test #29 4.19 Flashcards
what surface marker (cell type) is deficient in Bruton’s X-linked agammaglobulimemia?
CD19 (no mature B cells in circulation)
B cell markers
CD19, 20, 21
CD15
neutrophil marker. also present in reed sternberg cells
CD16
NK cells (and others)
two types of abnormal ventilation during sleep
(1) apnea (cessation of breathing for >10 seconds)
2) hypopnea (reduced airflow causing SaO2 to decrease >4%
obstructive sleep apnea
noturnal hypoventilation w/ a transient upper airway obstruction due to poor pharyngeal muscle tone
most common cause of excessive daytime sleepiness
exam: erythrocytosis, obesity, increased soft tissue in oropharynx
arterial blood gas in day: normal
obesity hypoventilation syndrome (aka Pickwickian syndrome)
obesity impedes expansion of chest and abdominal wall during breathing.
increased respiratory work & decreased respiratory drive.
underventilation during all hours (chronically elevated PaCO2 and reduced PaO2)
arterial blood gas = abnormal
differentiation obesity hypoventilation syndrome from sleep apnea?
sleep apnea: normal arterial blood gas in day time
central sleep apnea
patient’s central DRIVE to initiate breaths is absent.
neurological problem (not mechanical)
tumor w/ fat, smooth muscle, blood vessel
angiomyolipoma (benign tumor)
associated w/ tuberous sclerosis
tuberous sclerosis inheritance
autosomal DOMINANT
tuberous sclerosis symptoms
HAMARTOMAS
- hamartomas in CNS and skin
- angiofibromas (face, adenoma sebaceum)
- mitral regurgitation
- angiomyolipoma (renal)
- tuberous sclerosis
- autosomal dOminant
- mental retardation
- ash-leaf patch (hypopigmented)
- shagreen patch (thick leathery, dimpled, organge
also: subependymal astrocytoma and ungual fibromas
NF2
autosomal DOMINANT. bilateral acoustic neuromas.
also have multiple meningiomas, gliomas, ependymomas of spinal cord.
cerebellar hemangiomas, retinal hemangiomas, liver cysts, bilateral renal cell carcinoma, pheochromocytoma
von-hippel-lindau
sturge-weber syndrome
STURGE:
Somatic Tram track Ca2+ opposite gyrus Unilateral leptomeningeal angioma& port-wine stain Retardation GNAQ (activating mutation) & Glaucoma (episcleral hemangioma) Epilepsy
port-wine stain – nonblanching in V1/V2 distribution
developmental anomaly of neural crest derivatives (mesoderm/ectoderm)
hereditary hemorrhagic telangiectasia
Osler-Rendu-Weber syndrome
multiple tenangiectasia of skin & mucosa.
presentation is recurrent epistaxis or GI bleed (melena)
how does B agonists (increased camp) increase contractility?
cAMP increases conductance of Ca2+ channels in SR.
when patient takes exogenous glucocorticoids, worry about..
how is this prevented?
acute adrenal insufficiency (when used for 3+ wks)
prevent by tapering off treatment
where does suppression occur when extended exogenous glucocortoids are taken?
the WHOLE axis: hypothalamic, pituitary, and adrenal!
low CRH, low ACTH, low cortisol!
mutation in NF1
mutation in NF1, tumor suppressor that regulates Ras
autosomal dominant
how does alcohol lead to pancreatitis?
obstruction via ductal concreations & direct parenchymal injury
three types of damage in pancreatitis
(1) pancreatic autodigestion - proteases
(2) vascular damage & hemorrhage - elastase
(3) fat necrosis - lipase / phospholipase
amylase makes..
hydrolyze starch into maltose (a glucose-glucose dissacharide), trisaccharide maltotriose, limit dextins
17 alpha hydroxylase needed for (2)
(1) pregnenolone -> 17 hydroxypregnenolone
(2) progesterone -> 17 hydroxyprogesterone
17 alpha hydroxlase deficiency on secondary sex characterestics
prevents in both males & females.
no menarche in females
5-alpha reductase deficiency on secondary sex characteristics?
abnormal external genitalia development, but will have normal secondary sex (increased muscle mass and phallus enlargement) bc of testosterone
prostate and hair = DHT
urine from umbilicus
persistant allantois remnant
allantois becomes..
