Pathoma Pics Flashcards
Explain the ‘sawtooth appearance’ on histology of lichen planus
Lichen planus = inflammation (neutrophil infiltration) at the epidermal-dermal junction that gives a saw-tooth appearance of the basement membrane
Which cancer is associated w/ ‘starry sky’ appearance on histology
Buzzword: ‘starry sky’ = Burkitt Lymphoma = neoplasm of intermediate shaped B cells caused by c-myc translocation
These are hepatocytes- describe the changes
Fatty liver! Showing fat droplets inside hepatocytes
ex: CCL4 exposure, free radical production (CCL3 free radical) causes hepatocyte destruction = reduction in apolipoprotein production so fat gets trapped in the liver
Type of tissue necrosis seen in pancreatitis
Pancreatitis = when pancreatic enzymes get activated early, in the pancreatic parenchyma instead of in the lumen of the small intestines
- pancreatic parenchyma undergoes liquefactive necrosis = liquification 2/2 enzymatic breakdown of tissue
- peripancreatic fat undergoes fat necrosis = chalky white appearance due to saponification (deposition of calcium due to FFA deposition)
Image showing both liquefactive (black stuff) and fat necrosis (chalky white)
Differentiate the 5 kinds of neoplasms that can arise from hematopoietic stem cells
5 neoplasms from the HSC –> myeloblasts and leukoblasts
Acute leukemia arises from neoplastic proliferation of blasts due to maturation defect
- when myeloblasts accumulate b/c can’t mature = AML
- when lymphoblasts accumulate b/c can’t mature = ALL
- when mature circulating lymphocytes become neoplastic = chronic leukemia: CLL if mature cells of lymphoid lineage, CML if mature cells of myeloid lineage (granulocytes)
- when mature cells of myeloid lineage neoplastically accumulate = myeloproliferative d/o
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What are Anitschkow cells?
(a) Dx?
Anitschkow cells = histiocytes w/ squiggly nuclei giving them the name ‘catepillar cells’
Anitschkow cells are found in Ashoff bodies in the myocardium pathognomonic for acute rheumatic fever myocarditis
Hallmark histologic feature of basal cell carcinoma
Peripheral palisading of nuclei
Name the main histologic features of a granuloma
Granuloma = aggregate of epitheliod histocytes (meaning lots of cytoplasm so very pink)
- surrounded by ring of lymphocytes (squiggle)
- associated w/ multinucleated giant cells
Note that all histocytes contain their nuclei = noncaseating granuloma
Describe the histologic features of Polyarteritis Nodosa
Polyarteritis Nodosa = vasculitis of medium sized vessels
Histologically characterized by fibrinoid necrosis (see the ton of pink squiggled in the pic)
Explain the mechanism of O2 dependent killing of phagocytosed material
(a) Oxidative burst
(b) Which chemical kills the bacteria?
Overall O2-dependent killing = O2 used to make HOCl- (bleach), bleach then destroys the organism
(a) O2 –> O2- by NADPH oxidase = oxidative burst
(b) Then O2- –> H2O2 (by supraoxide dismutase), H2O2 –> HOCl- by MPO (myeloperoxidase)
- so need NADPH oxidase, SOB, and MPO (all 3 enzymes) for O2-dependent killing
What type of granuloma? Explain
Noncaseating = lack of central necrosis
Differentiate the three stages of nuclear loss during cell death
Starts w/ pyknosis (nuclear shrinkage), then karyorrhexis (nucleus breaks up), then karyolysis (little pieces are broken down into building blocks) and then nucleus gone!
Loss of nucleus = hallmark of cell death
Is this acute or chronic inflammation?
Two key features of acute inflammation = edema and neutrophils
- big white spaces seen btwn tissue = fluid = edema
- small circled multi-lobated cells = neutrophils
(while lymphocytes, plasma cells, and fibrosis would be indicative of chronic inflammation)
Name the two mechanisms of destruction of material inside phagolysosome
(a) Which is more effective?
O2-dependent and O2-independent killing
O2 dependent killing uses NADPH oxidase for oxidative burst and creates HOCl- (bleach) to kill bacteria, O2 independent directly uses enzymes (lysozme) to kill
(a) O2-dependent is much more effective
Name 2 disorders that are due to defects in O2-dependent killing
O2 dependent killing: first rxn is oxidative burst:
O2 –> (NADPH oxidase) –> O2-
O2- –> H2O2
H2O2 –> (myeloperoxidase) –> HOCl-
- NADPH oxidase defect = Chronic granulomatous disease
- MPO deficiency
Dx
Reed Sternberg (‘owl eye’ cells = multi-lobed nucleus w/ prominent nucleoi
- seen in Hodgkin’s Lymphoma: where RS cells release cytokines to draw in reactive inflammatory cells
- then these reactive inflammatory cells, w/ rare RS throughout, make mass
Name the layers of the skin
Basement membrane separates dermis and episdermis
- dermis (light pink, deeper) contains CT, hair follicles, sweat glands, and BV
- epidermis: stratum basalis (basal layer of stem cells, connected to basement membrane by hemidesmosomes) –> stratum spinosum (desmisomes) –> stratum granulosum –> stratum corneum –> keratin (anucleate)
What type of necrosis is shown in the left pic (compared to normal tissue on right)?
