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liquefactive necrosis

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Last updated

6 years ago

Date created

Mar 1, 2020

Cards (131)

Section 1

(50 cards)

liquefactive necrosis

Front

brain infarct, bacterial infections, pancreatitis

Back

Ziehl-Nielsen

Front

acid-fast bacteria

Back

Acetaminophen toxicity

Front

produces NAQI reactiva compound which binds to glutathione (depletes it) metabolism by P450 (CYP2E1) zone 3 necrosis/centrilobular necrosis (region with high concentration of P450) present with Jaundice, RUQ pain

Back

Vitamin C deficiency

Front

scurvy, hemorrhagic diathesis, poor wound healing purpura, bleeding, petechiae- collagen production inhibited

Back

Pyridoxine deficiency

Front

peripheral neuropathy, sideroblastic anemia, impaired immune function, weakness, dermatitis medication induced: isoniazid- always give B6 supplement B6

Back

Sideroblastic anemia

Front

defect in mitochondrial heme synthesis producing ringed sideroblasts

Back

Thiamine deficiencies

Front

Heart= Beriberi, dilated cardiomyopathy Brain= Wernicke-Korsakoff syndrome B1- alcoholics

Back

Vitamin D deficiency

Front

Rickets or osteomalacia bone mineralization inhibited Rachitic rosary- cartilage and unmineralized osteoid overgrowth Collagen 1- skin and bone Vitamin D made in the kidney (1-a-hydroxylase) then converted in the skin and increases absorption of calcium from the gut sxs: diet? renal? sun exposure? fat malabsorption?

Back

Vitamin A deficiency

Front

night blindness, dry skin without vitamin A; cells do not mature. Causes metaplasia White spots are squamous cell metaplasia

Back

Cachexia marker for cancer

Front

TNF (tumor necrosis factor)- pro-inflammatory cytokine suppresses appetite and depletes lipids elevated leptin levels

Back

desmin

Front

muscle: cardiac, smooth, skeletal muscle cells

Back

acid fast stain

Front

cryptosporidium oocyst

Back

pyknosis

Front

nuclear condensation "shrinking"

Back

brown granular casts in urine

Front

degenerative, sloughed off renal epithelial cells

Back

timeline of tissue repair

Front

1 day: acute necrosis 1 week: abscess, macrophages, granulation 1 month: wound healing via re-epitheliazation /scar formation *scarring if there is no underlying stem cell/regenerative tissue

Back

cytokeratin stain

Front

epithelial cells

Back

congo red

Front

amyloid

Back

Fat necrosis

Front

Fatty tissue is broken down into fatty acids saponification

Back

Appetite regulation

Front

Ghrelin: growls/grows Leptin: lowers

Back

chromogranin stain

Front

neuroendocrine cell

Back

Karyorrhexis

Front

nuclear fragmentation

Back

cystic fibrosis

Front

pancreatic insufficiency because of mucus plugs-> bile duct obstruction no bile= no fat absorption= no ADEK vitamins absorbed

Back

trichrome stain

Front

collagen (chirrosis of the liver)

Back

gram

Front

bacteria

Back

Mucicarmine

Front

Cryptococcus neoformans Aspergillus- 45 angle Pneumocystis Jirovecii vs. KOH= scrape specimen

Back

india ink

Front

cryptococcus neoformans CSF culture

Back

CD3 stain

Front

T cell (toddlers)

Back

carcinoid tumor

Front

tumor cells use tryptophan to produce serotonin (flushing)- high levels of 5-HTP liver metastasis only affects right side of the heart, broken down in the lungs to 5-HIAA present in the urine depletes all tryptophan-> niacin deficiency

Back

reversible cell injury

Front

decreased ATP synthesis decreased Na/K ATPase function anaerobic glycolysis decreased protein synthesis plasma membrane blebs and myelin figures

Back

Marasmus vs. Kwashiorkor

Front

Marasmus-low in both calories and protein Kwashiorkor-severe protein deficiency edema: due to increased capillary hydrostatic pressure OR decreased plasma oncotic pressure (hypoproteinemia)

