), Malignancy (Malignant melanoma), Endocrine (Hypopituitarism), halo Naevus, Trauma,
Endocrine, Drugs (Hydroxychloroquine).
ALbinism is Autosomal Recessive caused by Tyrosinase Enzyme Deficiency or defective Tyrosine
transporter or defective Neural crest cells migration. ALAR TED. Vitaligo is AuToimmune.
vitalImmine.
Contusion: Skin is continuous (not broken), bruise in soft tissue by blunt object.

White Oral Plaque:

Hairy leukoplakia- associated with HIV/EBV/HPV but Benign, does not progress to cancer. But
Leukoplakia is precancerous, later turn into Squamous cell carcinoma.
Lichen Planus may present with white oral plaque. It is characterized by intense Lymphocytic infiltration
of the dermoepidermal (or Mucosal-submucosal) junction with destruction of the basal layer of cells.

Blistering Skin Disorders:

Bullus Phemphigoid- Hemidesmosome- BPH, Nonulcerative, Tense bullae, does not involve Oral
mucosa. Pemphigus vulgaris- flaccid bulla, Ulcerative, involves oral mucosa. treated by Steroid. Bullus
phemphigoid affects mainly Bura.
Erythema multiforme , Steven Johnson & Toxic epidermal necrolysis have same pathophysiology and
presentation. but Erythema multiforme is least severe, when less than 10% skin is involved. then it is SJS,
when more than 30% skin is involved then it is TEN. more than Thirty percent is Toxic epidermal
necrolysis.
acanthoSiS is thickness of Stratum Spinosum (prickle cell layer). acanthocyte-Pricke cell.

Ans: Shingle. Varicella stays at Various stage and Crops. Various stage Crops.

Urticaria
Basal & Squamous Cell Carcinoma:

BAsal cell carcinoma is also called RODent ulcer and arises from Pilosebacious Adnexa {Remember
BARODA & BAPA}. Pearly/Waxy Papule, Pallisading nuclei at Periphery. Schwan cell has pallisading
nuclei with islands of tumor cells, telangiectasia. It occurs by ultraviolet light exposure (UVB>UVA). It
occurs in Upper lip, whereas Squamous cell carcinoma occurs in Lower Lip. Farmers are at high risk for
Malignant melanoma due to prolonged exposure to ultraviolet B light. Basal cell Carcinoma occurs
mainly in Bura, Border raised.
Fig: Basal cell carcinoma.
Squamous cell carcinoma arises from Prickle cell of Malphigian layer of skin (SPM: Social and
Preventive Medicine). Squamous cell carcinoma involves Mucous but Basal cell carcinoma does not
occur in Mucus. SCC contains keratin pearl.

Arsenic causes Squamous cell carcinoma of skin, Angiosarcoma of Liver, Lung cancer.

Melanoma Characteristics ABCD. Asymmetry, Border irregularity, Color Variation, Diameter>6mm and
Dark lesion. Chromosome 9- Melanoma. Melano Noy. Melanoma is S-100 Positive. 9 Chromosome Mile
100 koreche.

Dermatophyte:
Trichophyton Tonsurans causes Tinea Capitis. Ondhokare TT khelle Chul pore jay. Wood’s lamp test
negative. Microsporum Audouinii & Microsporum Canis also causes Tinea Capitis but they are Wood’s
lamp test positive.
Trichophyton Rubrum causes Tinea Corporis (body, rubbing in the body, body malish), Tinea cruris,
Tinea pedis. Wood’s lamp test positive.

Only TT is woodlamp negative.

Nervous system pathology

MMSE
Dementia:
Lewy body dementia: two out of three symptoms to diagnose it. Memory loss/Cognitive impairment,
Parkinsonism, Psychotic symptoms such as Paranoia, Visual haLLucination, DeLusion. reLapse &
remission pattern. Lewy body is found in Limbic cortex, basal nucleus of Meynert and substantia nigra.
Combination of Alzheimer’s, Parkinsons and Psychosis. Rapidly progressive like CJ disease.

Answer: C. of midbrain.
Alzheimer’s disease: Alzheimer’s disease presents mostly with cognitive changes initially and does not
involve motor dysfunction until the later stages of the disease. Paranoia and Delusion can be present but
not hallucination until late stage. Visual hallucination is not present in Alzheimer’s disease but
characteristic of Lewy body dementia. APP is a normal transmembrane protein on chromosome 21.
Abnormal degradation of APP is crucial event in formation of Aβ amyloid in sporadic and familial
alzheimer disease, whereas increased expression of APP leads to accumulation of Aβ Amyloid in the
brains of patients with trisomy 21. Alzheimer-associated amyloid Aβ derives from proteolytic cleavage of
APP and accumulates within the core of senile plaques. Apolipoprotein E gene on chromosome 19,
presenilin-1 gene on chromosome 14 and presenilin-2 gene on chromosome 1 are responsible for most
hereditary case of AD but they have no role to develop AD in Down syndrome.
21 years e alzheimer’s hole chromosome 21, presenilin 2, 1 is involved. Elderly te hole apo E4.
Alzheimer disease patients are prone to large Lobar hemorrhage that usually begin in the parietal lobe. It
is due to Cerebral amyloid angiopathy, deposition of amyloid into the walls of cerebral blood vessels,
similar to the amyloid plaques seen in the parechyma of the brain with this disease. Amyloid makes these
vessels weak and prone to rupture. Hemorrhage from parietal lobe can spread and compress an entire
cerebral hemisphere.
if one can not perform task of independent daily living (grocery, paying bills) then it is Alzheimer’s. If
can then normal aging.
alzheiMer disease linked with basal nucleus of Meynert and hippocapmus. locus Ceruleus secretes
Catecholamine (NE), is linked with Panic attacks, Panic disorder. CeruPan. Rafe-Reticular-Rotonin
(seRotonin).
Presenile (at age 21) alzheimer’s has Presenelin gene & APP (chromosome 21) mutation. Elderly
alzheimer’s have apo E4 gene mutation. Apo E2 gene is protective.
Both APP & Presenilin gene mutations are thought to promote the production of A β-amyloid. ApoE4
protein may be involved in the formation of Senile plaques.
Tau protein- TauPick (Topic), Pick disease/frontoTemporal dementia. Pick body is highlighted by Silver
stain. Pick Silver. Neurofibrilary Tangle, found in Alzheimer’s disease, is abnormally phosphorylated
Tau protein forming paired helical filaments (PHF). Pick has Parkinsonism, Personality change,
dementia.

Lewy body dementia has Parkinsonism, haLLucination, dementia.

Multnucleated cells are findings of HIV & HSV. AIDS dementia cause Multinucleated microgleal cells.
Microglea is reservoir of HIV.
Creutzfeldt-Jacob diseae: CJD. Cornea implant, Jerky movement (Myoclonus) Rapidly progressing
Memory loss, Motor abnormality & Myoclonus is characteristic. EEG shows high voltage, slow wave.

Parkinson’s Disease: your body becomes a TRAP (Tremor at rest, cogwheel Rigidity, Akinesia or
bradykinesia and Postural instability. PARKINSONS- Pill rolling, akinesia, rigidity, kyphosis, instability,
neck titubation, shuffling gait, oculogyric crisis, nose tap (glabellar), small writing. surgical treatment of
Parkinson’s disease is Pallidotomy (globus pallidus).

Multiple Sclerosis- MS is SIIIN: Scanning speech, Intention tremor/Incontinence/Internuclear

ophthalmoplegia, Nystagmus.

Demyelinating Diseases:
GBS causes both Inflammation & Demyelination of Peripheral nerve, Carcoat Marry tooth cause only
deMyelination.
Demyelinating disease: MS, Metachromatic leukodystrophy, Progressive multifocal
leukoencephalopathy, Central pontine myelinolysis, GBS, Charcoat-Marie-Tooth disease, Acute
disseminated (postinfectious) encephalomyelitis.
Seizures:
Complex Partial Seizure: 4A- Aura, Alteration of Consciousness, Automatism, Amnesia.
Generalized Seizure: ATMS: Absence,?Atonic, ?Tonic, Tonic Clonic, Myoclonic, Status Epilepticus.
The type of seizure that would most closely resemble a fainting spell is the atonic, or drop seizure. In this
form of seizure, the patient suddenly loses muscle tone and falls to the floor. Tonic seizure is
characterized by stiffening of muscle. Tonic-clonic seizures are characterized by tonic contractions of
muscles throughout the body followed by intermittent relaxation of various muscle groups (clonic phase).
Absence seizure (Petit mal) occurs in Children (Pediatric).
Headache:
Tension headache: Two side/Bifrontal, Squeezing and Constant, no prodromal symptoms, Nausea may be
present, no photophobia, No vomiting. NSAIDS is effective.
Cluster headache: No prodromal symptoms, Episodic, Eye pain/Lacrimation, rhinorrea, always unilateral.
around eye or Temple, short duration, prefers to stay active. prevention- Ca channel blocker & 100%
Oxygen.