(a) Mechanism
(b) Classic clinical example
On the left you see tissue that has preserved cell shape and structure (maintained architecture) but no nuclei
= Coagulative necrosis
(a) Maintain architecture by coagulation of cellular proteins (hence coagulative necrosis…)
(b) This is the type of necrosis that happens 2/2 ischemic infarction of any tissue EXCEPT brain
Free radicals
(a) Name the 3 free radicals produced by partial O2 reduction
(b) Name the rxn by which free Fe produced free radicals
Free radicals are physiologically produced during oxidative phosphorylation if O2 doesn’t get all 4 electrons (so gets partially reduced)
(a) O2 –> O2- (superoxide) –> H2O2 (hydrogen peroxide) –> OH- (hydroxyl free radical) –> H20
- glutathione peroxidase is key free radical containing enzyme that catalyzes OH- to water
(b) Fentin rxn = Fe creates free radical
What type of necrosis is indicated by this picture?
(a) Most likely mechanism
Coagulative necrosis 2/2 ischemic infarct- see wedge-shaped pale area of infarction
(a) Ischemic infarct of any tissue besides the brain causes coagulative necrosis
- wedge shaped b/c of the way vessels branch (so obstruction at tip of the wedge causes necrosis in a wedge shape pattern outwards)
Type of necrosis shown in pic
(a) 2 mechanisms of this necrosis
Fibrinoid necrosis = necrotic damage to blood vessel wall
- intracellular proteins are leaked into the vessel wall giving the characteristic pink staining of the wall (squiggled lines)
(a) Seen in malignant HTN and vasculitis
Name the two histological features used to diagnose amyloidosis on fat pad biopsy
- Congo red staining- so see extracellular amyloid deposition (squiggles) around central blood vessel (dot)
- Apple-green birefringence under polarized light
What is the highlighted cell significant for?
Cell is undergoing apoptosis
- first step is cell shrinking = cytoplasmic condenses = eosinophilic (more pink looking)
- nucleus is smaller
Histologic feature of chronic cholecystitis
Chronic GB inflammation causes formation of Rokitasky-Aschoff sinuses = pseudodiverticula, basically inpouchings/pockets in the GB wall
-not dagernous on their own, but can indicate chronic cholecystitis
Classic EKG finding of Digitalis toxicity
‘Scooped’ concave ST segments
Caseating vs. noncaseating granulomas histologically
In pic see central area of necrosis = non-nucleated cells, shrinked/small cells = dead cells in the middle
-characteristic of Tb and other fungal infections
Dx
Blister btwn the basal layer and stratum spinosum = Pemphigus vulgaris
-2/2 IgG against desmosomes
(don’t confuse w/ IgG against hemidesmosomes = Bullous pemphigoid which would make blister btwn dermis and epidermis, see attached to answer card)
Briefly explain mechanism of neutrophil phagocytosis
(a) Name a d/o in which this is defective
Neutrophils (first cells on the scene in acute inflammation) extend out pseudopods that gets ingested as a phagosome, then this phagosome fuses w/ lysosome forming phagolysosome
Key here = phagolysosome
(a) Defective phagolysosome formation (and therefore in overall phagocytosis) seen in Chediak-Higashi syndrome
Clinical significance of FAS ligand
(a) Physiologically
(b) Pathologically
FAS ligand is expressed on a cell and binds to FAS death receptor (CD95) on cytotoxic CD8+ cells to activate extrinsic receptor-ligand pathway of apoptosis
(a) Causes apoptosis of immature T cells in thymus that fail negative selection- aka have too high an affinity for self-antigen)
(b) pathway goes awry in certain cancers
H2 blockers vs. PPI
(a) End of drug name
(b) Mechanism
(c) Duration of action
H2 blockers are (b) Reversible H2 receptor blockers
(a) ‘idine’ like ranitidine
(c) Immediate onset, short acting => take right before a meal
PPIs (a) irreversibly block the H+/K+ ATPase
(a) ‘prazole’ like omeprazole
(c) Long term => take daily for 24 hr protection
What type of granuloma? Explain
Caseating granuloma = presence of central necrosis
Key histologic feature of atherosclerotic emboli
Cholesterol clefts
-how to differentiate atherosclerotic plaque rupture causing embolization from thrombosis etc = cholesterol clefts in the emboli
Non-Hodgkins Lyphoma
(a) MC: T or B cell?
