test #13 4.1 Flashcards
pleuritic pain 2-4 days post-MI
pleuritic (changes w/ cough & swallowing, radiating to neck). fibrinous or serofibrinous early-onset pericarditis. 10-20% fever. rxn to transmural necrosis. short-lived, rx: aspirin
pericarditis vs. myocardial ischemia pain
pericarditis: pleuritic & sharp, changes w/ cough. MI: constant, substernal, crushing
dressler’s syndrome
diffuse pericardial inflammation (& lung pleura) due to autoimmune reaction to necrotic tissue. 1 wk-months post MI (fewer than 4%). fever, pleuritis, leukocytosis, pericardial friction rub, chest radiograph evidence of new pericardial / pleural effusions. autoimmune polyserositis. rx: aspirin, NSAID, glucocorticoids
viral pericarditis usu follows..
upper respiratory infection.
3 major symptoms of klinefelter 47 XXY
(1) primary testicular failure: (hyalinization and fibrosis of seminiferous tubules) —> subsequent lack of testosterone.
(2) eunuchoid body habitus: due to testosterone deficiency: tall w/ gynecomastia. lack body hair.
(3) cognitive symptoms: mild retardation, but mostly normal.
arachnodactyl, scoliosis, and aortic root dilation
Marfan. inherited defect of extracellular matrix protein: fibrillin
short stature, hypotonia, obesity.
prader-willi. microdeletion on chromosome 15 (inherited from fatheR). mental retardation.
exact direction of translocation in CML. karyotype.
t(9,22). fusion gene on shortened 22. BCR gene on 22 to ABL gene on 9. karyotype: long 9
kartagener syndrome
autosomal recessive mutation in gene coding for dynein. male infertility, recurrent sinusitis, bronchiectasis. situs inversus.
karyotype analysis of fragile X syndrome
karyotype of cells cultured in folate-deficient medium, discontinuity of staining on the long-arm of X chromosome.
chromosome of sickle cell anemia
chromosome 11
1 gram of hemoglobin holds how much oxygen?
1.34ml oxygen / 100ml blood
PaO2 100 = how much oxygen dissolved?
0.3ml oxygen dissolved / 100ml blood
cyanide intoxication leads to what blood gas finding
inhibition of cytochrome C, failure of electron transport chain & aerobic metabolism. SaO2 of venous blood INCREASES (oxygen cannot unload)
what 3 factors affect total oxygen content of blood
(1) hemoglobin concentration (2) oxygen saturation of hemoglobin (SaO2) (3) partial pressure of xygen dissolved in blood (PaO2)
SCID presentation
bacterial (i.e. recurrent otitis media), viral (bronchiolitis), and fungal (candidiasis) w/ poor growth & thymic hypoplasia (absent thymic shadow).
absent thymic shadow can mean.. (2)
SCID or DiGeorge (very uncommon)
Bruton’s agammaglobulinemia
X-linked, boys, 6 months after passive immunity passes. BTK gene. insufficient production of mature B cells
common variable immunodeficiency
defect in B cell maturation. many causes.
Ab abnormalities w/ Wiskot-Aldrich
low to normal IgG and IgM. increased IgE and IgA
4 basic payment methods (most contracts between health insurance plans & physicians)
capitation, fee-for-service, discounted fee-for-service, salary
capitation
paid fixed amount per enrollee (not per service). fixed budget aloocated: incentives to contain costs. motivated to catch illness early (preventative care) so less tests needed as patient ages.
fee-for-service
paid fixed amount for every service & diagnostic test. face little financial risk, enticed to increase visits per patient and services per visit.
discounted fee-for-service
similar to FFS, but are reimbursed a discounted price. physician will be more conservative when ordering tests / providing services
salary
fixed amount, pay not tied to service or enrollee. no financial risk. no financial incentive to change treatment patterns.