Migraine headache: Family history, Prodromal symptoms, with Nausea & Vomiting, prefers to stay in
dark and quiet room. Sumatriptan works in Acute stage. Methylsergide, Propranolol works in Migraine
Prophylaxis. MP works for MP.
Vertigo:

Meniere’s disease: Meniere’S TV. Sensorineural deafness, Tinnitus, Vertigo. Vertigo is due to increased
endolymphatic pressure on Crista ampullaris. Cristi r upor beshi pressure porle ore matha ghure. Stria
vascularis Secretes Endolymph.
macule of uTRICle is not sensitive in verTRICal acceleration, it is sensitive to horizontal acceleration.
Macule of sacule is sensitive to vertical acceleration.

Neurocutaneous Disorders:

Neurofibromatosis Type: Both are autosomal dominant. Type 1 is due to mutation in NF 1 tumor
suppressor gene in chromosome 17, 90% NF cases are Type 1. Type 2 is due to mutation in NF 2 tumor
suppressor gene in chromosome 22, 10% of NF cases are Type 2 . Neurofibroma, café au lait spot
(pigmented skin lesion/Deep color. whereas hypopigmented, light color ash leaf spots are seen in Tuberus
sclerosis), Meningioma, Pheochromocytoma, are common in both types. Lisch nodule (pigmented iris
hamartoma) & Multiple neurofibroma are present in NF type 1, Bilateral acoustic neuroma are present in
NF Type 2.

HemangioVLastoma- VHL.

Tuberous sclerosis- OMA- cardiac rhabdomyOMA, renal angiomyolipOMA (composed of Blood vessel,
Muscle, Lipid. RCC occurs in VHL), adenOMA sebaceum, giant cell astrocytOMA (nodular proliferation
of multinucleated atypical astrocyte). multiple hemartOMA including cortical tuber, ash leaf spot,
shagreen pach, Mental retardation, Seizaure. Tube like Sigarete produces Ash leaf spot. Ash leaf spot is
Hypopigmented lesion but Cafe-au-lait spot is Hyperpigmented lesion/Coffe colored lesion. may have
Autistic behavior. TSC1 gene on Chromosome 9 or TSC2 on chromosome 16 are involved. Astrocyte
(Ash leaf spot) proliferation in subependyma casuse Seizure.
Fig: Ash leaf spot in Tuberous Sclerosis

Sturge Weber Syndrome: (?One sided lesion- Stain to one side of face, One sided weakness due to one
hemisphere atrophy of brain found in CT Scan, hemianopia), tram track calcification along the cortical
ribbon. STURGE- Seizure, Trigeminal Port-Wine stain, Unilateral weakness (often opposite side to
stain), Retardation (mental) in some patients, Glaucoma, Eye problems e.g Buphthalmos.
Adult Primary Brain Tumors: GM MOPS. Glioblastoma Multiforme, Meningioma, Oligodendroglioma,
Pituitary adenoma, Schwannoma.
Glioblastoma occurs in Cerebrum in Adult, Cerebellum/brainstem in Child. Medulloblastoma occurs in
Cerebrum in Adult, Cerebellum in Child. Meduloblastoma is Mixed tumor (both Glial cell & Neuron in
Tumor. Neuronal cells form rosette, Glial cells show spindle cell morphology, stain for GFAP, Glial
marker).
Glioblastoma Multiforme: Most aggressive tumor of astrocytic line. Bizarre Pleomorphic cells with
necrosis and hemorrhage. Brain stem in children and cerebral cortex in adult.

Fig: GBM.
Meningioma: Arise from AG DAM (Arachnoid Granulations/Dura or Arachnoid Matter). They are
uncommon in children and do not invade the brain. Meningioma often incite an osteoblastic reaction in
the overlying cranial bones. They frequently arise from superior parasagittal surface of frontal lobe, so
bilateral leg weakness is a common feature.
Calcification is present in Meningioma & Oligodendroglioma.
Tumor at Gray white matter junction- Metastatis.
Primary CNS lymphoma: Typically a late manifestation of AIDS (median CD4 Count: 40). Usually a B-
cell lymphoma that typically involves the leptomeninges. Associated with EBV infection.

Childhood Brain Tumor:

HEMAC. HemangioVlastoma, Ependymoma, Medulloblastoma, Astrocytoma, Craniopharyngioma.
Among childhood brain tumor, only craniopharyngioma is exclusively supratentorial, Pilocytic
astrocytoma are mostly posterior fossa tumor but can be supratentorial in rare case. Others are posterior
fossa tumor.
Hemangiovlastoma, Ependymoma & Medulloblastoma can cause obstructive hydrocephalus that present
with Increased ICP features (HEMar hydrocephalus. Nuchal rigidity, nausea, vomiting, headache,
altered mental status, bilateral papilloedema. Craniopharyngioma may also present with raised ICP
features, vision problem, bilateral papilloedema though they do not cause obstructive hydrocephalus).
Ependymoma locates in 4th ventricle but Medulloblastoma, pilocytic astrocytoma locates in Cerebellum &
compress 4th ventricle. So, in addition to raised ICP, Medulloblastoma & Pilocytic astrocytoma have
cerebellar features like ataxia and Nystagmus. Medulloblastoma form homer-wright rosettes but
ependymoma forms perivascular pseudorosette, GBM forms pseudopallisading, (medula brings rosette,
venturar/ventricular Epen brings pseudorosette/plastic rosette, GBM Pallisader). Medulloblastoma cells
are small blue cells. Medulloblastoma is only solid, Pilocytic astrocytoma is mixed solid and cystic.
PiloCytic astrocytoma is Partially Cystic.
Hemorrhage and necrosis are present in GBM in adult and Medulloblastoma in Child brain tumor.
Medulloblastoma arises from external granular cell layer in vermis of cerebellum. Gray white tumor with
multifocal areas of hemorrhage and necrosis. Medulloblastoma often seed the neuraxis via the CSF,
which explains the presence of Malignant cells in CSF, Medulloblastoma Metastasize in CSF. CSF study
also show increase in Protein and decrease in Glucose, latter due to metabolism of glucose by malignant
cells (features like bacterial Meningitis in Medulloblastoma). Medulloblastoma is Solid Mass with
hemorrhage & necrosis but Pilocytic astrocytoma is Partially solid & Liquid.
Craniopharyngioma is Calcified (visible on X-ray), Cholesterol rich Cystic & solid tumor occurs in
Children or young adult. It is most common non-glial brain tumor of children. Though histologically
looks benign, they invade the surrounding bones. Crankcase oil is used to describe the Oily componants
of Craniopharyngioma. It is multilocualted cystic and solid tumor containing dark brown, oily fluid.
These tumors arise from epithelial rests derived from Ratheke’s pouch. Histologically it can resemble
ameloblastomas, which are tumors derived from dental epithelium.
Pilocytic/Cystic Cerebellar Astrocytoma: Most common primary brain tumor in Pediatric/Children. most
frequently in Cerebellum, but may occur in hypothalamus. Cyst with a mural nodule, Rosenthal fibers is
characteristic. Immunostaining with GFA Protein is positive in Pilocytic astrocytoma. They do not invade
the fourth ventricle and can be surgically excised in most cases. no Obstructive hydrocephalus. rosenthal
astrocytoma.

Ependymoma: Ependymoma in children most commonly arise in fourth ventricle, where they cause
obstructive hydrocephalus. In adult, ependymoma usually are located in Cauda equina. Ependymomas do
not seed the Neuraxis via the CSF.
Brain abscess: Brain abscess appear as ring enhancing lesion on CT. 60% of Childhood brain abscess are
related to middle ear infection. Cerebellar abscess and Temporal lobe abscess are associated with middle-
ear infection.