URACHUS
urachus
duct between bladder (urogenital sinus) and yolk sac
failure of urachus to obliterate results in..
- patent urachus: umbilicus to bladder: pee from belly button
vesicourachal diverticulum
failure to close part of urachus adjacent to bladder.
outpouching of apex of bladder. commonly asymptomatic.
urachal sinus
failure to close distal part of urachus (adjacent to umbilicus)
periumbicilical tenderness & purulent discharge from umilicus due to persistent and recurrent infection.
vitelline duct
omphalo-mesenteric duct connect yolksac to midgut lumen.
connect small intestine w/ skin at umbilicus
failure of vitelline duct to obliterate
(1) vitelline fistula
(2) meckel diverticulum
vitelline fistula
failure of vitillene duct to obliterate
meconium from umbillicus
meckel’s diverticlum
partial closure of vitilline duct. patent portion attached to ileum (true diverticulum)
ectopic gastric mucosa / pancreatic tissue –> melena, periumbilical pain, ulcers
rule of 2!
2 inches, 2 feet from ileocecal valve, 2% of population, 2 epithelial
omphalocele
incomplete closure of anterior abdominal wall.
– failure of abdominal contents to return to body cavity
presents as ventral opening at the umbilicus, protruding viscera covered by peritoneum
SEALED in peritoneum
gastroschisis
inadequate enlargement of peritoneal cavity during fetal life.
viscera PROTRUDE through defect in anterior abdominal wall adjacent to umbilicus
NOT covered by peritoneum.
closure of abdominal wall (rostral, lateral, caudal)
rostral fold: sternal defects
lateral: omphalocele, gastroschisis
caudal fold: bladder extrophy
duodenal atresia results from..
failure to recanalize
jejunal, ileal, colonic atresia results from…
vascular accident – apple peel atresia
midgut development
6th wk: midgut herniates through belly button
10th: return to abdominal cavity, rotates around SMA, 90 degree counter clockwise
granules in whipple’s disease
diastase-resistant granules in macrophages (lysosomes w/ partially digested bacteria)
what medication can decrease formation of adenomatous polyp formation?
aspirin! cox-2 overexpression in colon mucosa help lead to adenocarcinoma in adenoma-to-carcinoma sequence
adenoma to carcinoma sequence
AK53 & DCC 1. APC (b-catenin) --> AT RISK (cox-2 overexpression & methylation increase too) 2. K-ras -->ADENOMA 3. p53 & DCC --> CARCINOMA
how does APC mutation lead to at risk colon?
APC keeps beta-catenin low –> maintains intercellular adhesion
FAP –> carcinoma always involves..
RECTUM (left, despite being an “exophytic mass’
HNPCC –> carcinoma always involves
PROXIMAL COLON (right, despite not being exophytic)
febuxostat
like allopurinol, inhibits xanthine oxidase
probenicid
blocks reabsorption of uric acid.
so does HIGH dose of salicylates
caspase
cysteine protease
what two enzymes can act on fructose intracellularly
fructokinase (fructose 1-phosphate) and hexokinase (fructose 6-phosphate)
where is fructose absorbed
proximal intestine, facilitative hexose transporter GLUT 5
how is fructose metabolised in essential fructosuria?
absent fructokinase, cannot make fructose-1-phosphate. mostly loose in urine.