HMO (health maintenance organization insurance plans) tend to use… Preferred provider organization insurance plans tend to use.. (payment plans)
HMO: capacitation. PPO: FFS or discounted FFS
latency in epidemiological studies
time elapsed from exposure to clinically apparent disease. short: infectious disease. long: heart disease/cancer.
or, exposure to risk modifiers occur significant time before effect on disease process. or must occur continuously over extended period before disease outcome is affected.
idiopathic hirsuitism. rx: (3)
(1) increased conversion of testosterone to DHT (5-alpha-reductase) or (2) increased sensitivity of hair follicles to DHT. rx: spironolactone, flutamide (testosterone receptor antagonist), finasteride (5-alpha-reductase inhibitor)
spironolactone on hirtsuitism
anti-adrogenic properties. block androgen receptors at hair follicles & decreases testosterone production.
flutamide
testosterone receptor antagonist
clomiphene? rx?
antiestrogen. inteferes w/ negative feedback of estrogens on hypothalamus and pituitary. increases GnRH. rx: infertility w/ anovulation
mitotaine? rx?
adrenocortiolytic. rx: adrenocortical carcinoma.
medroxyprogesterone? rx?
Depo Provera. progesterone only contraceptive (intramuscular injection once every 12 wks)
mifepristone? rx?
RU-486. synthetic steroid w/ anti-progestin & anti-glucocorticoid effect. abortifacient.
danazol? rx?
synthetic androgen used to treat endometriosis & hereditary andioedema.
where is vitamin E obtained from? deficiency? results in?
widely available in regular diet. deficiency is unusual: fat malabsorption, abetalipoproteinemia. low birth weight infants. deficiency – subacute combined degeneration of dorsal column & spinocerebellar tract
vitamin E deficiency mimics..
freidrich’s ataxia (ataxia, dysarthria, loss of position & vibration sense)
clinical presentation of acute intermittent porphyria
acute abdominal pain, peripheral neuropathy, hyponatremia
PSGN on light microscope? lab findings? EM?
hypercellular (leukocyte, endothelial, mesangian cell proliferation) glomerular.
lab: elevated titers of anti-streptococcal antibodies (anti-streptolysin O, anti-DNase B, anti-cationic proteinase). low C3. cryoglobulins.
EM: subepithelial humps
lab finding w/ drug-induced interstitial nephritis (tubulointerstitial nephritis)
high serum EOSINOPHILIA. offenders: beta-lactam antibiotics, NSAIDs, diuretics, anticonvulsants. nephritis. hypersensitivity.
early embryonic development, body veins divided into 3 main groups.. what is the fate of these groups?
(1) vitelline – become veins of portal system (2) umbilical – degenerate (3) cardinal – veins of systemic circulation
site of superior vena cava
right, posterolateral to ascending aorta. anterior to right pulmonary artery. below level of carina.
truncus arteriosus gives rise to..
aorta and pulmonary artery
embryological origin of descending aorta
fusion of embryonic left and right dorsal aortas
pupillary light reflex pathway
SENSORY: retina –> optic nerve –> bilateral pretectal nucleus in superior colliculus –> ipsilateral & contralateral edingerwestphal nuclei (decussating fibers traverse posterior commissure)
MOTOR: parasympathetic preganglionic fibers in Edinger-Westphal –> travel w/ oculomotor n. to ciliary ganglion –> synapse onto postganglionic neurons –> project fibers to sphincter of iris.
main contributor to nitrate effect in patients w/ stable angina?
reduced preload –> reduced left ventricular volume.
also have modest dilatory effect on coronary arterioles & decrease afterload, but less impt.
5 major symptoms caused by invasion of pancoast tumors
(1) invasion of parietal pleura, vertebrae, superior ribs: SHOULDER PAIN. (2) invasion of brachial plexus: weakness & paraesthesia of ARM , particular inferior trunk. (3) HORNER (superior cervical ganglion sympathetics) (4) SVC syndrome (5) invasion of recurrent laryngeal n (HOARSENESS
isoniazid mechanism
decrease synthesis of mycolic acid in cell wall. bacterial catalase-peroxidase needed (encoded by KatG) to convert to active metabolite.
ethambutol mechanism
decrease carbohydrate polymerization of cell wall (block arabinosyltransferase)
pyrazinamide mechanism
unknown, acidify intracellular environment (pyrazinoic acid) effective in acidic lysosomes
what feature of mycobacteria makes them acid fast?
mycolic acids in cell wall
mycolic acids are essential for what 2 things in mycobacterium?