Back

Niacin deficiency

Front

pellagra: dermatitis, diarrhea, dementia, death B9 due to inadequate tryptophan, diet primarily of corn (south america, impoverished)

Back

Periodic acid schiff

Front

carbohydrates alpa-1-antitrypsin basement membrane

Back

vinyl chloride

Front

risk for liver angiosarcoma risk: plastics

Back

Collagen types

Front

I = bONE, skin II = carTWOlage III = blood vessels, granulation tissue IV = basement membrane, lens

Back

prussian blue

Front

iron (hemochromatosis)

Back

vimentin stain

Front

mesenchymal cells, endothelial cells, vascular smooth muscle, fibroblasts

Back

Hyper-vitaminosis

Front

A= stored in stellate cells, liver disease, jaundice (eskimos d/t diet of whale, GNC supplements) Vitamin D= irritability, fatigue, muscle weakness, bone resorption, metastatic calcifications

Back

Carbon tetrachloride (CCl4)

Front

cytochrome p450 converts CCL4 to CL3 free radical- leads to membrane peroxidation damage to liver, kidney, brain risk: occupational

Back

Folate deficiency

Front

megaloblastic anemia vitamin B9

Back

Vitamin B12 deficiency

Front

pernicious anemia (cobalamin) neuropathy

Back

irreversible cell injury

Front

severe membrane damage marked mitochondria dysfunction rupture of lysosomes nuclear changes

Back

S100 stain

Front

neuroendocrine cell melanocytes (also neurocrest cell derived) schwannoma

Back

Karyolysis

Front

dissolution of nucleus "ghost nucleus"

Back

Vitamin K deficiencies

Front

bruising Vit K dependent clotting factors 2, 7, 9, 10, Protein S, C Warfarin: affects vitamin K dependent reaction sxs: usually pharmacologic we get Vitamin K from bacteria so if someone had a colonic resection- increased risk neonates get Vit K injection for this reason

Back

Necrosis vs. Apoptosis

Front

necrosis: pyknosis, kryorrhexis, karyolysis apoptosis: pyknosis, karyorrhexis

Back

Silver Stain

Front

H. Pylori Pneumocystis Jirovecii (black stain)

Back

synaptophysin stain

Front

neurons

Back

caseous necrosis

Front

degeneration and death of tissue with a cheese-like appearance seen in TB

Back

CD20 marker

Front

B cell

Back

tryptophan downstream products

Front

Back

Section 2

(50 cards)

ITP types

Front

acute (Child, viral, self-limited) vs. chronic (SLE) immune thrombocytic purpura IVIG given to help survival of the platelets by blocking Fc receptors on macrophages if steroid and IVIG do not work in patient with ITP splenectomy is last and final option

Back

Chediak-Higashi syndrome

Front

impaired phagolysosome formation. Pathophys: Microtubule polymerization disorder means the "tracks" to get around the cell are broken, as such transport of phagosomes is deficient. albinism, peripheral neuropathy, pyogenic infections

Back

Leukocyte adhesion deficiency

Front

Late seperation of umbilical cord, AR loss of CD18 necessary for integrin formation, recurrent infections without pus

Back

Chronic Granulomatous Disease (CGD)

Front

defect in NADPH oxidase → ↑ susceptibility to infections with catalase + organisms (S. aureus, Aspergillus, listeria, enterobacteria.)

Back

Immigrant swimming in nile with hematuria and malignant squamous epithelial cells- cause?