Herniation: 3 types.
Subfalcine (Cingulate) herniation: Cingulate gyrus (Central) is displaced underneath the falx to opposite
side with compression of anterior cerebral artery.
TransTentorial herniation: The Uncus of the Temporal lobe is displaced over the free edge of the
tentorium. Compression tof the third nerve, with pupillary dilatation on the same side. Infarct in
dependent territory. Advanced stage, Duret hemorrhage within the central pons and midbrain. Medial
Temporal lobe damaged, Midbrain can be damaged. Uncal herniation. TT MT Unca.
Cerebellar Tonsillar herniation occurs through the foramen magnum, compression of Medulla oblangata
leads to cardiorespiratory arrest.
 Arnold-chiari
malformation:
Type 1 is
common, mostly
asymptomatic
(headache, neck
pain), associated
with cerebellar
tonsil herniation.
type AK is
Asymptomatic.
Type 2 (Severe), Second is Symptomatic, Severe, Small posterior fossa, associated with Syringomyelia,
Meningomyelocele. Downward displacement of Cerebellar Vermis and Medulla through foramen
Magnum. Compression of fourth ventricle causes obstructive hydrocephalus.
Dandy-walker malformation: Dhaush size posterior fossa, Dilated fourth ventricle due to failure of
foramen of luschka and magendie to open. cerebellar vermis is absent, replaced by ependyma lined
midline cyst. Splenium of corpus callosum is also absent.
NPH- ADI roshattok- Ataxia, Dementia, Incontinence. Wet, Wobbly, Wacky.

Pathologic findings:
Disease of Basal ganglia: Huntingtons’s disease, Parkinson’s disease, Wilson’s disease, Hemibellism,
Tourette syndrome.

ALS: Degeneration of Both UMN & LMN due to excitatory toxicity to neurons caused by glutamate.
Riluzole is glutamate release inhibitor, glutamate receptor blocker and Na + channel blocker. Baclofen is
used in ALS to reduce muscle spasticity. ALS-Amyotrophic- Atrophy of muscle. SOD1 gene defects are
in ALS. SODALS. Spare third cranial nerve & cognitive function is normal.

Brainstem Lesion:
Anterior Spinal Artery syndrome has two presentation. If it is blocked at Medulla level, it causes Medial
Medullary Syndrome (ASA MiMS). Secondly, If Anterior Spinal Artery is lesioned at Spinal cord level,
it will damage all tracts except Dorsal column.
Medial Midbrain syndrome/Weber sydrome: It is caused by Posterior ?Cerebral artery. It consists of
Contralateral spastic hemiparesis mostly the upper limb and lower half of the face. Damage to CN 3
fibers can also lead to a dilated pupil, ptosis and lateral strabismus.
Fibers of CN 3: Ipsilateral occulomotor nerve palsy causing lateral strabismus, dilated pupil, ptosis.
Corticospinal tract: Contralateral spastic hemiparesis.
Corticobulbar tract: Contralateral spastic hemiparesis of lower face.
Dorsal Midbrain Syndrome/Parinaud syndrome: It is caused by Pineal gland tumor. Superior
colliculus/Pretectal area: Paralysis of upward gaze, various pupillary abnormalities. Most fibers from the
optic tract project to the lateral geniculate body (LGB), some also project to the pretectal area (center of
light reflex), Superior colliculus (center of reflex gaze/?Vertical gaze) and the suprachiasmatic nuclei
(circadian rhythm). The LGB projects to the primary visual cortex(striate cortex, brodmann area 17) of
the occipital lobe via the optic radiations.
In occulomotor nerve, Middle-Motor-supplies Muscle. Periphery- Parasympathetic.
Light reflex: afferent limb is CN2, Efferent limb is CN 3.
Light stimulates ganglion retinal cells>impulse travel up through Optic nerve, which projects bilaterally
to pretectal nuclei of midbrain> The pretectal nucleus projects bilaterally> Edinger-Westphal nuclei.
Efferent limb: Edinger-Westphal nucleus (preganglionic parasympathetic)-Ciliary ganglion
(postganglionic parasympathetic)>pupillary sphincter muscle>Miosis.
Because this reflex does not involve the visual cortex, a person who is cortically blind can still have this
reflex.

Pontine Lesion: Horizontal gaze paralysis, as MLF is there.

Contralateral Pyramidal tract & Dorsal column lesion is common in Medial Pontine, Lateral
Pontine, Medial Medullary Syndrome. Cranial nerve lesion makes the difference (CN 6 lesion in
Medial Pontine, CN 7 & 8 in Lateral Pontine, CN 12 Lesion in Medial Medullary Syndrome). CN 9
& 10 Lesion is in Lateral Medullary syndrome.
AICA LIPS- Anterior Inferior Cerebellar Artery occlusion gives rise to Lateral Inferior Pontine
Syndrome. It produces similar symptoms like Lateral Medullary syndrome (Contralateral Pyramidal
tract /Corticospinal tract lesion causes spastic paralysis, Contralateral Dorsal column medial lemniscus
tract lesion causes loss of position & Vibration sense) except that a lesion in the lateral Pons can affect
fibers of CN 7 & 8, which would produce a facial droop and hearing loss, respectively. ipsilateral
Hypoglossal nerve will be damaged. Facial nucleus lesion is specific to AICA lesion. AICA lege Face
nosto hoye gese.
Medial Pontine syndrome: Contralateral Pyramidal tract/Corticospinal tract lesion causes spastic
paralysis, Contralateral Dorsal column/Medial lemniscus tract lesion causes loss of position & Vibration
sense & CN 6 lesion causes medial strabismus. Damage to CN 6 distinguishes Medial Pontine Syndrome
from Medial Medullary Syndrome (CN 12 is damaged).
Medullary Lesion: Hoarseness of voice/Dysphonia, Dysphagia, Palate droop (N. Ambiguous, formed by
CN 9 & 10) & Loss of taste (N. Solitarius) are present only in Medulla. Tasteless hoarse in medulla.
ASA MiMS: Anterior Spinal Artery lesion causes Medial medullary syndrome: Contralateral Pyramidal
tract/Corticospinal tract lesion causes spastic paralysis, Contralateral Dorsal column/medial lemniscus
tract lesion causes loss of position & Vibration sense & Hypoglossal nerve (Ipsilateral flaccid paralysis
of Tongue) is affected. Damage to CN 6 distinguishes Medial Pontine Syndrome from Medial Medullary
Syndrome (CN 12 is damaged).
a. Pyramid: Contralateral spastic paresis (body)
b. Medial lemniscus: Contralateral loss of tactile, vibration, conscious proprioception (body)
c. CN 12 Nucleus/Fibers: Ipsilateral flaccid paralysis of tongue.