(1) proper cell wall structure (2) synthesis of mycobacterial virulence factors (sulfatides, wax D, and cord factor)
streptomycin is indicated in the treatment of… (3)
(1) mycobacteria: TB (2) plague: Yersenia pestis (3) tularemia: Francisella tularensis
skin findings in sarcoidosis (3)
variety: 1. subcutaneous nodules (erythema nodosum), 2. erythemtous plaques 3. macules that are slightly reddened / scaling
liver pathology in sarcoidosis
scattered noncaseating granulomas (75% of cases). affect portal triad far more than lobular parenchyma.
fatty (steatosis) change in liver occurs in.. (3)
reversible (1) hypoxic (2) toxic (3) metabolic injury (i.e. protein malnutrition, diabetes, obesity)
hepatic centrilobular necrosis can be caused by..
death of hepatocytes immediately surrounding terminal hepatic vein. cause: ischemic injury (right heart failure), drugs, toxins, fulminant hepatitis
portal inflammation can be found in
VERY NONSPECIFIC: alcoholic heptatitis, acute/chronic viral hepatitis, secondary biliary cirrhosis due to biliary tract obstruction, primary biliary cirrhosis, sclerosing cholangitis, chronic graft vs. host disease, acute cellular rejection of liver transplant, idiopathic neonatal hepatitis.
periportal fibrosis is a common pathologic finding in..
chronic viral hepatitis
prolactinomas in men v. women? why?
female: < 10mm (micro). male: >10mm (macro). bc men don’t present until it is very large (i.e. no menstrual abnormalities)
renal failure and calcium problems…
VITAMIN D synthesis occurs in kidney. low vitamin D, low Ca2++, high PTH
which bacteria are capable of producing dextrans using sucrose as a substrate?
s. viridans
what is the most likely adherence site for S. viridans?
fibrin & platelets (think: subacute endocarditis, valvular vegetation)
role of subendothelial collagen and subendothelial glycosaminoglycans
subendothelial GAGs form subendothelial fibrous cap over the central core of atherosclerotic plaque. can activate platelets
antithrombin III inactivates..
thrombin, IX, X, XI, and XII (prevent conversion of fibrinogen to fibrin)
golgi tendon organ
sensory receptors located at junction of muscle and tendon. innervated by group Ib sensory axons
what does contraction of muscle do to golgi tendon organ? passive stretch?
GTO located in junction between tendon and extrafusal muscle fibers. contraction: increased tension transmitted through the tendon, activates golgi tendon organ (in SERIES w/ extrafusal muscle).
note, passive stretch: no effect, GTO insensitive to changes in muscle length (which affects muscle, not tendon)
golgi tendon organ circuit
group IB sensory axon from GTO contact inhibitory interneurons in spinal cord, synapse w/ alpha motor neurons that innervate SAME muscle. NEGATIVE FEEDBACK: regulates & maintains muscle tension. note: too much force on muscle –> GTO inhibit contraction –> SUDDEN MUSCLE RELAXATION (prevents damage)
A-delta fibers..
thin, myelinated nerve fibers, free never endings –> temperature and pain
muscle spindle aka..
intrafusal muscle fibers
muscle spindle / intrafusal muscle fibers
connected in PARALLEL w/ extrafusal fubers. innervated by group Ia and II sensory axons, sensitive to muscle LENGTH. mediate STRETCH reflex (myotactic reflex – DTR). stretch of muscle, monosynaptic reflex ACTIVATION of alpha-motor neuron, contraction that resists stretch.
pacinian corpuscles
rapidly adaptive mechanoreceptors in subcutaneous tissue of skin, mesentery, peritoneum, joint capsule. vibration and pressure. A-beta fibers.
ruffini’s end organs
slowly adaptive mechanoreceptors in skin, subcutaneous tissue, and joint capsule. pressure. A-beta fibers.
monitor and maintenance of muscle length
muscle spindle system (intrafusal)
monitor and maintenance of muscle force
golgi tendon organ
atrial fibrillation
irregularly irregular, absent P waves w/ irregularly irregular QRS waves. no coordinated atrial contraction
palpitations are.. caused by..
subjective sensation/awareness of one’s heart beating. any significant acute change in HR, rhythm, or force of ventricular contraction.
precipitating factors for isolated atrial fibrillation
(1) binge alcohol consumption (holiday heart syndrome) (2) increased cardiac sympathetic tone (3) pericarditis
high QRS voltage in precordial leads suggests..
ventricular hypertrophy. HR is regular.
prolonged QRS interval..
sign of ventricular dysynchrony or slowed intraventricular impulse conduction (i.e. bundle blood). HR is normal.