Front

Squamous cell carcinoma in bladder triggered by schistosomiasis haematobium

Back

Crigler-Najar Syndrome

Front

a) Complete deficiency in UDP glucuronyltransferase b) present in childhood unconjugated bilirubin deposits in the brain

Back

PECAM

Front

neutrophil migration

Back

Psammoma bodies

Front

dystrophic calcification of apoptotic neoplastic cells meningioma papillary thyroid serous cystadeno of ovaries mesothelioma

Back

Complement deficiencies

Front

recurrent neisserial infection

Back

Fibrinoid necrosis

Front

HPS type 3 due to vasculitis be careful with these stems; vs: if the patient has amyloidosis it could be amyloid deposition vs: also could be hyaline arteriosclerosis

Back

ristocetin

Front

measures platelet aggregation with the help of von Willebrand factor (vWF) and exogenous antibiotic ristocetin added in a graded fashion.

Back

giant cell arteritis

Front

temporal artery granulomatous vasculitis; ipsilateral blindness (ophthalmic artery) older female, polymyalgia rheumatica increased ESR: giant cells on bx

Back

Hemophilia A

Front

Factor VIII deficiency, sex-linked recessive. Spontaneous hemarthosis. Excessive bleeding especially deep tissue (muscle). Prolonged PTT (normal PT). Treat by replacing factor & fresh frozen plasma. Genetic counseling

Back

Pathologic vs physiologic LVH

Front

Athletes will have a normal end diastolic LV internal diameter (42-60mm) *be careful with these questions

Back

If cryoprecipitate transfusion improves bleeding coagulation

Front

vWB disease cryoprecipitate provides: vWF, fibrinogen, factor 8, factor 13, fibronectin

Back

Crescendo-decrescendo murmur

Front

AORTIC STENOSIS

Back

Histamine

Front

Chemical stored in mast cells that triggers dilation and increased permeability of capillaries.

Back

Dubin-Johnson syndrome

Front

Conjugated hyperbilirubinemia due to defective liver excretion. Grossly black liver. Benign.

Back

Indomethacin MOA

Front

Prostaglandin inhibitor (NSAID) via COX-2 pathway

Back

C3b

Front

opsonization

Back

Thromboxane

Front

potent platelet activator, vasoconstrictor

Back

ICAM

Front

neutrophil adhesion molecule

Back

Polyarteritis nodosa

Front

Hep B +, affects multiple medium-sized arteries EXCEPT PULMONARY Transmural inflammation young adults, skin, GI tract, liver, kidney

Back

Sialyl Lewis X

Front

Found on leukocytes, binds to P and E selectins during Neutrophil Rolling

Back

Heparin-induced thrombocytopenia (HIT)

Front

Development of IgG antibodies against heparin- bound platelet factor 4 (PF4). Antibody-heparin-PF4 complex activates platelets leading to thrombosis and thrombocytopenia. Prolonged PTT

Back

Kawasaki disease

Front

(inflammation of blood vessles, hence the strawberry tongue) causes coronary artery aneurysms. asian child <4yo fever, conjuctiva, rash next steps: ECHO- look for coronary artery aneurysm tx: ASA (only exception to the rule of Reyes)- prevent thrombosis OR IVIG

Back

Councilman bodies

Front

Toxic or viral hepatitis (dying/ apoptotic hepatocytes); small round eosinophilic masses found in dying hepatocytes often containing chromatin remnants

Back

Gangrenous necrosis

Front

death of tissue from severe hypoxic injury torsion, ischemia

Back

Abciximab

Front

Blocks glycoprotein IIa/IIIb receptor to decrease platelet binding to fibrinogen

Back

DIC

Front

causes: acute promeylocytic leukemia AML, M3 Adenocarcinomas- mucin activated extrinsic pathway STOP Making New thrimbi: Sepsis, trauma, Obstetrics, Pancreatitis, Malignancy, Nephrotic syndrome (minimal change disease)

Back

CD11b/CD18

Front

marker for integrin

Back

Abnormal neutrophil respiratory burst activity

Front

NADPH oxidase activity deficient

Back

Glanzmann thrombasthenia

Front

Due to a genetic GPIIb/IIIa deficiency; platelet aggregation is impaired abnormal aggregation with epinephrine, ADP

Back

Which chemical is most responsible for the symptoms of asthma?