BUT small amount converted by hexokinase in liver into fructose-6-phosphate –> phosphoglucomutase turns it into –> glucose 6 phosphate.
can be used for glycogenesis, glycolysis, HMP, etc.
aldolase B converts..
fructose 6-phosphate –> DHAP (dihydroxyacetone P) and glyceraldehyde
glyceraldehyde –> glyceraldehyde 3-phoshpate via triose kinase
galactose metabolism
galactose –> galactose-1-phosphate
(via galactokinase)
galactose 1-phosphate –> glucose 1-phosohate
(via galacose-1-uridyltransferase, which also converts UDP-glucose –> UDP-galactose
UDP glucose is regenerated from UDP galactose with UDP-galactose-4-epimerase
aldose reductase
[low affinity for glucose, only relevant when glucose is high]
converts glucose –> sorbitol.
also galactose –> galactitol
will accumulate if there is no sorbitol dehydrogenase to convert sorbitol —> fructose
which tissues (4) lack sorbitol dehydrogenase? what is the manifestations of this?
lens, schwann cells, retina, kidney.
glucose –> sorbitol via aldose reductase. sorbitol accumulates (can’t convert to fructose).
has osmotic pull. results in..
cataracts, peripheral neuropathy, retinopathy, nephropathy (as seen in diabetes)
acute interstitial pancreatitis vs. acute necrotic pancreatitis
acute interstitial: GROSS EDEMA: microscopic: calcifications. l
ipase digests adipose cells, form fatty acids that bind Ca2+ & ppt calcium salts.
if inflammation continues, trypsin activated, autodigestion of pancreas –
acute necrotic pancreatitis: GROSS CHALKY. destroy vessels –> white chalky fat necrosis. spread onto mesentery, omentum, other parts of abdominal cavity.
mesenteric ischemia on gross
bowel is dusky red and congested. see subserosal ecchymoses, edema, defined necrosis
(probably related to arcades, mult sources of blood to bowel)
calcification on bowel mesentary, omentum, etc
pancreatitis. lipase release free fatty acids, which bind Ca2+ and ppt calcium salts
gastroesophageal mural injury: mallory-weiss vs. boerhaave syndrome?
both caused by forceful vomiting
mallory-weiss: MUCOSAL tear. submucosal arterial or venous plexus bleeding
boerhaave: esophageal TRANSMURAL tear. esophageal air/fluid leakage into mediastinum & pleura
ethanol metabolism
in cytosol:
ethanol –> acetaldehyde
(alcohol dehydrogenase, makes NADH)
in mitochondria:
acetaldehyde –> acetate
(acetaldehyde dehydroganse, makes NADH)
overall increase in NADH/NAD+
why does alcohol cause lactic acidosis?
high NADH/NAD+
need NAD+ for glycolysis, will regenerate AND+ via lactic acid production
pyruvate -> lactate
consume NADH –> NAD+
why does alcohol cause steatosis in liver (2)?
high NADH/NAD+
- glyceradehyde-3-phosphate –> glycerol-3-phosphate. combine w/ fatty acids –> triglycerides
- high acetyl-CoA (due to inhibition of TCA) promotes lipogenesis
TCA inhibited bc oxaloacetate is converted to malate (to regenerate NAD+)
what 4 metabolic pathways are affected by alcohol?
high NADH/NAD+
- pyruvate -> lactate
(consumes NADH–> NAD+) - oxaloacetate -> malate
(consumes NADH –> NAD+) - glyceraldehyde-3-phosphate –> glycerol-3-phosphate
(combines w/ fatty acids to make triglyceride) - blocked TCA, build up acetyl-CoA, permits ketogenesis & lipogenesis
supine hypotension syndrome
aortocaval compression syndrome
hypotension, pallor, sweating, nausea, dizziness
when preggers lady > 20wks lay on back
inheritance of hemochromatosis
autosomal recessive
fairly common among northern europeans
intestinal absorption of iron
usu C282Y mutation on chr 6 in HFE gene
symptoms of hemochromatosis (5)
- micronodular cirrhosis
- diabetes mellitus
- skin pigmentation
- testicular atrophy
- CHF
increased risk of HCC
all related to DEPOSITS of Fe2+
most common source of e. coli bacteremia
URINARY TRACT!
urosepsis risk: BPH, fecal incontinence, neurogenic bladder secondary to diabetes, frequent indwelling catheterization.
why does mucor, rhizopus, absidia <3 diabetic ketoacidosis
have ketone reductase.