3 ways PTH increases serum calcium
(1) increasing osteoclastic bone resorption (2) increasing distal tubular Ca2++ resorption (3) increasing formation of 1,25 dihydroxy vitamin D (upregulation of 1-alpha-hydroxylase). impt for GI reabsorption of Ca++
how does chronic renal failure affect PTH?
secondary parahyperthyroidism. (1) decrease vitamin D, less Ca2++ resorption in gut (2) poor PO4- excretion, which further stimulates PTH and lowers serum Ca2++
primary hyperparathyroidism
high PTH, high Ca2++
PTH-independent causes of hyperparathyroidism
(1) humoral hypercalcemia of malignancy (2) vitamin D toxicity (3) excessive injestion of calcium (4) thyrotoxicosis (5) immobilization
homeobox gene
highly conserved sequence of DNA (180 nucleotides). typically codes for DNA-binding transcription factors (alter expression of genes involved in morphogenesis.
viral bronchitis in a child < 2 years old. rx?
RSV infection. ribavarin (nucleoside analog, inhibits synthesis of guanosine nucleotides) active against RSV and Hep C
ribavarin controversy
ribavarin for RSV is controversial for most children, but indicated in infants at risk for disease progression (immunodeficiency, prematurity, cardiopulmonary disease)
osteltamavir
sialic acid analogue, inhibitor of influenza A and B viral neuraminidases.
ganciclovir differs from acyclovir bc..
gancyclovir is more specific for cytomegalovirus DNA polymerase
amantadine
impairs uncoating of influenza A virion after endocytosis
IFN-alpha used to treat?
combat hep B and hep C infxn
acute obstruction in small airways of infant usu secondary to…
RSV bronchiolitis
2 promoter regions in eukaryotic DNA
CAAT box and TATA box. CAAT is 60-80 base upstream 5’ end. TATA is 25 bases upstream beginning of coding region. Gene transcription begins when RNA pol II attaches at one promoter site. facilitated by TFs. mutations here alter expression levels.
hyperinfection (widespread dissemination of worms in body) w/ strongyloides usu occurs in.. (2)
(1) immunosuppressant (i.e. taking corticosteroids) or (2) HTLV-1 infection. impaired Th2-directed cellular immunity
physical sign of stronglyoides infxn?
larva currens (pruitic, erythematous, linear streaks on thighs and buttocks as larva migrate subcutaneously away from perianal region).
diagnosis of stronglyoides? rx?
diagnosis: larvae in stool. eggs & adult parasites in intestinal biopsy. rx: ivermectin
diagnosis of tapeworms (t. solium, t. saginata, d. latum)
proglottids in stool
trophozoites & cysts in stool
giardia lamblia and entamoeba histolytica
eggs in stool
schistosomiasis
features of nephrotic syndrome
(1) massive proteinuria (>3.5g/day) (2) hypoalbuminemia (<2.5g/dl) (3) generalized edema (4) hyperlipidemia (5) lipiduria. will see increased aldosterone and aldosterone & Na+ & H20 retention due to low intravascular volume
protease inhibitor (-navir) side effects
(1) LIPODYSTROPHY – increased deposition of fat on back & abdomen, decrease adipose on extremities. buffalo hump w/ central obesity & peripheral wasting. (2) HYPERGLYCEMIA – increased insulin resistance, leads to frank diabetes.
(3) INHIBITION of P-450 – leading to drug drug intxn
rifampin in patients on protease inhibitors (-navirs)? what should be used instead if TB + HIV?
rifampin ramps P450 & gets rid of -navir. use rifabutin instead
impt side effects of TMP-SMX
megaloblastic anemia, steven-johnson’s syndrome, toxic epidermal necrolysis
impt side effects of NRTI (zidovudine)
bone marrow toxicity resulting in anemia (40% of patients)
impt side effect of acyclovir
crystalline nephropathy
fosacarnet rx? side effects
treatment of CMV infxn in HIV patients. nephrotoxicity, electrolyte disturbances (hypocalcemia, hypomagnesemia, hypokalemia)
what drugs increase rise of gallstones (2)?