Front

Bradykinin other chemicals: IL-1= fever LB4= chemotaxis PGE2= pain, vasodilation TAXA2= vasoconstriction

Back

Hyaline change

Front

nonspecific term used to describe any intracellular or extracellular alteration that has a pink homogenous appearance on H&E stain

Back

mallory body

Front

An irregular red-staining structure in the cytoplasm of injured liver cells, usually resulting from alcohol-induced liver injury

Back

Prostaglandins

Front

vasodilation

Back

Bud Chiari Syndrome

Front

thrombosis of hepatic veins

Back

Leukotriene B4

Front

cause neutrophil migration to sites of inflammation. Other importnat ones to know are C5a and IL-8. chemokine

Back

Von Willebrand Disease

Front

bleeding disorder caused by a deficiency of von Willebrand factor, a "sticky" protein that lines blood vessels and reacts with platelets to form a plug that leads to clot formation Autosomal Dominant vs. Bernard Soulier

Back

CGD and nitroblue Tetrazolium test

Front

negative NBT test in CGD patients (no reduction occurs)

Back

Hypertrophic scar vs. keloid

Front

Hypertrophic scar does not extend beyond the boundary of the wound Keloid wound grows past the boundary of the original injury (see the histology)

Back

Bernard-Soulier syndrome

Front

genetic GPIB deficiency; platelet ADHESION impaired, blood smear shows thrombocytopenia with enlarged platelets. abnormal platelet aggregation with ristocetin enlarged because they are slightly more immature PTT will be normal Autosomal Dominant

Back

Diabetes and chronic cystitis

Front

DM2 are more susceptible to resistant bacteria

Back

Takayasu arteritis

Front

Granulomatous (giant cell) inflammation of media and adventitia of large elastic arteries. Asian women. Female-to-male ratio of 10:1. Most often affects thoracic aorta and its proximal branches and pulmonary arteries.

Back

Unopposed estrogen effect

Front

Can lead to carcinoma in post-menopausal females

Back

scar formation

Front

Myofibroblasts-> type 3 collagen replaced by type 1 collagen (except keloid: collagen 3 remant)

Back

TTP

Front

Pentad: FAT RN Fever Anemia (microangiopathic hemolytic) Thrombocytopenia (petechiae, mucocutaneous bleed) Renal dysfunction / uremia Neuro sxs (HA, CVA, AMS) Primary: MC idiopathic AI --> Ab vs ADAMST13 Secondary: malignancy, HIV Dx: thrombocytopenia, NORMAL coags (same as in HUS; DIC will also have abn coags) hemolytic anemia: incr retic, schistocytes, incr LDH, incr INdirect bili, decr haptoglobin Tx: Plasmapheresis Tx/oC, steroids DON'T do platelet transfusion (more thrombi formation)

Back

Bcl-2 overexpression

Front

follicular lymphoma t(14;18) inhibits apoptosis- lymphoma cells survive

Back

Hageman factor

Front

Factor XII Converts pre-kalikrein to kalikrein Kalikrein is responsible for producing bradykinin

Back

Section 3

(31 cards)

syphilic aortitis

Front

wrinkling of intimal surface thoracic dilation with atrophy of the muscularis 3rd stage of syphilis

Back

C-ANCA vs P-ANCA

Front

C= cytoplasmic; antiprotease 3 P= perinucleolar; myeloperoxidase

Back

Marfans

Front

Arachnodactyly- long slender fingers high risk of aortic dissection gene: Fibrillin, FBN1 support protein for elastic fibers

Back

Stanford type A vs. B

Front

A: ascending B: descending

Back

ASO titer

Front

Blood draw used to detect prior infection by group A Streptococcus, responsible for diseases such as: Bacterial endocarditis, glomerulonephritis,rheumatic fever,scarlet fever, strep throat