PICA LiMS/WS- Lateral Medullary Syndrome/Wallenberg Syndrome. Most common Brainstem stroke,
it is due to the involvement of any of the following five vessels: Vertebral artery, posterior inferior
cerebellar artery, Superior Medullary Artery, Inferior Medullary Artery, Middle Medullary Artery.
Thrombosis of Vertebral Artery is the most common cause. as CN 9 to 11 are located in lateral Medulla,
so symptoms related to these nerve’s lesion will be present. Same side horner syndrome, loss of Pain
& Temperature sensation of Ipsilateral Face and Contralateral half of Body will be there. Nucleus
Ambiguus lesion (Paralysis of the Vocal cord, Dysphagia and Palate droop) are specific to PICA lesion.
PICA: Don’t pick (PIC A) a horny (horner syndrome) horse (hoarseness) that losT Pain
(Temperature & Pain) & swallowing (dysphagia). Horner syndrome is due to lesion in descending
sympathetic fibre, not due to Occulomotor nerve lesion. But no CN 12 sign because it is located in
Medial Medulla (present in Medial Medullary syndrome). Nucleus Ambiguous consists of fibres of CN 9
& 10, Lesion lead to Ipsilateral paralysis of the Vocal cord causing Hoarseness of voice, Dysphagia and
palate droop. Taste sensation is altered if solitary nucleus is lesioned. The solitary nucleus and tract
transmit and receive visceral sensation and taste from the CN 7, 9, 10 as well as CN11. Majority of taste
is sensed by CN 7. she Eka eka (Solitary Nucleus) taste check kore. True vocal cord is lined by
Squamous cell. True Quasom.
a. Inferior cerebellar peduncle: Ipsilateral limb ataxia.
b. Vestibular nuclei: Vertigo, Nausea/Vomiting, Nystagmus (away from lesion)
c. Nucleus ambiguus (CN 9,10,11) Ipsilateral paralysis of larynx, pharynx, palate cause
dysarthria/Hoarseness, dysphagia, loss of gag reflex.
d. Spinal nucleus of trigeminal nerve: Ipsilateral pain/temperature loss (Face).
e. Spinothalamic tract: Contralateral pain/temperature loss (body)
f. Descending hypothalamics: Ipsilateral horner syndrome.
Retinal pathology:
Retinopathy of prematurity (Retrolental fibroplasia): excess proliferation of vessels in inner layer of
retina. may be mild to progressive vasoproliferation, scarring causing white pupillary reflex an potentially
blinding retinal detachment. Major risk factors include prematurity and high oxygen.
Retinitis pigmentosa : Pigmented epithelium degeneration.
Seile macular degeneration: Pigmented epithelium degeneration.
Glucoma: Ganglion cell and optic nerve degeneration.
Progressive Supranuclear Palsy: a degenerative disorder characterized by ophthalmoplegia, pseudobulbar
palsy, axial dystonia and bradykinesia. The pathologic changes consist of widespread neuronal loss and
gliosis in subcortical sites with sparing of the cerebral and cerebellar cortices.

Pupils: Small HAPPY. Horners, Argyll-Robertson, Pontine haemorrhage, Pilocarpine, Happy

(morPhine).

Argyll Robertson Pupil- ARP- PRA (Accomodation Reflex Present but Pupillary Reflex Absent)
Argyll Robertson SADE (accommodates but doesn’t react – c.f. prostitute). Syphilis, Alcohol, DM,
Encephalitis.

Auditory Test:
Normally, AC>BC. Air Conduction is better than Bone Conduction.
Rinne Test: It remains Normal (AC>BC) in Sensoryneural hearing loss but Opposite in Conduction
deafness.
Weber test: Coaffe SENd UNan to Weber (UN secretary general). (in Conduction deafness, lateralized to
Affected side means Vibration is louder in affected ear, in SENsoryneural deafness to UNaffected side
means vibration is louder in unaffected ear). CLL- in Conduction deafness Lateralized to Lesioned side.

SubArachnoid hemorrhage- Aneurysm rupture/Arteriovenous malformation. Pontine Hemorrhage- 3Ps-

Paralysis (bilateal), Pin point pupils, Pyrexia,Coma.
Premature senile dementia- DEEP SHIT- Deficiency of B12, Epilepsy, Endocrine (myxoedema),
Parkinsonism, Syphilis (GPI), Huntingtons, Injury, Tumor.

Neurosyphilis: 3 types. In tabes dorsales, Tendon reflex is absent. But in General paresis, Tendon reflex is
hyper.

Tabes Dorsalis features: DORSALIS. Dorsal column degeneration, Orthopedic pain (Charcot joints),
Reflexes decreased (deep tendon), Shooting pain, Argyll-Robertson pupils, Locomotor ataxia, Impaired
proprioception, Syphillis.

Cerebellar sign: 3 Deadly ANTS Playing on ur cerebellam: Dysarthria, Decreased tone,

Dysdiadochokinesia, Ataxia, Nystagmus, Tremor, Slurred speech/Scanning speech, Pendular knee jerk.
OR
Cerebellar Sign- DANISH- Dysdiadokinesia/Dysmetria, Ataxia towards the side of lesion, Nystagmus,
Intention tremor, Slurred speech, Hypotonia.
Romberg Sign: Sway with open eye indicates Cerebellar Sign, Sway with Close eye indicates Dorsal
column sign.

Causes of Pure motor neuropathy: PHD is A TALL degree. Poliomyelitis, Hereditary spinal muscular
atrophy, Dapsone intoxication, Adult variant of Hexosaminidase deficiency, Tick bite paralysis, Acute
intermittent porphyria, Lead intoxication, Lambert Eaton Syndrome, LMN form of Amyotrophic lateral
sclerosis.

Nerve thickening: ISLAND. Idiopathic hypertrophic neuropathy, Sarcoidosis, Leprosy, Amyloidosis,

Neurofibromatosis, DM.

Neuropathic Ulcer- TADS- Tabes Dorsalis, Alcohol, DM, Syringomyelia.

Small muscle wasting: MARS BAR: MND / Myopathies, Apical tumours, RA, Syringomyelia, Brachial
Plexus injuries, Aging, Cervical Rib.
Pes Cavus : Disease Can Shorten The Foot: DM, Charcot Marie Tooth, Syringomyelia
Tabes dorsalis, Fredreich’s Ataxia.
Polyneuropathy- VITAMINS- Vitamin deficiency/Vasculitides, Infection (TB, Leprosy, Syphilis, Polio),
Toxin (Amiodarone, Antiseptics, INH, Lead, Metronidazole, Phenytoin, Vincristine), Amyloid, Metabolic
(Alcohol, DM, Hyperthyroid, Porphyria, Liver & Renal failure), Idiopathic/Inherited, Neoplasm,
Systemic (SLE, PAN, Multiple myeloma).

Respiratory Pathology
CHeyne-STokes respiration is caused by CHF, Stroke, brain Trauma.
Centroacinar emphysema: Cigarette, most Common type (95%). Pan acinar: α-1 antitrypsin deficiency.
chronic Bronchitis- Blue Bloater, emPhysema- Pink Puffer. Chronic bronchitis- Cough with Copious
sputum production is dominant symptom.
Asthma: Two types: Intrinsic & Extrinsic.

Intrinsic: occurs by Aspirin, Cold, Exercise, Toluene. caused by Increased Leukotrene in Respiratory
tract. Leukotrene antagonist (Zileuton, Montelukast). Leukotrienes attracts Leukocyte and increase
vascular permeability during inflammation and type 1 hypersensitivity reaction.
Extrinsic: Atopy or Allergic. ASpergilus fumigatus.
Asthma is a Curse. has Cursman spiral.
Pneumonia: Alcoholic can have pneumona by two organisms. e.g- Klebsiella (?No abscess in lung) or
Anerobes (particulary In unconscious state form Abscess in lung).
Streptococcus Pneumonia causes Lobar Pneumonia but Streptococcus Pyogenes causes
Bronchopneumonia (? rare).
Postviral Pneumonia: Staph. Aureus, Strep. Pneumonia, Hemophilus Influenza.
Pneumoconioses: Silicosis causes eggShell calcification in lung hilum, affects Superior lobe.
AsBASEstosis causes calcification of pleura, affects lower lobe/BASE. anthracosis is inhalation of
carbon only, in city dewellers, harmless. Coal worker pneumoconiosis is inhalation of Coal dust,
Combination of carbon and silica, harmful. Silica attacks Hilum.
pRussians are Ferrocious for Asbestos. asbestosis forms ferruginous body that is prussian blue stain
positive.
Pleural Effusion: Exudative effusion: Excess Protein & LDH. Chylous effusion, Empyema is Exudative
effusion.
Cavitary Lung Lesion - Staphylococcus Aureus, Mycobacterium Tuberculosis (M. TB produces Niacin),
Anerobic infection/Aspiration pneumonia in Unconscious/Alcoholic.
Calcifying Lung lesion is most likely Fungal Lesion.
AIDS patient are vulnerable to TB, they may not form Granuloma or it may be Non caseating granuloma
due to lack of CD4 cell. Granuloma occurs mainly by Intracellular organism or by Chronic Infection
producing organism which cant be eradicated by immune system. Granulomatous disease in neonate
occurs by Listeria Monocytogenes.