(b) Name the 3 types of small cell NHL
NHL
(a) Almost all are B cell
(b) Small cells are well differentiated- meaning they better resemble normal tissue, so these 3 cause proliferation of certain zones
- Follicular lymphoma = more follicles
- Mantle cell lymphoma = expansion of compartment just adjacent to the follicle
- Marginal Zone Lymhoma
Describe the histologic features of temporal cell arteritis
Temporal giant cell arterities = large vessel vasculitis
Two features = granulomatous inflammation (meaning presence of giant cells) w/ intimal fibrosis
- usually intima and media are up next to each other, here see the thick F (fibrosis) separating the two, therefore narrowing the lumen
- see multinucleated giant cells in peripheral (granulomatous inflammation)
Histologic finding on biopsy of HOCM
Hallmark = myofiber hypertrophy w/ disarray
Key is DISARRAY
-basically super unorganized myocardium
Explain the embryologic defect that leads to cleft lip/palate
5 facial prominences early in pregnancy that form and fuse, must fuse properly to form face
-cleft lip and palate often co-occur since failure to fuse properly causes both
Facial prominences: one from the top, 2 laterally, 2 form bottom
Differentiate gross pathologic features (aka what you’d see on endoscopy) of benign vs. malignant gastric ulcer
Gastric ulcers:
- benign MC due to H. pylori (70%), NSAIDs (20%): small (under 3cm), sharply demarcated
- malignant features: larger, irregular w/ heaped up margins
Name 2 key biopsy findings in Celiac disease
Celiac disease- take biopsy of duodenum (most commonly involved site) and see
- flattening of villi- villi are the upward-going things
- deepening of crypts (downwards protrusion)
(a) What type of stain?
(b) Dx?
(a) Chromogranin A
- neurosecretory granules released from carcinoidtumors stain positive for chromogranin
(b) Dx = carcinoid tumor
Two unique features of difuse type gastric carcinoma
(a) Histologically
(b) Grossly
(a) Signet ring cells = nucleus pushed off to edge by mucus inside the cell
- signet ring cells characteristic of carcinoma, MC gastric but can also be appendix etc
(b) Grossly- get diffuse thickening of the stomach wall (linitis plastica) that clinically causes early satiety
Give exact steps of insulin release (dude this is important just memorize it already)
What is this cell?
(a) Seen in what d/o
Schistocyte or ‘helmet cell’
(a) Seen in microangiopathic hemolytic anemias- basically there are microthrombi in the BVs that shear the RBC as they move thru
- HUS (hemolytic uremic syndrome) and TTP (thrombotic thrombocytopenic purpura)
Differentiate platelet receptors used in aggregation vs. adhesion
Primary hemostasis (formation of weak platelet plug): vasoconstriction, plt adhesion, plt degranulation, plt aggregation
- vasoconstriction
- Plt adhesion- Gp1b receptor on plts binds to vWF that is bound to subendothelial collagen
- Plt degranulation- releases ADP (increases Gp2b3a) and TXA2 (promotes aggregation)
- Plt aggregation- plts bind to each other via Gp2b3b receptor that links fibrinogen molecules
Explain secondary hemostasis to form stable fibrin clot
Coagulation cascade generates thrombin,
thrombin converts fibrinogen (binding plts in weak plt plug via Gp2b3a receptors) into fibrin
-the fibrin is then cross-linked, yielding a stable plt-fibrin thrombus
Name the clotting factors involved in the 3 pathways of the coagulation cascade
Mneumonic to memorize: first draw X in the middle
- Start on the left (intrinsic pathway): count down from 12 –> 11 –> (skip 10 b/c is already there) –> 9 –> 8
- Then place 7 on the right side (extrinsic pathway)
- then common pathway from the bottom: 1 x 2 x 5 = 10
Differentiate which coagulation factors are measured by PT vs. PTT
Mneumonic to memorize: first draw X in the middle
- Start on the left (intrinsic pathway): count down from 12 –> 11 –> (skip 10 b/c is already there) –> 9 –> 8. More factors on this side => measured by PTT (more letters than PT)
- Then place 7 on the right side (extrinsic pathway) => fewer factors => measured by PT (fewer lettesr)
- then common pathway from the bottom: 1 x 2 x 5 = 10
Differentiate which lab test (PT or PTT) is best used to measure effect of heparin vs. coumadin
Mneumonic to memorize: first draw X in the middle
- Start on the left (intrinsic pathway): count down from 12 –> 11 –> (skip 10 b/c is already there) –> 9 –> 8. More factors => test w/ more letters PTT. Hep has 3 letters, so does PTT => use PTT to measure effect of heparin
- Then place 7 on the right side (extrinsic pathway). Fewer factors => use test w/ fewer letters (PT) => PT used to measure effect of coumadin
- then common pathway from the bottom: 1 x 2 x 5 = 10
Explain how thrombus is removed in normal fibrinolysis
tPA (tissue plasminogen activator) converts plasminogen –> plasmin, plasmin then cleaves fibrin and serum fibrinogen, destroys coagulation factors, and blocks plt aggregation
Then once clot is broken down, alpha2-antiplasmin inactivates plasmin (don’t want plasmin just continuing to go and break up stuff)
Virchow’s triad
3 RF for thrombosis (pathologic intravascular clot)