Back

Microscopic polyangiitis

Front

palpable purpura; crescentic GN; p-ANCA variant of PAN

Back

rheumatic heart disease

Front

damage to the heart muscle or heart valves chorea fever subcutaneous nodules

Back

coagulative necrosis

Front

4h-3days

Back

fluffy infiltrates on chest XR 3 days after MI in RCA

Front

posteromedial papillary muscle rupture mitral valve regurgitation-> infiltrates in the lungs

Back

GPA vs. Good pasture syndrome

Front

GPA: hemoptysis, hematuria, ulcers in nasal mucosa Good pasture: hemoptysis, hematuria

Back

Prinzmetal angina

Front

episodic chest pain unrelated to exertion can see ST elevation on EKG

Back

von Hippel-Lindau disease

Front

a hereditary disease that includes the development of cysts within the pancreas and other organs such as kidney (von Hippel Rindau; r for renal) hemangioblastoma pheochromocytoma autosomal dominant HIF gene (Hypoxic Induction Factor)

Back

Osler Weber Rendu

Front

autosomal dominant. Hereditary hemorrhagic telangiectasia. GI bleeds, epistaxis, AVM in liver/lung/brain. high output cardiac failure vs. Padget disease of the bone also has high output cardiac failure

Back

dressler syndrome

Front

Onset is typically 1 week to 3 months postinjury. Fever, chest pain, pericarditis, pericardial effusion, and pleuritis, with pleural effusion usually more prominent on the left. Dressler syndrome responds well to anti-inflammatory medications.

Back

Fibromuscular dysplasia

Front

Most commonly affects renal artery and carotid artery young women

Back

Sturge Weber

Front

Port wine stain of the face/ hemangioma think of Andrew LLoyd Weber->phantom of the opera mask

Back

polycystic kidney disease

Front

autosomal dominant berry aneurysm, circle of Willis

Back

most likely vessel to have atherosclerotic involvement

Front

abdominal aorta- round ostia turbulent blood flow then: coronary, popliteal, interna carotid

Back

neurfibromatosis type II

Front

which type of neurofibromatosis, gene on chromosome 22 (merlin gene), bilateral acoustic neuromas (8th cranial nerve), multiple meningiomas

Back

homocysteine

Front

increased levels indicate risk for ischemic heart disease, stroke, and PVD

Back

Mid-systolic click

Front

mitral valve prolapse

Back

Tuberous sclerosis

Front

Skin lesions: Adenoma sebaceum. Ash-leaf spots. Brain lesions: Subependymal hamartomas. Cortical tubers. Subependymal giant cell astrocytomas located at foramina of Monro (May lead to hydrocephalus) heart: rhabdomyeloma

Back

timeline for cardiac tamponda

Front

3-7 days after MI neutrophils switching out with macrophages granulation tissue is incomplete (collagen 3)- WEAKEST point in timeline for MI

Back

Abdominal Aortic Aneurysm (AAA)

Front

pulsatile non tender mass history of CVD or previous MI

Back

Eosinophilic granulomatosis with polyangiitis (Churg- Strauss)

Front

P-ANCA eosinophilia variant of PAN asthma, sinus, skin, GI tract, kidney (chug your pee)

Back

Treg secrete TGF-beta

Front

prevents macrophage inflammation and promotes smooth muscle cell proliferation fibrous cap formation= stable plaque fibrous cap ulceration can result in MI

Back

Myocardial Infarction Patterns

Front

Back

The MOA of most MI cause of death

Front

ventricular fibrillation

Back

Henoch-Schonlein Purpura

Front

IgA-anti-IgA immune complexes -> palpable purpura on buttocks/legs, IgA GN, arthritis

Back

Fibrinous pericarditis causes

Front

dressler syndrome, uremia, radiation, rheumatic fever, lupus, presents with loud friction rub DIFFUSE ST SEGMENT ELEVATION

Back

Granulomatosis with polyangiitis (Wegener)

Front

C-ANCA older males upper & lower resp tract kidney (W has 3 points; disease has 3 locations and also corresponds to antiprotease 3) ulceration in the nasal mucosa can cause a saddle nose

Back