Lung Cancer:
ADenocarcinoma is linked with K-ras. AD Kras. Small cell carcinoma is linked with L-myc. Small myc.
All lung cancer except CDBA (bronchial CrcinoiD and BronchioloALveolar, one subtype of
ADenocarcinoma, BAAD) are associated with smoking. Nonsmoker’s BAL hoy.
2 lung cancer are located centrally, 2 S- Squamous & Small. 2 are peripherally-AL- Adenocarcinoma &
Large cell carcinoma.
Smoking is related with Small cell & Squamous cell carcinoma of Lung.
Large cell carcinoma presents with Large breast in men and large amount Milk in woman.
Small cell carcinoma- 4A- ACTH (Cushing syndrome), ADH (SIADH), Antibody against presynaptic
Ca++ (LES), Amplification of L- myc oncogene. (K-ras gene in Adenocarcinoma). Small blue cell with
Scanty cytoplasm. Surgery is contraindicated in small cell carcinoma as there is no improvement in
survival.
Squamous cell carcinoma- 4C, C square- Central, Cavitation, Cigarette, Calcium increase
(parathormone). Keratinized Squamous cells & Komola (Orange) stain in Pap smear, small cell
carcinoma are Blue color. Pancoast’s tumor though located at apex but it is usually Squamous cell
carcinoma. Pancoast Square.
Adenocarcinoma occurs in both Smoker & Non smoker, female (Most frequent cancer in Nonsmoker). It
is also the most frequent peripheral cancer (other one is Large cell cancer, Peripheral Awami Leaguer).
BroncheoloAlveolar Carcinoma is a subtype of Adenocarcinoma which occurs to Nonsmoker.
aDenocarcinoma occurs in Damaged lung such as history of recurrent pneumonia. It also looks like
pneumonia and Dense alveolar wall/alveolar wall thickening on X-ray. Nonsmoker der BAL hoy.

Small cell carcinoma & Large cell carcinoma are both highly anaplastic/undifferentiated. But small cell
carcinoma is located centrally, treated by chemotherapy. Large cell carcinoma are located peripheraly,
treated surgically.

Hamartoma & ? Histoplasmosis looks like Coin. Hamara Coin.

Neuroendocrine cells are present in Small cell carcinoma and bronchial carcinoid/?serotonin.
complication: SPHERE. Superior venacava syndrome, Pancoast tumor, Horner’s syndrome, Endocrine
(Paraneoplastic), Recurrent laryngeal symptoms, Effusion (pleural or pericardial).
CyaNide Poisoning: Almond smell, no Cyanosis. Treatment is amyl Nitrite, thiosulfate,
hydroxyCobalamin.

CO presents with Cherry red color. Mono Red.

Methemoglobinemia: Methylene blue, Vitamin C. Cyanosis & Muddy/Brown color blood. Cyanosis,
Chocolate color blood, Tachypnea is highly suggestive of Methemoglobinemia. Treatment is Methylene
blue.

CO poisoning cause left shift of oxy hemoglobin curve, Cyanide does not shift. Cyanide does not allow
tissue to use O2, so venous blood O2 remains high. CO increase O2 affinity to Hb, so venous blood has
high O2.
Renal Pathology:
Cast:
Waxy cast: CRF, PSGN (rarely)
Epithelial/Granular cast/Tubular cast: Intrinsic Renal failure/ ATN. Great ATN.
RBC Cast: Nephritic Syndrome.
Fatty cast: Looks Maltese cross (Fat looks carbohydrate, maltose) Nephrotic syndrome.
Hyaline cast: found in any proteinuric state. Without proteinuria , they have no significance. Hay! protein
chole jacche.

HyalINe Deposit- in HIV, Diabetic or Normal patient.

Fig: Hyaline deposition in a vessel.

ATN:
BUN: Creatinine elevation Causes ABCD. Azotemia (Pre renal, Bleeding (GI), Catabolic Status, Diet
(High protein parenteral nutrition).
Nephritic Syndrome: Bloody HERO CUP. Hypertension, Edema, RBC in urine, Oliguria, Cast of RBC
in urine, Uremia, Protienuria.
Berger, acute PSGN, RPGN, Diffuse PGN, AlPort syndrome. (berger and all P except
MembranoProliferative are nephritic syndrome. MPGN are mostly nephrotic but could be nephritic. MP
dui dikei tal rakhe).
Berger disease e Barbar (recurrent) hematuria hoy, Ig A deposit in Mesangium, Mesangial
hypercellularity are characteristics. 50% patient needs kidney transplant. develops CRF after Bish (20)
years.

Acute PSGN: Classic presentation. Throat, bloat & coke. Throat: 1 week ago, Bloat: facial edema, Coke:
coke-colored urine. occurs before Puberty (2-14 yrs).

RPGN- GoLANCA. -Tyep 1-Goodpasture syndrome, type 2-SLE, type 3-Wegener’s granulomatosis, C-
ANCA positive. Type 3 has no immune complex deposition.
Nephrotic Syndrome: Foreign Secretary, MP, GM or DGM, Minimum, Amyloidosis, DM. (Focal
Segmental glomerulosclerosis, MembranoProliferative glomerulonephritis, Membranous
Glomerulonephritis or Diffuse membranous glomerulopathy, Minimal change disease, Amyloidosis,
Diabetic glomerulopathy).

Nephrotic Syndrome- Its NEPHROTIC- (Na & Water retention, Edema, Proteinuria >3.5 gm/day, HTN
& Hyperlipidemia, Renal Vein Thrombosis, Thrombotic & Thromboembolic complications. Infection
with Staphylococci & Pneumococci. Hypercoagulable state. proteinuria makes urine frothy, Liver
produces protein to compensate protein loss and Lipid is also synthesized simultaneously.
LEAP to Nephrotic syndrome: Lipiduria/hyperLipidemia, Edema, hypoAlbuminemia, Proteinuria.
nephrOtic- prOteinuria. nephrItic syndrome- Inflammatory process.
Diabetic patient develop Diffuse glomerulosclerosis. SLE can present as Diffuse proliferative GN
(Nephritic) or Membranous GN (Nephrotic). Diabetic nephropathy has PAS positive KW nodules &
mesangial deposition.

Kidney Stones:
Kidney stone: Cause of Magnesium Ammonium Phosphate (Struvite) stone is Alkaline urine. but
Treatment of Cystine & Uric acid stone is Alkalinization of the Urine. Urate stone is radiolUcent and
associated with goUt.

Kidney Tumor:
Wilm’s tumor is Unilateral tumor but ARPKD & ADPKD are bilateral tumor. ADPKD occurs in ADult.
Tumor Origin: Embryonic renal cell of metanephros- Wilm’s Tumor/Nephroblastoma (one side lesion),
Renal tubular cell- Clear Cell Ca (Renal Tube is Clear. Smoking is a risk factor), Uroepithelial cell-
Transitional cell carcinoma (from renal calyx to Urinary bladder). Obesity is Clearly a risk factor for
Clear cell carcinoma.

Wilm's Tumor : WAGR complex: Wilm’s Tumor, Aniridia, Genitourinary malformation, mental-motor
Retardation.

Bilateral renal cell carcinoma- VHL. RCC may present as left sided Varicocele. RCC is Clear cell
Carcinoma.
Pyelonephritis:
Dialysis Indication: five vowels: AEIOU: Acidosis refractory to bicarbonate, sever Electrolyte disorder
refractory to medical intervention specially hyperkalemia, Intoxication with some drugs, volume
Overload refractory to diuretics, Uremic symptoms (cardiac friction rubs and altered mental status).
Microscopic Findings:

Wegener's granulomatosis affects the upper and lower respiratory tracts and the kidney. It does not affect
GIT. It is characterized by focal necrotizing vasculitis and necrotizing granuloma. URTI, LRTI,
Epistaxis, Hemoptysis, Glomerulonephritis are few of the manifestations of this disease. It is C-ANCA
positive. Treatment is with antibiotics, corticosteroid, Azathiopurine.

c-ANCA (PR3 ANCA)- CPR3 ANCA- World Cup 3- Wegener’s granulomatosis.

p-ANCA (p ANCA U r PMC)- Ulcerative Colitis, PSC (Not Polyarteritis Nodosa), Microscopic
polyangitis, Churg strauss disease.
Messangial deposit: Berger disease, HSP, MPGN, FSGN.

SubePithelial deposit: PSGN. Granular lumpybumpy humpy Streptococci. Granular, lumpybumpy or

subepithelial hump deposit in PSGN.

Subendothelial deposit: Goodpasture syndrome, SLE, MPGN, Membranous GN.