- Disruption in normal blood flow: non-laminar flow, plts and factors less dispersed
- immobilization, Afib, aneurysm (irregular flow thru abnormal lumen) - Endothelial damage b/c endothelium is very protective against clots (blocks collagen exposure, produced PGI2, NO, heparin-like molecules, tPa, thrombomodulin
- Hypercoagulable states: deficient or inactive protein C/S
Explain how vitamin B12 deficiency can cause endothelial cell damage
Vitamin B12 is needed to demethylate THF (so that THF can be active in DNA precursor synthesis). Then methylated vit B12 converts homocystine –> methionine
W/o Vitamin B12 (or w/o folate), homocystine precursor builds up and directly damages endothelium
MC cause of homocysteinuria
(a) Clinical presentation
Homocystine in the urine 2/2 deficiency in enzyme needed to convert homocystine –> cystathionine (enzyme called cystathionine beta synthase)
(a) Vessel thrombosis (b/c homocysteine directly damages endothelium), mental retardation, lens dislocation, long slender fingers
Histologic finding of amniotic fluid embolism
Characterized by squamous cells and keratin debris (from fetal skin) in the embolism
-differentiate from fat embolism (see fat chunks in embolism) and atherosclerotic embolism (see cholesterol clefts in embolus)
MC location of osteoma
Osteoma = benign tumor of bone, MC on surface of facial bones
Explain the finding
(a) Dx
(b) Other Xray finding
Finding = ‘Codman’s triangle’ = periosteal lifting due to underlying tumor growth
(a) Dx = osteosarcoma
(b) Classic ‘sunburst’ appearance of osteosarcoma
Describe the general anatomy of a joint
Joint: two bones join w/ articular cartilage (made of collagen type II = hyaline cartilag)
- then synovium laterally that secretes synovial fluid rich in hyaluronic acid to lubricate the joint
- all articular surface and synovium surrounded by joint capsule
Explain what rheumatoid factor is
RF = IgM autoantibody against Fc portion of IgG
-IgM against IgG
Explain how eating a steak can precipitate podagra
Steak (full of animal RNA and DNA) can precipitate podagra (gout of great toe) b/c AMP and GMP break down into uric acid
Cell is characteristic of what tumor?
Lipoblast = cell w/ multiple fat globules independent of the nucleus
-characteristic of liposarcoma = malignant tumor of mesenchymal (fat) tissue
Hypospadias vs. Epispadias
(a) Location
(b) Physiology
Hypospadias
(a) Hypo = under, urethral opening under the shaft of the penis
(b) 2/2 failure of urethral folds to close (urethral folds below genital tubercle embyologically, 2 urethral folds fuse around the urethra)
Epispadias
(a) Epi = above, urethral meatus on superior surface of penis
(b) Due to abnormal positioning of the genital tubercle (not failure of ureteral folds to fuse)
Describe histology of the prostate gland
Have both glands and stroma
-both which are maintained by androgens, both of which undergo hyperplasia in BPH in response to DHT
Differentiate location of BPH and prostatic carcinoma
BPH = hyperplasia (benign, no increased risk of cancer) of glands and stroma in the periurethral zone
-so the zone in the center around the prostatic urethra, compresses urethra => early urinary symptoms
MC location of prostate adenocarcinoma is in the posterior periphery => doesn’t produce urinary symptoms (or possibly very late), and much more easily palpable by DRE b/c this is the surface facing the rectum
Explain the histologic appearance of iron deficiency anemia
Microcytic, hypochromic anemia: bone marrow makes smaller and fewer RBCs that lack central pallor
-help to tell RBCs are smaller than should be (macrocytic) b/c RBCs should normally be the same size as lymphocyte nucleus
Explain the histologic finding of siderobalstic anemia
Ringed sideroblast = build up of iron inside mitochondria that form a circle around the nucleus
-so sideroblastic anemia = defect in protoporphyrin synthesis, so iron enters the mitochondria to make heme but is then trapped b/c doesnt have protoporphyrin to combine with
Histologic difference btwn mature RBC and reticulocyte
Reticulocyte is slightly larger and has a blurish tint 2/2 RNA still in the cytoplasm
Histologic finding of hereditary spherocytosis
(a) Explain why there is anemia
Sperocyte w/ loss of central pallor
- loss of membrane (b/c of defective cytoskeleton-membrane tethering proteins) causes spherocyte instead of disc-shaped RBC
(a) It’s not the production, but spherocytes are less able to maneuver in the sinusoids of the spleen => RBCs consumed by splenic macrophages
Characteristic peripheral smear finding of Hb C
Hb C = aut recessive mutation in beta globin gene where glutamic acid is replaced by lysine
Characteristically see HbC crystals in RBCs on blood smear
“C, lyCine, Crystals”
Histologic finding to screen G6PD deficiency
(a) How to diagnose disease
Use heinz preparation to screen for disease- see Heinz bodies containing precipitated Hb inside the RBC (oxidative stress precipitates Hb as Heinz bodies)
(a) Diagnose w/ enyzme study (lacking G6PD) weeks after the hemolytic episode resolves
- b/c if do enzyme studying during the hemolytic episode, all the cells w/ the enzyme are dead anyway!