proliferate in vasculature, causes downstream tissue necrosis –> black eschar
differentiate paranasal infxn w. aspergillus and mucor?
histology.
aspergillus: acute angle septate
mucor: broad angle, nonseptate
diagnosis of allergic bronchopulmonary aspergillosis
SEROLOGICAL TESTING.
increased IgE and Ab to aspergillus fumigatus = diagnostic
quadratus lumborum
muscle of posterior abdominal wall
erector spinae
large group of back muscle. longitudinally along spinous processes. contraction = spine extension
transversus abdominis (transversalis)
most internal component of anterior abdominal wall musculature. below inferior oblique
ligamentum flava
paired elastic ligaments, connect vertebral laminae.
form posterior wall of spinal canal. help hold body erect.
psoas major
anterior surface of transverse processes & lateral surface of vertebral bodies of T12-L5
long delay between diet change and vitamin deficiency (~4yr) suggests..
cobalamin B12
hepatic reserves last for up to several years
which vitamins present w/ deficiency rapidly
WATER SOLUBLE, quickly wash out of body (except B12 and folate – have stores in liver)
time frame of B12 and folate deficiency
B12: hepatic reserves last for years
folate: about 1/2 stored in liver, lasts 3-4 months.
folate deficiency faster
storage of vitamin D (25-vitD)
in adipose tissue.
deficiency takes a few months
vitamin A storage
90% stored in liver, perisinusoisal stellate (Ito cells)
last 6 months
vitamin K storage
small amount in liver, lasts 1-3 weeks only.
heavily dependent on that made from large intestinal microbes
diagnosis of hashimoto
usu (1)hypothyroidism, (2) high TSH, low T4/T3, and (3) anti-TPO antibody
can do biopsy: see intense mononuclear infiltration w/ lymphocytes and plasma cells. germinal centers.
characterestics of papillary thyroid cancer (3)
tall variant?
MOST COMMON. GOOD PROGNOSIS.
(1) branching papillary structure
(2) psamomma bodies
(3) ground glass nucleus w/ intranuclear grooving “orphan annie eyes’
tall variant: follicular hyperplasia, lined by tall epithelial cells. older individuals, worse prognosis compared to well-differentiated papillary thyroid cancer.
in thyroid; follicular hyperplasia lined by tall epithelial cells in older individual?
tall variant of papillary thyroid carcinoma. worse prognosis.
mixed cellular infiltration w/ occasional multinuclear giant cells in thyroid
subacute thyroiditis or,
de Quervain thyroiditis or,
granulomatous thyroiditis
presentation of subacute thyroiditis, de Quervain, granulomatous thyroiditis
painful tender thyroid. first thyroxoticosis, then hypothyroid
usu post-viral illness
origin of Riedel’s thyroiditis
IgG4-related systemic illness
Riedel’s thyroiditis vs. anaplastic carcinoma
both are firm, fixed, painless masses, but..
Riedel – young female. anaplastic – old people.
rapid relief for rheumatoid arthritis
glucocorticoids
NSAIDs woud help too
sulfasalazine, hydroxychloroquine, minocycline in rheumatoid arthritis
used to treat mild, early, seronegative rheumatoid arthritis.
do NOT have anti-inflammatory.
effects work as immune modulators (disease modifying)
colchicine
NOT used in rheumatoid arthritis.
binds to tubulin and inhibts MT polymerization of neutrophils. reduce inflammatory response to uric acid crystals
rx for acute gout:
NSAID, glucocorticoids (short-term only), colchine
rx for chronic gout:
allopurinol, febuxostat, probenicid, also colchine
mechanism of pain in migraines
(1) trigeminal afferents to meninges activated
(2) release substance P and CGRP (calcitonin gene related peptide)
(3) causes neurogenic inflammation –> vasodilation and plasma protein extravasation
sumatriptan for cluster headache and migraines
agonist of 5-HT 1B/1D on post-synaptic vasculature & presynaptic trigeminal neuron. inhibit release of vasoactive peptides. blocks vasodilation.