Linear Subendothelial Ig G & C3 deposit: Goodpasture. Linear is Good.
Granular SubEndothelial Wire-Loop deposit- SLE. Wire-Loop- Lupus Nephritis.
Granular subendothelial tram-track appearance deposit: MPGN. Tram e chore MP ashe.

Granular, Spike & Dome appearance – Membranous GN. GSM- Granular Spiky Membrane.
Splitting of basement membrane: alPort syndrome, MPGN. Alport is Andha, Boyra, affect Abujh Baccha.
alPort & MPgn- basement Membrane Phare. Fair/Fibrin deposition and GBM disruption in Goodpasture
due to Fibrinoid necrosis.

Thickening of Both or Only Capillary wall & GBM: Membranous GN (Mota banay). Thickening and
splitting of GBM: MPGN (Mota banay & Phare).
Mesangial hypercellularity is seen in HSP, Berger’s disease, PSGN, MPGN. proliferative means
hypercellular.
Effacement of Foot process/podocyte: Minimal change disease, FSGN (very rare).
Mesangial Ig A deposit: Berger’s disease, HSP.
Mesangial hypercellularity with Ig A & C3 deposit: HSP.
Mesangial hypercellularity with Ig G & C3 deposit: MPGN.

C1 C3, IgM, IgG- 13 GM are found in Principal Secretary & Foreign Secretary & MP’s Office (C 1 C3, IgM,
IgG complement are found in PSGN, FSGS, MPGN). Ig M is usually found in FSGN. Mota Foreign
Secretary.

FSGS is associated with Obesity, HIV or Heroin, Interferon use. amader Mota Foreign Secretary Heroin,
Interferon kheye HIV hoise.

MPGN: mostly Nephrotic syndrome, can be Nephritic syndrome. MP dui dikei tal rakhe.

Type 1: Subendothelial IC deposit and granular immunofluroscence. Tram-track appearance. Type 1 is

associated with HBV, HCV.
Type 2: Intramembranous IC deposit. Dense deposit disease. it is associated with C3 Nephritic factor.
Crescentic GN:
Papillary Necrosis:

Cortical necrosis is in Mural thrombosis, Hypotension/Shock/DIC. TSC, Thrombosis Shocked Cortex.

DIC causes Diffuse cortical necrosis.

Renovascular Hypertensionn: Increased Renin secretion is the mechanism. two cause. Fibromuscular
dysplasia/ Fibrodysplasia is common in woman between 30-50 years of age. Renal artery atherosclerosis
is the most common cause in Man over 50 years age.

Fibromuscular dysplasia/Fibrodysplasia is a non-inflammatory, non-atherosclerotic disorder, beaded

pattern, that leads to arterial stenosis, usually of the renal and internal carotid arteries, Renal bruit is a
common finding. Patients resent with HTN, TIA and stroke.

Chronic Vs Acute renal disease: SNAB. Small kidney, Neuropathy (peripheral), Anaemia, Bone disease.

Creatine
Reproductive Pathology:
Sex chromosome disorders:
Klinfelter Syndrome: Increased LH, FSH, Estrogen but Low Testosterone. Ledyg cell hyperplasia but
nonfuncional, Seminiferous Tubule is hyalinized, Small Testis, Small Penis but Big Breast. ? Fibrosis of
Seminiferous tubule causes Azospermia & low Inhibin which causes High FSH by negative feedback and
hyperplasia of Ledyg cell by increased LH. Increased aromatase activity in Ledyg cell converts all
testosterone to estrogen, results in Low Testosterone & High Estrogen. Small testes is also found in
Fanconi’s anemia. Klinfelter syndrome & cryptorchidism has increased risk of testicular cancer.
In complete androgen resistance/Testicular feminization syndrome/Androgen Insensitivity syndrome, the
external genitalia are feminized but neither the male type nor the female type internal tracts develop. In
the absence of the androgen receptor, the wolffian ducts will degenerate. The mullerian ducts will also
degenerate because of the normal effect of testicular mullerian inhibiting factor. Normal male genotype
with Normal female phenotype except short vagina, undescended or inguinal testes, Sparse pubic hair,
absent Uterus. Blind vaginal pouch is found. Blind to Androgen.
5α reductase deficiency- 5 TEN- Testosterone, Estrogen are Normal. Vs Androgen insensitivity
syndrome/Testicular feminization syndrome where Testosterone, Estrogen are high.
Penis at 12- Congenital 5α reductase deficiency. Girl’s clitoris becomes enlarged, genotypically male.
Serum TEL (Testosterone, Estrogen, LH) are normal. In contrast, Androgen insensitivity syndrome /
Testicular feminization syndrome shows genotypically male but phenotypically female, bilateral testes in
labia majora or undescended & has high Serum Testosterone, Estrogen, LH. They are also Male
Pseudohermaphrodite (Male genotype but Female Phenotype). 5 α affects at 12.

Female look like male, 21 or 11 hydroxylase deficiency.

In 17- hydroxylase deficiency, the testes cannot synthesize testosterone, resulting in feminization of the
external genitalia and degeneration of the wolffian ducts. Normal secretion of Mullerian regression factor
should also cause the degeneration of the Mullerian ducts. Because of excessive secretion of
deoxycorticosterone by the adrenal cortex, these individuals are usually hypertensive. Female are born
with a normal female internal and external genitalia because the default program is for the female
phenotype to develop in utero. With 17 hydroxylase deficiency, sex steroid can not be synthesized and
secreted. Affected females do not mature sexually at puberty and remain infantile.
In sertoli only syndrome, only the sertoli cells of the seminiferous tubules are present (germ cell aplasia).
Spermatogenesis is absent in these individuals, who also show increased plasma levels of FSH due to
decreased Sertoli cell secretion of Inhibin. They may exhibit both male type and female type internal
tracts due to the absence of Mullerian regression factor. The Leydig cells, however, have normal function
and result in normal secretion of testosterone so that male type both internal tracts and external genitalia
develop.

Testicular dysgenesis is poor intrauterine development of the testes with concomitantly decreased
secretion of testosterone and Mullerian regression factor. The Wolffian duct structures may degenerate
and the external genitalia may be feminized. Female type internal tracts may develop because of the
decreased secretion of Mullerian regression factor.
In utero differentiation of the Wolffian ducts into the normal male phenotypic internal reproductive tract
requires testosterone, but not dihydrotestosterone. On the otherhand, differentiation of the indifferent
external genital slit into the penis, prostate and scrotum does require dihydrotestosterone. A congenital
absence of 5 alpha reductase in these tissues will result in feminization. If left untreated, the affected
individuals are generally phenotypic females until puberty, at which time increased amounts of
testosterone results in virilization (penis at twelve syndrome). If discovered early, a male gender
assignment can be supported with administration of dihydrotestosterone to increase peinis size. If
discovered after infancy, a female gender assignment can be supported with estrogen substitution therapy
and prophylactic orchiectomy.
5α reductase deficiency: Male baby looks like female, almost similar to Complete androgen insensitivity/
Testicular feminization syndrome, but at puberty female external genitalia becomes musculinized.
Testosterone, Estrogen, LH are normal but these are high in Complete androgen insensitivity/Testicular
feminization syndrome. Male have normal male genotype with hypospadias and poor development of
male EXTERNAL genitalia. Finasteride is pregnancy risk category X and is absolutely contraindicated
for use in women during pregnancy or in females who potentially may be pregnant. Finasteride causes
abnormality in the external genitalia of the male fetus. Pregnant women trying to conceive should not
ingest the drug or even handle crushed or broken finasteride tablet.
Turner syndrome:
Two high risk of turner syndrome is Bacterial endocarditis and Cerebral hemorrhage due to coarctation of
aorta.
Bicuspid aortic valve is most common cardiac anomaly, then infantile type Coarctation of aorta.
Turner syndrome has more risk for Horseshoe kidney that increases chance of developing Wilm’s tumor.
Ms. Wiliam Horse Turner.

Hydatiform Mole: PARTial derived from both Parents, has fetal PARTs. In complete mole, 2 haploid
sperm fertilizes one empty egg, so there is no fetal parts. Mole is treated by Methotrexate.
HTN, Proteinuria & Edema before 20 weeks of pregnancy is Hydatiform mole. After 20 weeks- pre
eclampsia.
Bleeding after 20 weeks pregnancy. Two cause- Placenta Previa (Painless), Abruptio Placenta (painful).
ABRUPTio placenta- ABRUPT detachment of Placenta. PainFUL, dark red bleeding. Abrupt Pain,
Abrupt Bleeding.
Placenta Previa- PainLESS, Bright red bleeding.
Placenta ACCRETA- ENCASED IN myometrium.