Embryologic derivatives of
(a) CNS
(b) PNS
(c) Ventricles
(a) CNS derived from the wall of the neural tube
(b) PNS from neural crest cells
(c) Ventricles and spinal cord canal derived from the lumen of the neural tube
- notocord gives rise to nucleus pulposis
Appearance of anencephaly
(a) Complication
Anencephaly = failure of neural tube to close cranially => absence of brain and skull
Frog-like appearance b/c no brain/skull above the eyes so flat head on top of eyes :-(
(a) Polyhydramnios b/c no brain to make fetus swallow amniotic flud
Initial presentation of syringomyelia
(a) Features of expansion
Syringomyelia = general term for cyst or cavity within the spinal cord.
Initially presents as sensory loss of pain and temp (knocked out anterior white commisure) w/ sparing of fine touch and position sense, in a “cape-like” distribution of the upper extremities (b/c MC location is C8-T1)
(a) As syrinx expands, it knocks out anterior horn => muscle atrophy, weakness, hypotonia, impaired reflexes.
Knocks out lateral horn of hypothalamospinal tract = loss of sympathetics => Horner’s syndrome (anhydrosis, miosis, ptosis)
List (in order) the histologic changes seen after cerebral infarction
- Red neurons = acutely damaged neurons undergo eosinophilic change in the cytoplasm, in first 12 hrs of infarction (before 1 day)
- Days 1-3: neutrophilic infiltration
- Then microglial cells (CNS macrophages) come days 4-7
- Gliosis in weeks 2-3 = fluid-filled cystic spaces (cystic b/c underwent liquefactive necrosis) surrounded by gliosis
Gliosis = reactive astrocytes = key finding of old brain infarct
Dx
Lack of cerebellar vermis causing dilation of 4th ventricle = Dandy Walker Malformation
Locate the cerebral hemorrhage
Left pic showing blood under the dura matter and above the brain (so extracranial) = subdural hemorrhage
Right pic showing blood on the surface of the brain = subarachnoid hemorrhage
Dx
(a) Cause
See little lakes or ‘lacunes’ of dead tissue = Lacunar stroke
(a) MC 2/2 hyaline arteriolosclerosis from chronic HTN
(a) First histologic finding of cerebral infarct
(b) Type of necrosis seen 2/2 cerebral infarct
(a) First sign are red neurons = eosinophilic cytoplasm of neurons, occurs w/in first 12 hrs
(b) Liquefactive necrosis where brain parenchyma literally just liquefies (gross)
Multiple sclerosis
(a) MRI findings
(b) LP findings
Multiple sclerosis
(a) MRI: plaques indicating areas of white matter demyelination
(b) LP: classic oligoclonal IgG bands, increase lymphocytes and immunoglobulins, myelin basic protein (2/2 myelin destruction)
Gross pathologic findings of Alzheimer disease
Degeneration of the cortex = cerebral atrophy w/ narrowing of gyri and widening of sulci leading to dilation of ventricles (hydrocephalus ex vacuo
Distinguish the intracellular and extracellular histologic findings of Alzheimer disease
Intracellular neurofibrillary tangles = aggregates of hyperphosphorylated tau (microtubule) protein
Extracellular deposition of Abeta amyloid entangled w/ neuritic processes
Name the three pathological findings of Alzheimer disease
- Grossly: cortical degeneration/cerebral atrophy causing hydrocephalus ex vacuo
- Extracellular Abeta amyloid plaques
- Intracellular deposits of hyperphosphorylated Tau
Parkinson disease pathology
(a) Gross path finding
(b) Histologically
Parkinson disease
(a) Grossly see loss of pigmentation of neurons in the substantia nigra
(b) Histologically: round, eosinophilic inclusions of alpha-synuclein (Lewy bodies) in affected neurons
Explain the role of the two central dopamine receptors involved in Parkinson disease
Parkinson disease = degenerative loss of dopaminergic neurons in the substantia nigra of the basal ganglia
- loss of D1 action, D1 increases stimulation of cortex
- loss of D2 action which reduces inhibition of the cortex => overall reduced input to cortex so movement is impaired
- nigrostriatal pathway of the basal ganglia uses dopmaine to initiate movement
Gross pathology findings of Huntington disease
Huntington disease = loss of GABAergic neurons in the caudate nucleus
- grossly see degeneration of the caudate nucleus (inferior boundary of the lateral ventricles)
- loss of striatal tissue => hydrocephalus ex vacu as ventricles expand into extra space
Creutzfeldt-Jakob disease
(a) EEG
(b) Histology
Creutzfeldt-Jakob disease
(a) EEG finding: periodic sharp waves
(b) Histologically: intracellular vacuoles (vacuolization of cytoplasm) = spongiform changes
Histologic characteristic of glioblastoma multiforme
GBM = malignant high grade tumor of astrocytes
- characterized by regions of necrosis surrounding the tumor cells (pseudopalisading, and endothelial cell proliferation
- tumor cells stain GFAP positive
Buzzword = pseudopalisading necrosis
Histologic hallmark of meningioma
Whroled pattern of cells w/ psammoma bodies = laminated calcific conceretions
Histologic hallmark of oligodendroglioma
‘Fried-egg’ appearance of cells on biopsy
Pilocytic Astrocytoma
(a) MC location
(b) CT finding
Pilocystic astrocytoma = benign tumor arising from astrocytes
(a) MC arises in cerebellum
- MC primary CNS tumor in children and recall that CNS tumors in children are mostly infratentorial (so fits that it develops in the cerebellum)
(c) CT finding: cystic lesions w/ mural nodule
Histologic findings on pilocytic atrocytoma
Pilocytic astrocytoma = benign tumor of astrocytes seen in children
Rosenthal fibers = thick eosinophilic processes of astrocytes and eosinophilic granular bodies
-GFAP positive b/c GFAP is the intermediate filament in astrocytes
Perivascular pseudorosettes are a characteristic finding of what CNS tumor?