ABORTIVE.
contraindicated in prinzmetal angina and CAD bc can cause coronary vasospasm
buprprion activity
NDRI and nicotine agonist
which drugs block presynaptic reuptake of 5-HT and NE?
(1) TCA
(2) SNRI (venlafaxine and duloxetine)
note: TCA also have..
(1) anti-alpha adrenergic
(2) anti-muscarinic
(3) anti-H1 histamine
SNRI used for? specific extra use of each>
rx: depression.
venlafaxine also: generalized anxiety disorder & panic
duloxetine: also peripheral diabetic neuropathy
drugs used for migraine prophylaxis
b-blockers
antidepressants (TCA and SNRI)
anticonvulsants (valproate and topiramate)b
didanosine
nucleoside reverse transcription inhibitor.
side effect: pancreatitis
ganciclovir toxicity
interfere w/ human host cell DNA synthesis
zidovudine toxicity
inhibit mammalian cellular and mitochondria DNA polymerases
bone marrow suppression (anemia, granulocytopenia)
common side effect in non-nucleotide reverse transcriptase inhibitors (nnRTIs: efavirenz, nevirapine, delaviridine)
specific ones?
rash and hepatotoxicity
efavirenz: vivid dreams and CNS
delaviridine and efavirenz contraindicated in pregnancy
rx for reducing risk of fetal transmission of HIV?
zidovudine
common side effect of nucleotide reverse transcriptase inhibits (nRTIs)
bone marrow suppression (reverse with G-CSF and EPO)
peripheral neuropathy, lactic acidosis (nucleosides)
anemia: zidovidine
didanosine: pancreatitis
what is more toxic: acyclovir or gancyclovir?
gancyclovir
toxicity with gancyclovir
bone marrow suppression & renal toxicity
toxicity with acyclovir
obstructive crystalline nephropathy & acute renal failure
foscarnet toxicity
nephropathy, results in electrolyte abnormalities: hypocalcemia, hypokalemia, hypomagnesemia, hypophosphatemia
cidofovir toxicity
nephrotoxic! give w/ probenecid and IV saline to reduce toxicity
nonselective beta and alpha blockers
carvedilol and labetalol (modified endings)
nebivolol
combines cardioselective B1 blockage w/ stimulation of B3 (activates NO synthase in vasculature)
short acting benzo (<10hr)
MOAT
midazolan, oxazepam, alprazolam, triazolam
medium acting benzo (10-20)
LET
lorazepam, estazolam, temazepam
long acting benzo (days)
chlordiazepoxide, clorazepate, diazepam, flurazepam
choosing duration of a benzo?
long-acting: more severe drowsiness, but less addicting/dependent
older people: short acting or they will fall
drug addict: long acting, or they will get addicted!
association between risk of dependence and rate of clearance.
directly proportional.
rate of clearance high, more dependence
association between duration of action and withdrawal symptoms
shorter duration of action, more likely withdrawal symptoms will occur
short acting benzo vs. zolpidem
short acting benzo = addictive.
zolpidem = rapid onset of action & short half-life, but LOW POTENTIAL for tolerance and dependence
normal P50 (partial pressure of oxygen at which hemoglobin is 50% saturated)
26mmHg.
shifted to lower numbers in lungs (LEFT = lungs)
shifted to higher numbers in tissue (RIGHT = tissue)
oxygen dissociation curve for sickle cell
shifted to RIGHT (easier to release oxygen)
subperiosteal thinning w/ cystic degeneration filled with brown fibrous tissue?
hyperparathyroidism! usu cortical bones
excessive osteoid matrix accumulation around trabeculae. and widening between osteoid seems
(as measured by bone histomorphometry and double tetracycline labeling)
vitamin D deficiency
trabecular thinning w/ few interconnections
osteoperosis
lamellar bone structure resembling mosaic?
paget’s disease of bone
spongiosa filling medullar canal with no mature trabeculae
osteopetrosis
after vitamin D is absorbed from GI tract or skin..