Characteristic Findings on Endometrial Biopsy in benign Endometrial Disease:

Anovulatory bleeding: Proliferative endometrium with stromal breakdown.
Asynchronous Secretory endometrium (a form of DUB that can cause infertility): Secretory endometrium
with mismatch of 2 or more days between glands and stroma.
OCP use: Decidualized stroma with inactive glands.
Secretory phase of menstrual cycle endometrium: Long, coiled glands with small nuclei and clear apical
vesicles
Proliferative endometrium: Smaller glands lined with columnar epithelium without apical vesicles.
 d

Anovulation & DUB: Anovulation is the most likely cause of DUB, caused by an interruption in the
normal sequence of the follicular and luteal phases of the menstrual cycle. Bleeding that occurs in
anovulation is estrogen breakthrough bleeding, caused by a continuous estrogen stimulation of the
endometrium without interruption by cyclic progesterone secretion and withdrawal. PCOS is a common
cause of anovulation in young female. Progestine challenge will cause menstrual bleeding and confirm
anovulation. Clomiphene is not appropriate until the diagnosis is confirmed with the progestin challenge
test.
HPV produces E6, E7 protein. E6 binds with P53, E7 binds with Rb. 653, 7Rb. HPV causes APC
carcinoma and Anal wart (APC-Anal, Penile, Cervical).
In Theca cell, Cholesterol is converted to Testosterone/Androstenidione by Desmolase (Stimulated by
LH). Thick Desh, Chol Andru. Ladies hormone stimulates Purush Hormone production.
In Granulosa cell, Androstenedione is converted to Estradiol by Aromatase (stimulated by FSH). Grand
Arrow Follicle.
? Theca Interna cell produce Estrogen, Granulosa Lutein cell produce Progesterone. TIE GLP (Kaplan).
PCOS: Increased GnRH, Increased Ladies hormone (LH), Increased Purush hormone (Testosterone),
Estrogen may be Increased or Normal. High TEL But Low FSH & Progesterone. Increased GnRH makes
a partiality, it Stimulates more LH but less stimulation to FSH. High LH causes Theca cell hyperplasia &
excessive Testosterone secretion but low FSH causes Granulosa cell atrophy & insufficient aromatase
activity to convert Androgen to Estrogen.

Ovarian Tumor:
Ovarian germ cell tumors are TYCe & DYSe (Teratoma, Yolksac tumor, Choriocarcinoma and
DYSgerminoma. Dysgerminoma is ovarian counterpart of male Seminoma, both express Placental
alkaline phosphatase antigen). Testicular germ cell tumors are Semi TYCE (Seminoma, Teratoma, Yolk
sac tumor, Choriocarcinoma, Embryonal Carcinoma).
Choriocarcinoma can be Ovarian choriocarcinoma, Placental choriocarcinoma and Testicular
choriocarcinoma. all produce human chorionic gonadotropin/HCG. Placental choriocarcinoma are
responsive to chemotherapy whereas Ovarian choriocarcinoma are non responsive.
Similar to testicular tumors, ovarian tumors can be classified into Cell of origin. There are three main
categories: Tumors of surface epithelium, Tumors of germ cell origin and tumors of sex cord-stromal
origin. Ovarian surface epithelium (Coelomic mesothelium) may differentiate along Tubal (Serous),
Cervical (Mucinous) or endometrial lines, giving origin to serous cystadenoma/cystadenocarcinoma,
mucinous cystadenoma/cystadenocarcinoma and endometroid tumors, respectively. Serous tumors
represent 40% of all ovarian tumors and serous cystadenocarcinoma is the most frequent serous tumor.
Serous cystadenocarcinoma occur primarily in women aged 40-65 years. About two-thirds of these
tumors are bilateral, Serous in two Side. As the name suggests, it is a cystic tumor containing clear fluid.
The cystic wall is lined by malignant epithelial cells forming papillary fronds.
Less frequent than serous cystadenocarcinoma, endometroid adenocarcinoma and mucinous
cystadenocarcinoma also derive from surface epithelium. Endometroid carcinoma is histologically similar
to endometrial adenocarcinoma, whereas Mucinous cystadenocarcinoma is composed of Mucin producing
cells similar to cervical epithelium. Both these neoplasms have solid and cystic areas and may be
bilateral. Intraperitoneal accumulation of Mucus/PseudoMyxoma peritonei is rare presentation of ovarian
Mucinous cystadenoma (benign) or Mucinous cystadenocarcinoma. MUcINous tumor are Multilocular,
Intestine like tissue, Unilateral frequently whereas Serous tumor are Unilocular and Bilateral/two Side
frequently.
Granulosa cell tumors originate from ovarian stroma and consist of variable mixtures of granulosa cells
and theca cells. Since they frequently produce large amounts of estrogens, these tumors manifest with
precocious puberty in preadolescent girls. Mature woman with granulosa cell tumors develop endometrial
hyperplasia, endometrial carcinoma and fibrocystic change of breast. Histologically, these neoplasms are
composed of uniform Cuboidal cells, forming structures like ovarian follicle with Eosinophilic material
(Call-Exner YellowGranule). CEG-Call Exner Granule. Exner is Eosinophilic.

Three Ovarian tumor produce Steroid hormone. Sertoli-Ledyg cell tumor produce mainly Androgen,
causing defeminization/Musculinizing feature in woman, Granulosa cell tumor produce mainly estrogen.
Fibroma-Thecoma produce Estrogen but less in amount.
Ovarian Fibroma/Thecoma-Fibroma/Fibrothecoma has Fibrous Capsule with Lipid & Fibroblast cell
inside. Spindle shaped Fibroblast, produces excess Collagen. makes classic triad of Meig’s syndrome-
Pleura effusion, Ascites, Fibroma. Meig Fibre/Fibroma. ? fibromaThecoma is Theca cell & Fibroblast
dominant tumor, so produce Estrogen & Collagen.
Brenner tumor: Surface epithelium tumor. Benign or malignant, looks like Bladder transitional epithelium
with abundant fibrous stroma. It resembles transitional cell carcinoma. Coffee Bean nuclei, Encapsulated.
Yolk sac tumor produces Schiller-Duval Body which looks like Glomeruli. Yolkshire Duvai kidney.
Teratoma, derived from germ cells, can be further classified into mature cystic, immature and
monodermal teratomas. Mature cystic teratoma is the Most frequent neoplasm derived from germ cells.
Since they originate from More than one germ layer, these neoplasms contain an amazing mixture of
Mature tissue components, often including skin, teeth, neural epithelium, thyroid cartilage. STTruma
Ovary is a Single layer Teratoma (Monodermal teratoma) associated with Thyroid hormone elevation.
Breast Carcinoma:
Lobular Carcinoma: Parallel arrays of small monomorphic cells with Scant cytoplasm. mass found
accidentally. cells are found in clusters or in a Linear formation.
Intraductal papilloma: branching fibrovascular core extending from a dilated duct.
Medullary carcinoma: Lymphocytic infiltration and scant stroma.
Paget disease: skin Patch/Eczema, Large cells with clear halos. Pus/serosanguinous discharge from
nipple.
Mucinous/Colloid carcinoma: Gelatinous consistency and pools of extracellular mucous surrounding
clusters of tumor cells.
Epithelial hyperplasia: Proliferation of normal-looking epithelial cells.
Intraductal papilloma: Proliferation of normal-looking glands and ducts.
Fibroadenoma: Fibrosing stroma around normal glandular tissue.
Invasive Ductal carcinoma: Sheets of pleomorphic cells infiltrating adjacent stroma, Peau d’orange skin,
Unilateral bloody nipple discharge.

Paget’s disease r Deep e Ductal cell carcinoma in situ/Ductal carcinoma thake. Paget’s disease is skin
Patch/Eczematous lesion of breast. Phyloides can have Ulcer in breast but it is bulky tumor.
Comedocarcioma has Cheesy consistency due to Central Caseous necrosis, Calcification. Phyloides
tumors has Pata like porjection.