(1) bile acid binding resins: cholestyramine, colestipol, colesevelam –> block enterohepatic circulation of bile acids, which can increase bile acid production/secretion, which increases cholesterol content of bile (2) fibrates: gemfibrizol, fenofibrate –> increase cholesterol content of bile.
how do bile acid resins decrease LDL?
hepatic cholesterol is consumed in re-synthesis of bile acids (increases uptake of LDL from circulation)
etoposide & podophyllin
targets topoisomerase II. inhibits topoisomerase II’s ability to seal the strand break it induces.
topoisomerase I vs. topoisomerase II
topo I: single stranded nicks to relieve negative supercoiling. topo II: transient breaks in both DNA strands simultaneously to relieve both positive and negative supercoiling.
rx: etoposide. rx: podophyllin
etoposide: testicular cancer and small cell lung cancer. podophyllin: genital warts
irinotecan and topotecan..
inhibit topoisomerase I (normally induces single strand breaks in DNA to relieve negative supercoiling during replication
bioavailability defined as.. how is it determined?
fraction of administered drug that reaches systemic circulation in a chemically unchanged form. plot plasma drug concentration over time (for a dose) IV and then other route: F = divide AUC of route / AUC of IV. if doses are not equivalent: F= (area under oral curve x IV dose)/(area under IV curve x oral dose)
ABPA (allergic bronchopulmonary aspergillosis) can affect…
colonize bronchial mucosa and complicate (1) asthma (5-10%) or (2) cystic fibrosis
ABPA causes
high serum IgE, eosinophilia, and IgE plus IgG against Apergillus. intense airway inflammation and mucos plugging w/ exacerbation and remission. repeat exacerbation –> transient pulmonary INFILTRATES and proximal BRONCHIECTASIS.
progression of femoral hernias
(1) prone to INCARCERATION [femoral canal is small]: cannot be reduced (2) impaired blood flow for few hrs –> STRANGULATION (ischemia and necrosis)
pectineal (cooper’s ligament)
thickened part of pectineal fascia. overlies pectineal ridge of the pubic bone. located posteriorly to the femoral canal.
where is traversalis fascia found
between transversalis muscle and extraperiotoneal fat.
hesselbach’s triangle
medial border: rectus muscle shealth. lateral: inguinal ligament. superior: femoral artery & vein
round ligament in women homologous to what in men?
spermatic cord in men. in women: leaves pelvis through deep inguinal ring, passes through inguinal canal
femoral hernia borders
inferior to inguinal ligament. medial to pubic tubercle. lateral to femoral artery/vein
rx for allergic asthma?
1st: LTD4 antagonist (zafirlukast and montelukast). short term relief: inhaled ipratropium –> cholingeric m3 antagonist
leukotrienes in lungs
synthesized by mast cells, eosinophils, basophils. causes (1) bronchial constriction and (2) hyperreactivity. (3) promote mucosal edema and (4) mucous hypersecretion
uremic platelet dysfunction
qualitative (platelet count, PT, PTT normal). BLEEDING TIMe – VERY PROLONGED. build up of dialyzable platelet-inhibitory factors (inhibit platelet fxn –> leading to intrinsic platelet defects and impairment of platelet-endothelial interactions.
what stabilizes factor VIII in circulation
vWF
H. pylori-associated antral gastritis..
decrease in number of somatostatin-producing antral cells (ssn inhibits gastrin release)
where does H. pylori live? how?
mucus layer overlying the epithelium of gastric antrum and fundus, as well as any ectopic gastric tissue in duodenum or esophagus. h. pylori does not invade, and IS susceptible to gastric acidity. protected by (1) mucus layer (2) urease production
increased acidity from h. pylori specifically associated w/
duodenal ulcer. though h. pylori is also associated w/ gastric adenocarcinoma, gastric ulcer, gastritis, gastric lymphoma (via unclear mechanisms)
tetrahydrobiopterin is..
BH4
BH4 (tetrahydrobiopterin) is a cofactor for the synthesis of..