Ependymoma = malignant tumor of ependymal cells (line the ventricular space)
-typically seen in children
Pseudorosette b/c central structure isn’t part of the tumor, perivascular b/c the tumor cells are collected around a blood vessel
Differentiate the CXR appearance of the three patterns of pneumonia
- Lobar- consolidation of entire lobe
- Bronchopneumonia- scattered patchy consolidation around bronchioles
- Interstitial pnemonia- diffuse interstitial infiltrates, the interstitium (the CT of the alveoli air sacs) contain the neutrophils/debris
- visualized on CXR as increased air spaces
Differentiate primary and secondary Tb
(a) Gross pathologic findings
(b) Location
Primary Tb arises from initial exposure = Ghon complex- focal caseating necrosis in lower lobe and hilar LN, undergoes fibrosis and calcification
vs
Secondary Tb after reactivation- forming cavitary foci of caseating necrosis at the apex of the lung (poor lymphatic drainage and high O2 tension)
Describe the histologic features of fat necrosis of the breast
Fat necrosis often biopsied b/c causes calcifications on mammography => biopsy to distinguih from cancer
Bx shows necrotic fat w/ assocaited calcifications and giant cells
What is the Reid index in the diagnosis of chronic bronchitis?
Reid index = thickness of mucus glands relative to bronchial wall thickness
-usually under 40%, while increases to 50% in chronic bronchitis
Centriacinar vs. panacinar emphysema
Centriacinar emphysema- predominantely upper lobe (b/c cig smoke rises) and central acini affected b/c thats where cig smoke gets trapped
Panacinar emphysema most severe in lower lobes due to deficiency in antiprotease alpha-1 antitrypsin
2 findings of sputum in asthmatics
- Curschmann spirals = spiral-shaped mucus plugs
- Charcot-Leyden crystals = eosinophil-derived crystals
Explain what forms Charcot-Leyden crystals in asthmatics?
Charcot-Leyden crystals = crystalline aggregates of major basic protein from eosinophils, present in sputum of asthmatics and parasitic infections
Late CT findings of idiopathic pulmonary fibrosis
Honeycombing of lung parenchyma when fibrosis is diffuse
-fibrosis strats as subpleural patches, then eventually becomes diffuse involving the entire lung
Asteroid bodies- seen in what conditions?
Asteroid bodies = stellate inclusions seen w/in giant cells of noncaseating granulomas
- sarcoidosis
- also seen in foreign body inclusions
Histologic hallmark of pulmonary hypertension
Plexiform lesions w/ longstanding pulmonary hypertension: smooth muscle hypertrophy of pulmonary arteries w/ intimal fibrosis
-tufts of capillaries
(justk now Plexiform lesion)
CXR finding of ARDS
‘White out’ on CXR
- thickened diffuse barrier by hyaline membranes
- collapsed air sacs from increased air tension
Histologically differentiate the two lung cancers that present w/ chromogranin positive cells
Small cell carcinoma = poorly differentiated small cells that arise from neuroendocrine cells
- seen in male smokers, centrally located, associated paraneoplastic conditions
- Histologically: diffuse, not in nests
Carcinoid lung tumor = well differentiated neuroendocrine cells in nests
-not significantly related to smoking
2 histologic features of squamous cell carcinoma of the lung
- keratin pearls
- intercellular brides
Differentiate the histologic features of the two subgroups of intrarenal azotemia
Renal azotema divided into acute tubular necrosis (ATN) and acute interstitial necrosis (AIN)
ATN- tubular cells die (see anucleated pink cells) and slough off into lumen (no patent lumen in tubules = obstruction of filtrate)
AIN- tubules intact but inflammatory infiltrate in the CT btwn tubules
How does renal papillary necrosis present clinically?
Renal papillae = collection of the collecting ducts, renal papillae come together to form the minor calyx –> major calyx –> ureter
Pt w/ nephrotic syndrome and this H&E- Dx?
Normal glomeruli on H&E = minimal change disease
-change so ‘minimal’ that H&E is normal, its only on electron microscopy that you can see the podocyte effacement (flattening)
Pt w/ nephrotic syndrome and this H&E- Dx?
(a) EM finding
See part of (segment of) the glomeruli (not the entire thing) sclerosed = focal segmental glomerulosclerosis
- focal b/c not all glomeruli are involved, segmental b/c only part of the involved glomeruli are sclerosed (so the name tells you it all!)