must be activated by LIVER and KIDNEY
genu varus, rachitic rosary, harrison’s sulci, craniotabes, growth retardation
vitamin D deficiency
- genu varus: bowed legs
- rachitic rosary: bony prominence at costochondral junction
- Harrison’s sulci: indentations in lower ribs
- craniotabes: softening of skull
strong neutrophil chemotactic agents
leukotriene B4, C5a, 5-HETE
3 fates of arachodonic acid
(1) cox 1-2: prostacyclin, prostaglandin, thromboxane
(2) 5-lipooxygenase: leukotrienes
(3) 12-lipooxygenase:
lipoxin
fxn of lipoxins
made from arachadonic acid via 12-lipooxygenase
lipoxin A4 and B4
- vasodilate
- inhibit neutrophil chemotaxis
- stimulate monocyte adhesion
LTC4, LTD4, LTE4
made from arachadonic acid via 5-lipooxygenase
- increased bronchial tone
- vasoconstriction
- increased permeability
think: constrict everything
LTB4 & 5-HETE
neutrophil chemotaxis
prostacyclin (PGI2)
made from arachadonic acid via cyclooxygenase (PGH2 intermediate)
- inhibit platelet aggregation
- vasodilate
- reduce bronchial tone
- reduce uterine tone
- increases permeability
relaxes everything
prostaglandins (PGD2, PGE2, PGF2a)
made from arachadonic acid via cyclooxygenase
- vasodilate
- increase permeability
- increase uterine tone
- reduce bronchial tone
main difference between prostacyclin and prostaglandins?
prostaglandin (PGD2, PGE2, PGF2) INCREASE uterine tone
prostacyclin reduces uterine tone and reduces platelet aggregation
misoprostol
PGE1 analogue. used to increase production of gastric mucosa & decrease acid production.
also an abortifactant, increases uterine tone
thromboxane
made from arachodonic acid via cyclooxygenase
counteracts prostacyclin (PGI2)
(1) increases platelet aggregating
(2) vasoconstriction
(3) increases bronchial tone
‘increases everything’
important neutrophil chemoattractants (6)
5-HETE LTB4 C5a IL-8 PAF kallikrein
bradykinin on vasculature
- vasodilation
- increases vascular permeability
- stimulates muscular contraction
- mediates pain
initial concern w/ given ACE inhibitors?
hypotension, esp if using a diuretic, hyponatremic, renal impairment
esp worry if taking a thiazide!
reduce venous return, secondary to decrease in angiotensin II levels
can activate Bezold-Jarisch reflec: vagally mediated hypotension and bradycardia
don’t combined ACE with.. (2)
- beta blockers, won’t help much
2. thiazides, will give too much hypotension
three exposures related to liver angiosarcoma
- arsenic (pesticides)
- thorotrast (radioactive contrast)
- polyvinyl chloride
angiosarcoma on stain
CD31+, PECAM, impt for leukocyte extravasation
QT interval encompasses
start of QRS and end of T wave
inherited long QT? predisposed to
- K+ channel
- predisposed to torsades de pointes
(1) romano-warD
autosomal Dominant
no deafness
(2) lange-jervell-nielsen
autosomal recessive
sensorineural deafness
mutations in cardiac cell cytoskeleton & mitochondrial enzymes of oxidative phosphorylation related to..
inherited dilated cardiomyopathy
progressive fibrofatty replacement of right ventricular myocardium
arrhythmogenic right ventricular cardiomyopathy – mutation in calcium-binding sarcoplasmic reticulum protein
follicular carcinoma on histology
sheets of follicular cells or large cells w/ eosinophilic cytoplasm (hurthle)
adenoma: no capsular / vascular invasion
carcinoma: capsular / vascular invasion
urease test
H. pylori
give isotopic urea.