(1) tyrosine: precursor of dopa and melanin (2) DOPA (antecedent of catecholamines) (3) 5HT (4) nitric oxide. works w/ dihydrobiopterin reductase, which reduces dihydrobiopterin (BH2) to tetrabiopterin (BH4)
how is serotonin made
hydroxylation and decarboxylation of amino acid tryptophan
2 possible enzyme deficiencies resulting in phenylketonuria
(1) most common: phenylalanine hydroxylase (2) dihydrobiopterin reductase deficiency
formation of GABA
decarboxylation of glutamate via glutamatic acid decarboxylase (GAD)
most common congenital abnormality of small intestine
meckel diverticulum. present in 2% of population. incomplete obliteration of omphalomesenteric duct that connects midgut lumen and yolk sac cavity early in life. connected to ileum (2 ft proximal to ileocecal valve)
tissue found in meckel diverticulum? most common?
could be gastric, pancreatic, colonic, jejunal, duodenal, endometrial. most common – GASTRIC. (significant bc epithelium produces acid –> cause ulceration of adjacent tissues & lower GI bleed)
most common presentation of Meckel diverticulum
painless melena. could also become inflamed and stimulate clinical presentation of acute appendicitis.
ectopy
identification of microscopically and fxnally normal cells/tissues in abnormal location due to embryonic maldevelopment (i.e. meckel’s diverticulum)
criteria for anorexia nervosa
(1) body weight at least 15% below normal, accompanied by a refusal to maintain body weight at normal levels (2) amenorrhea for 3 months (3) distortion of body image in which individual views self as obese (4) fear of gaining weight or becoming fat despite being underweight. often observe female athlete triad: eating disorder, amenorrhea, osteoperosis
two subtypes of anorexia nervosa
(1) restricting subtype (2) binge eating / purging subtype
clinical signs of significant vomiting history (i.e. in anorexia nervosa / bulemia)
(1) parotid gland hypertrophy (2) anterior tooth enamel erosion
primary biliary cirrhosis
chronic liver disease characterized by autoimmune destruction of intrahepatic bile ducts & cholestasis
two enzymes that need B12 as a cofactor
(1) methylmalonyl CoA mutase (methylmalonyl CoA –> succinyl CoA) and (2) methionine synthase
B12 deficiency lab values
(1) increase in methylmalonic acid (2) homocysteine
elevated levels of serum protoporphyrin in..
(1) iron-deficiency anemia, (2) lead poisoning, (3) erythropoietic protoporphyria
anthracyclines are..
daunorubicin, doxorubicin, epirubicin, idarubicin
side effect of anthracyclines
severe cardiotoxicity (generation of free radicals). DILATED CARDIOMYOPATHY (cumulative dose dependent)
early sign of doxorubin-associated cardiomyopathy (histologically, and symptoms)
swelling of sarcoplasmic reticulum, followed by loss of cardiomyocytes “myofibrillar dropout”. same symptoms of biventricular CHF, including dyspnea on exertion, orthopnea, and peripheral edema
effective method of preventing doxorubicin cardiomyopathy
dexrazoxane (iron-chelating agent that decreases formation of oxygen free radicals)
fructose absorption in GI
GLUT 5, proximal small bowel
respiratory epithelium from nose to terminal bronchioles?
ciitated mucosal epithelium. goblet cells give mucous
clara cells
(1) secretory constituents of TERMINAL respiratory epithelium – clara cell secretory protein. also source of some surfactant (2) role in detox of inhaled particles via a cytochrome p450 mechanism
absorption of copper in GI system
60% absorbed in STOMACH and DUODENUM
pathway of copper upon absorption
stomach/duodenum absorption –> bound to albumin loosely –> liver –> incorporated into an alpha-2-globulin to form CERULOPLASMIN. ceruloplasmin accounts for 90-95% of circulating copper.
normal total body copper
50-150 mg
copper excretion
senescent ceruloplasmin & remainder of ingested unabsorbed Cu –> bile and extreted in stool. also small amt –> renal tubular secretion
3 forms of aspergillus infxn
(1) colonizing (2) hypersensitivity rxn (3) invasive
colonizing aspergillosis
occurs in old lung cavities (i.e. from TB, emphysema, sarcoidosis) – fungus ball. does not invade lung tissue. asymptomatic or cough w/ hemoptysis. chest x-ray: radiopaque structure that shifts when pt changes position
hypersensitivity rxn to aspergillus
allergic bronchopulmonary aspergillosis – wheezing, fever, migratory pulmonary infiltrates
invasive aspergillosis
characterized by primary lung involvement (cough, hemoptysis, pleuritic chest pain, fever). can form necrotizing pneumonia and granuloma. hyphae INVADING lung tissue.
necrotizing aspergillosis
can occur bc predilection for vasculature –> ischemia