(a) On EM (just like minimal change disease) see podocyte effacement/flattening on top of the basement membrane of the filtration barrier
Describe the 3 components of the glomerular filtration membrane
Glomerular membrane
- Endothelial cells lining the capillaries
- Basement membrane
- Epithelial cells on top of basement membrane = podocyte foot processes
Name the type of nephrotic syndrome caused when immune complexes deposit in the 3 different possible places of the filtration membrane
(a) Subepithelial
(b) Intramembranous
(c) Subendothelial
Immune complex deposition causing nephrotic syndrome (proteinuria over 3.5 g/day)
(a) Subepithelial deposits (above basement membrane, below epithelial podocyte food processes) = membranous nephropathy
(b) Intramembranous (IC in the basement membrane) = type II membranoproflierative glomerulonephritis (MPGN)
(b) Subendothelial (IC below the capillary endothelial cells) = type I MPGN
Describe Kimmelstiel-Wilson nodules characteristic of diabetic nephropathy
Diabetic nephropathy due to hyaline arteriolosclerosis by nonenzymatic glycosylation of the vascular basement membrane- get mesangial sclerosis = Kimmelstiel-Wilson nodules
Typical molecular finding diagnostic of amyloidosis on renal biopsy
Apple-green birefringence under polarized light after staining w/ Congo red
Pt w/ nephrotic syndrome and this H&E- Dx?
Nephrotic syndrome categories: normal H&E (MCD), FSGN with partial area of sclerosis, Membraneous w/ thickened BM
-here see thickened diffuse membrane 2/2 immune complex deposition, so Ddx = membranous nephropathy or membranoproliferative glomerulonephritis (depends on exact location of immune complexes)
Immunofluoresence findings in nephrotic syndrome
(a) MCD
(b) MPGN
(c) Membranous Nephropathy
(d) FSGS
IF findings
(a) MCD- normal, no immune complexes
(b,c) MPGN and membranous nephropathy both show ‘granular’ appearance on IF 2/2 immune complexes
- so see all the little ICs as little granules outlining the filtration membrane
(d) FSGS- also nothing on IF b/c there are no immune complexes, issue here is focal and segmental sclerosis of the glomeruli
Describe how systemic amyloidosis causes nephrotic syndrome
Systemic amyloidosis, MC organ involved is the kidney
Amyloid deposits in the mesangium causing nephrotic syndrome, mesangium = CT btwn capillaries
Diagnostic apple green birefrigence under congo red stain
H&E findings of post-strep glomerulonehpritis
(a) Immunofluorescence
Nephritic syndrome => has hypercellular, inflammed glomeruli
- nephritic syndrome is characterized by glomerular inflammation and bleeding => see lots of lymphocytes in the glomeruli
(a) Granular appearance on IF b/c immune complex mediated
20 yo 2-3 weeks after step pharyngitis p/w hematura and periorbital edema
25% of adults who develop post-strep GN progress to rapidly progressive glomerulonephritis seen on this H&E by glomerular crescentic formation
Composition of deposition seen in rapidly progressive glomerulonephritis
Rapidly progressive glomerulonephritis causes crescentic formation in glomeruli, crescents of Bowman space comprised of fibrin and macrophages
**fibrin**
Goodpasture syndrome
(a) Clinical presentation
(b) Diagnosis of renal involvement
(c) Immunofluoresence finding
Goodpasture syndrome
(a) Clinically: hematuria and hemoptysis 2/2 antibody against collagen in the basement membrane of both glomeruli and alveli
(b) Renal involvement = rapidly progressive (also called crescentic) glomerulonephritis
(c) IF: linear pattern b/c showing anti-BM antibody
Mechanism of IgA nephropathy
IgA nephropathy = IgA immune complex deposition in themesangium of the glomeruli
-IC => see mesangial pattern on immunofluorescence
Differentiate clinical features of nephrotic vs. nephritic syndrome
Nephrotic syndrome- peeing out tons of protein due to glomerular dysfunction, clinically get pitting edema (hypoalbumin), hypercoagulable state
Nephritic syndrome- glomerular inflammation and bleeding, clinically get oligura and azotemia w/ periorbital edema (2/2 salt retention)
Clinical triad of Alport Syndrome
Alport syndrome = X-linked inherited defect in type IV collagen
- Renal: nephrotic syndrome => hematuria
- Hearling loss
- Ocular/visual disturbance
Renal involvement of Alport syndrome
Alport syndrome = X-linked inherited defect in type IV collagen causing hematuria (nephritic syndrome), hearing loss, vision loss
Type IV collagen defect => thinning and splitting of glomerular basement membrane => hematuria (nephritic syndrome)
Histologic finding of chronic pyelonephritis
‘Thyroidization of kidney’ seen in chronic pyelo
-atrophic tubules (2/2 multiple bouts of acute pyelonephritis)
Differentiate flat vs. papillary transitional carcinoma
Two pathways of urothelial (transitional cell) carcinoma
- Flat: starts at high grade then invades, associated w/ early p53 mutation
- Papillary: starts as low grade then high grade then invades, not associated w/ early p53 mutations
Describe appearance of erythema multiforme
Erythema multiforme = hypersensitivity rxn of targetoid rash and bullae
- targetoid sometimes not super obvious but look for lesions of dif shapes (multiforme) w/ central pallor
- targets = central epidermal necrosis surrounded by erythema
MC site of endometriosis
Endometriosis = endometrial tissue (both glands and stroma) located outside of the uterine endometrial lining
-MC involves the ovaries, which classically forms a ‘chocolate cyst’ due to accumulation of endometrial debris
Classic gross pathologic finding of endometriosis in soft tissue
‘Gun powder’ nodules = yellow/brown bits of endometrial tissue outside of the uterine endometrial lining
What is endometrial hyperplasia?