H. pylori converts urea into CO2 and ammonia. isotpically labelled CO2 absorbed in blood and exhaled. measured 30min later.
distinguish ARDS from cardiogenic pulmonary edema?
pulmonary capillary wedge
histology: extreme myofiber disarray w/ interstitial fibrosis
hypertrophic cardiomyopathy
immunity to hepB indicated by
Anti-Hbs (HbsAb)
HbsAg
- detectable during acute infection
- persistence after 6 months – chronic infection
anti-HBc IgM vs IgG
IgM:
- present acute infection & window phase when HbsAg and HbsAb absent
IgG:
- detectable w/ HbsAb & HbeAb after recovery
- present w/o HbsAb in chronic infxn
- not present after vaccination
window period in hep B
no HbsAg or HbsAb.
can have HbcAb IgM
HBeAg
another component of core
- appears AFTER HBsAg
- marker for viral replication activity
- detetable in chronic infectoin
HBeAb
present after recovery from acute infection
- HBeAg/anti-HBe seroconversion indicates transition of chronic infection from high to low viral replication & infectivity
hepatitis B infection presentation
- long asymptomatic incubation period (6-8 wks)
- acute disease, lasting several week to months
when does HBsAg appear in blood? when does it peak?
appear in blood: before symptom onset
peak: when patient is most ill
undetectable in 3-6 months
markers for active viral replication (hep B)? what else rises in this time
HBeAg and HBV DNA in serum. rises shortly after HBsAg comes in.
also increase in anti-HBc IgM and serum transaminases [shortly after symptoms arise]
exacerbation of chronic hepatitis B?
abrupt increase in liver enzyme, increased levels of HBV DNA.
exacerbation frequently occurs w/ HbeAg seroconversion & accompanying transition from high infectivity to low infectivity.
acute hepatitis that has progressed to chronic hepatitis w/ low infectivity
HbsAg (>6 months), HbeAb, HbcAb
no HbeAg, no HbsAb
acute hepatitis that has progressed to chronic hepatitis w/ high infectivity
HbsAg (>6 months), HbeAb, HBV DNA
no HbeAb, no HBsAb
vaccinated against Hep B? resolved HepB?
vaccine: HbsAb, no anything else
resolved hepB: HbsAb, HbcAb
inguinal hernia vs. direct hernia
inguinal hernia: failure of processus vaginalis to oliterate, travels through indirect inguinal. out of external inguinal canal, scrotum
external hernia: weakness in abdominal wall (hesselbach’s triangle, between rectus abominus, inferior epigastric, inguinal ligament). come out near external inguinal ring. NOT in scrotum bc has no passage (no processus vaginalis)
hernia in scrotum? hernia above inguinal ligament? hernia below inguinal ligament?
in scrotum: indirect inguinal
above inguinal ligament: direct
below inguinal ligament: femoral
hernias relative to inferior epigastrics
indirect: lateral.
direct: medial
deep inguinal nodes receives drainage from?
reside under fascia lata, medial side of femoral vein.
glans penis // clitoris & superficial nodes
superficial inguinal nodes receives drainage from?
scrotum & all cutaneous structures inferior to umbillicus. including genitalia and anus up to pectinate line
testes drain to? scrotum? glans penis?
testes: para-aortic nodes.
scrotum: superficial inguinal nodes –> deep
glans penis –> deep inguinal nodes
specific iron deficiency signs (anemia)
dysphagia, spoon nails or koilonychia (disfigured finger nails)
filgastrim
G-CSF
what help w/ iron absorption
vitamin C, reduces it to Fe2+ state
factor V leiden
resistant to cleavage by protein C – thrombophilia
antiphospholipid presents with (3) abnormal lab finding?
- venous thromboembolism
- arterial thromboembolism
- frequent fetal loss
LONG aPTT
most common cause of long PTT?
lupus anticoagulant
why is folic acid deficiency –> prothrombotic?
hyperhomocysteinemia
lipofuscin is composed of..
product of lipid peroxidation.
lipid polymers and protein-complexed phospholipids.
‘wear & tear’
seen in heart & liver of aging or cachectic, malnourished patients.
mediators of cachexia?
TNF-alpha!!!!
also: IFN-gamma, IL-6
chromogranin + lung cancer?
small cell carcinoma!
also: neuron specific enolase, synaptophysin. secretory granules on EM