Obesity is risk factor for CRP. (Colon, Renal, Pancreas cancer).

Prolonged exposure to Estrogen is risk factor for Breast and Endometrial Carcinoma, Estrogen BrEnd.
so, Early menarche, late menopause, Nuliparity, late pregnancy, Positive family history, Tamoxifen use,
estrogen only pill, Obesity (have high estrogen as testosterone is converted to estrone in fat cell) are risk
factor for them. But Cervical cancer is not sensitive to Estrogen exposure. So these are not risk factor for
them. Sexy ladies are more prone to develop cervical cancer. e.g- Early sex, multiple sexual parter,
Smoking, low socioeconomic status. Sexyder Servical cancer hoy.
Paget disease of the breast: Older woman, one form of intraductal carcinoma, Eczematous skin lesion,
Ulceration and Oozing from skin of Nipple and Areola. Paget cells are Large cells with Clear halo. Clear
& Large Page.
Comedocarcinoma: Solid pattern, Cheesy consistency with Central Caseous necrosis. It is also an
intraductal ca in situ but not associated with Paget disease.
Colloid (Mucinous) Carcinoma: Older woman, islands of Tumor cells with Abundant Mucin secretion.
Older woman breast cancer: Paget’s disease, Comedocarcinoma. PC der hoy.
Invasive Lobular Carcinoma: Multicentric/multiLobular, usually have estrogen receptor. Monomorphic
cell. Small tumor cell and may be arranged in Rings. (Lobular carcinoma te cell Line e thake). ? Bilateral.
nonpalpable lump (Invisible Lobule) as small. 1nvasive Lobular Carcinoma: 1 Line, single file
distribution of Cancer cells.
Medullary Carcinoma: Meyeder hoy (Young woman). Fleshy Mass, little fibrous tissue so Soft
consistency, foci of necrosis and hemorrhage is common & Surrounded by a fibroid lymphoplasmacytic
reaction.
Medullary breast carcinoma and Medulloblastoma of brain, Glioblastoma Multiformi all have
haemorrhage and necrosis.
Intraductal Papilloma: Benign solitary lesion, occurs in Premenopausal woman, serous or bloody nipple
discharge, branching fibrovascular core extending from a dilated duct. Proliferation of Normal looking
Glands & Ducts. May confuse with Invasive Papillary carcinoma for bloody discharge in both. double IP
have serous or bloody nipple discharge.
Abortion:
Suspect a Robertsonian translocation in an apparently healthy woman who has many first-trimester
spontaneous abortions. Robert causes first trimester abortion. Low plasma progesterone can cause
repeated early pregnancy loss. If hCG is ineffective in maintaining the corpus luteum, it will regress. The
resulting loss of progesterone causes the endometrium to atrophy and the pregnancy will be terminated.

Male Reproductive Pathology

Undescended Testes Complication: TESTIS- Torsion, Epididymo orchitis, Sterility, Trauma, Inguinal
hernia, Seminoma.

Hydrocele & Varicocele:

Testicular Tumor: The classification of testicular tumor is based on cell of origin. Germ cell tumor
originate from the cell line maturing into sperm cells. Non-germ cell tumors originate from Sertoli cells,
Leydig cells and fibroblasts. Germ cell tumors represent 95% of all testicular neoplasm. To simplify,
approximately one third are seminomas, one-third are nonseminomatous germ-cell tumors (NSGCT), and
one-third are mixed tumors, i.e tumors that include seminomatous and nonseminomatous differentiation.
Germ cell tumor: Seminoma & Non seminoma (TYCE. Teratoma, Yolk sac tumor, Choriocarcinoma,
Embryonal Carcinoma).
Non germ cell tumor: Sertoli cell tumor, Leydig cell tumor, Lymphoma.
Hormone secretion: Yolksac tumor & Embryonal Carcinoma have increased α Fetoprotein level. YEF.
Choriocarcinoma has increased β HCG level. Seminoma & Pure Teratoma have normal α Fetoprotein &
β HCG levels, TeraSemin has no Hormone. but Seminoma has high Placental Alkaline Phophatase & if
Teratoma is mixed with Embryonal Carcinoma then it have increased α Fetoprotein level. Semi Placenta.
Semi has Double PLAP.
Choriocarcinoma is Choto, does not cause enlargement of entire testicle but Seminoma is painleSS
enlargement of testis.
Seminoma: Most common testicular tumor, painless tumor, occurs in young age, Homogenous tumor,
good prognosis, Radiosensitive, Large cell in lobule with watery cytoplasm (Prominent nucleoli and clear
cytoplasm. Nuclear atypia present), Fried egg appearance. reactive with Placental alkaline phosphatase,
CD117. Seminoma is painleSS, Semifried egg/halfboiled egg.
Fried egg cells: Seminoma, Oligodendroglioma,
Teratoma: Common in infants and younger children. Presents with different types of tissues, such as
nerves, muscles, cartilage and hair. Benign in childhood, variable (Benign or malignant) during
adulthood.
Yolk sac tumor: More common in Infants & Children. Aggressive tumor. histologically Yellow (like egg
yolk), alternative name is Endodermal Sinus Tumor (YES-Yolk, Endodermal Sinus)/Infantile embryonal
carcinoma. Yolk sac tumors produce a yellow, mucinous mass that histologically shows endodermal sinus
formation. Resembling glomeruli, called schiller duval bodies. Yolk sac tumors occur in pure form in
infants and children and may be part of mixed tumors in adults. Glomerular Yolk.
Embryonal Carcinoma: Painful, occurs 20-30 years old. Elevated alpha fetoprotein. Very
Undifferentiated and consists of epithelial cell arranged in tubular/GlanduloPapillary pattern. EC has GP.
Choriocarcinoma: Men 15-25 years old. Malignant. Elevated HCG levels . It recapitulates chorionic
villus differentiation, looks like Syncytiotrophoblast cells with abundant hemorrhage and expresses hCG.
This tumor is identical to choriocarcinoma of Placental tissue or Ovary. Patients Have ? Gynecomastia.
Choriocarcinoma contains both Cytotrophoblast & Syncytotrophoblast. Inner layer of chorionic villi is
Cytotrophoblast, Outer layer is Syncytiotrophoblast and Secretes hCG. I COSh.
Ledyg cell tumor: Unilateral, often benign. produces estrogen or androgen, masculinization or
feminization in children, gynaecomastia in adult, precocious puberty in boy. has Reinke crystal. Ledyg
Rein.
Sertoli cell tumor: Unilateral. Sholpo Small amount of Estrogen or Androgen produced. Not enough to
cause clinical symptoms. 90% are benign. Sertoli cell tumor form cordlike structures resembling
Seminiferous tubules.
Lymphoma: Most common in the elderly, often disseminated.
Mixed tesicular tumor are 60% of testicular tumors, with the most common pattern being teratoma,
embryonal carcinoma, yolk sac tumor and hcg containing syncytiotrophoblast. This pattern’s tumor also
contains elements of seminoma. The prognosis of these tumors is determined by the presence or absence
of more aggressive elements, notably choriocarcinoma.
Orchitis:

Penile Carcinoma in Situ:

Bowen disease: Single, white flat plaqe.
Bowenoid Papulosis: multiPle reddish-brown papule.
Erythroplasia of Queyrat: ? Single Soft red plaque.

Genetic disease
Port Wine stain-Permanent stain (not like strawberry-temporary), found in Sturge Weber syndrome.
Niemann-Pick disease: is Neonatal disease (actually child). NPS: Niemann-Pick Sphingomyelinase. No
man Picks (Niemann-Pick) his nose with his Sphinger (Sphingomyelinase). Hepatosplenomegaly is
present in Niemann-Pick disease & Gaucher disease. Two Sax also has the same feature like Niemann-
Pick disease except hepatosplenomegaly.
Gaucher’s tissue paper- gaucher’s cells are crampled tissue paper.

Anti Centromere Ab- CREST Syndrome

Anti Scl-70 (anti DNA- Topoisomerase)- Scleroderma.
Epidural Hematoma- EPI LUCID Lucid Interval.
Hairy Leukoplakia- associated with HIV but does not progress to cancer (or EBV, HPV), but Leukoplakia
is precancerous, not associated with virus.