(a) Cause
Hyperplasia specifically of the endometrial glands relative to the stroma, so more glands than stroma (CT that holds together the endometrium)
(a) Caused by unopposed estrogen: obesity, PCOS, menopause transition b/c estrogen w/o progesterone afterwards)
Differentiate histologic features of hyplerplastic vs. sporadic endometrial carcinoma
Which cestode is Taenia saginata?
Left = Taenia solium (piggies oink oink), Right = Taenia saginata (cattle)
Characteristic T. solium have hooks on proglottid heads visible on O&P (see those hooks on the thing on the left)
So w/o hook = Taenia saginata
Clinical presentation when see this bad boy on Stool O&P
Characteristic image of giardia => clinically p/w foul smelling diarrhea from camper/traveler drinking river water
-see the trophozoites in stool O&P
Clinical presentation when see this bad boy on stool O&P
Image showing trophozoite w/ endocytosed RBCs, characteristic of Entamoeba Histolytica
Clinically: R. liver lobe abscess, intestinal amebiasis w/ blood diarhea and colonic ‘flask shaped’ ulcerations
Clinical presentation of Bartholin cyst
(a) Demographic
(b) Physiologic fxn of Bartholin duct
Unilateral, painful cystic lesion at the lower vestibule (opening to vaginal canal)
Arises due to infalmmation and obstruction ot he gland
(a) F of reproductive age
(b) Fxn: produces mucus-like fluid that drains via ducts into lower vestible
What is extramammary paget disease?
(a) Clinically
(b) Bx to distinguish from what?
Malignant epithelial cells in the epidermis of the vulva, so see random malignant cells in the epithelial layer of the vulva on histology
(a) Clinically presents as erythematous, pruritis, ulcerated vulvar lesion
(b) Biopsy w/ stains to differentate from melanoma- which doesn’t commonly affect vulva but is also a malignancy of the skin…
Differentiate the stages of CIN
(a) Percent that reverse
CIN I involving less than 1/3 of epithlium thickness
CIN II: 1/3 to 2/3 of epithelium thickness
(a) 66% reverse
CIN III: slightly less than entire thickness of epithelium invovled
(a) 33% reverse
CIS = all epithelium involved but basement membrane not invaded
-involved means presence of HPV infected cells (microscopically tell by koilocytic change: raisinoid nucleus, also increased N:C ratio w/ hyperchromic nucleus)
Describe the anatomy of an ovarian follicle
Ovarian follicle: oocyte (egg) in the middle, first surrounded by granulosa cells (respond to FSH, produce estradiol)
Then outer surrounding by theca cells that respond to LH by producing androgens from cholesterol
Estrogen from granulosa cells work directly on oocyte for maturation
Composition of corpus luteum
Corpus lutuem is made of the granulosa and theca cells that are leftover after the egg leaves (ovluation)
Fxns to secrete progesterone to maintain thick endometrium for possible pregnancy
5 yo girl p/w adnexal mass, biopsy shows gomerular-like cells
Dx?
Dx = Endodermal sinus tumor = germ cell tumor from yolk sac tissue
-elevated serum AFP (b/c the yolk sac produces it…)
Schiller-Duvalbodies = glomerulus-like structures that are classically seen on histology
Krukenberg tumor
(a) Key histologic finding
Krukenberg tumor = b/l mets of mucionus tumor to the ovaries (MC diffuse gastric adenocarcinoma)
(a) Signet ring like a finger w/ a ring on periphery b/c abundant mucus in cytoplasm pushes nucleus to the periphery
What is placenta previa?
(a) Clinical presentation
(b) Clinical consequence
Placenta previa = implantation of placenta in the lower uterine segment causing the placenta to overlie the cervical os
(a) Presents as third-trimester bleeding
(b) Usually means C-section will be required, b/c delivery would compress th placenta and cut off fetal blood supply
If undetected by prenatal care, how does hydatidiform mole present?
W/o prenatal care: presents in second trimester by passage of grape-like masses (clear) thru the vaginal canal
Grape-like masses = abnormal edematous villi passing
Differentiate genetic cause of partial and complete molar pregnancy
Partial molar pregnancy: normal egg gets fertilized by two sperm (or two sperm that duplicates chromosomes) => 69 chromosomes
Complete molar has no maternal genes: empty ovum is fertilized either by two sperm or by one sperm w/ duplicated chromosomes = 46 chromosomes
