membranous nephropathy is associated w. underlying..
- systemic disease: DM, solid tumor, immunologic disorders (i.e. SLE)
- drugs: gold, penicllamine, NSAID
- infection: hep B, hep C, malaria, syphillis
focal sclerosing glomerular sclerosis
HIV
obesity
sickle cell
heroin abuse
spike & dome in membranous glomerulonephropathy
immune complex deposition
subepithelial
IgG & C3
no increase in cellularity
intoxication, slurred speech, impaired decision making at what alcohol level?
marked motor impairment, loss of consciousness, memory blackouts at what level?
- 0.10% (100mg/dl)
2. 0.2% (200mg/dl)
alveolar-arterial oxygen gradient helps determine
CAUSE of hypoxemia
normal alveolar PaO2
assumed to be partial pressure of oxygen in alveolar air.
healthy person at sea level, usu around 100mmHg
alveolar gas equation
to determine A-a gradient
PAO2 = 150 - PaCO2/0.8
ratio of carbon dioxide production to oxygen consumption
0.8 (important in calculating alveolar gas)
normal A-a gradient?
no more than 10-15mmHg
hypoxemia w/ normal A-a gradient? (2)
- high altitude (FiO2 down)
2. hypoventilation
hypoxemia w/ increased A-a gradient? (3)
- V/Q mismatch
- diffusion limitation (pulmonary edema, intersitital fibrosis
- right-to-left shunt
what values are needed to calculate A-a gradient
PaCO2! will assume normal FiO2, etc
PAO2 = 150 - PaCO2 / 0.8
when is diffusion capacity of lungs decreased (2)
alveolar walls thickened
- pulmonary fibrosis / hyaline membrane / edema
alveolar walls destroyed
- emphysema
when is mixed venous blood oxygen increased (2)
(1) abnormal hemoglobin binds w/ greater affinity to oxygen, preventing unloading
(2) oxidative metabolism inhibited (i.e. cyanide or CO toxicity)
thiazolidinediones (-glitazones) bind..
intracellular nuclear receptor
PPAR-gamma
pioglitazone, rosiglitazone increase expression of..
most importantly, ADIPONECTIN
(a cytokine released by fat cells, what is decreased in type 2 DM
exenatide, liraglutide are..
GLP-1 analogs, related to incretin effect
increase insulin, decrease glucagon release
linagliptin, saxagliptin, sitagliptin are..
DPP-4 inhibitors, related to incretin effect
normally cleave GLP-1
also increase insulin, decrease glucagon
repaglinide is..
meglitinide
like sulfonylurea but does not release insulin when blood glucose is low
weaker binding affinity & faster depolarization
GLP-1 is secreted by..
intestinal L cells in response to food
‘incretin effect’
GLP-1 works on what receptor
Gprotein - adenyl cyclase
which diabetes drugs work via enzyme inhibition (2)
metformin (block enzymes related to liver gluconeogenesis, etc)
alpha-glucosidase inhibitors (acarbose, miglitol)
miglitol
like acarbose, alpha-glucosidase-inhibitor,
diabetes med.
hyperestrinism state of cirrhosis due to (2)
- decrease metabolism of androstenidione, results in excess estrogen.
- increase in sex-hormone binding globulin (SHB) -> binds testosterone, decreases free testosterone
results in: gynecomastia, testicular atrophy, spider angiomata, less hair
edema in cirrhosis due to..
hypoalbuminemia (liver synthetic processes diminshed)
fetor hepaticus (musty breath) and encephalopathy are signs of..
hyperammonia (liver failure)
4 signs of portal HTN
- esophageal varices
- caput medusa
- hemmorhoids
- splenomegaly
what is major determinant for rate of bone mass decline post menopause
RACE. black have higher bone density than caucasians
BMI on bone density
higher BMI = higher bone density
smoking on bone density?
overall, anti-estrogenic
–> risk for osteopersosis
what does smoking actually decrease risk of?
fibrocystic breast disease & uterine cancer
bc anti-estrogenic
overall bad for you though!
3 ways glucocorticoids decrease bone formation
- decrease osteoblast activity
- decrease GI absorption of Ca2+
- increased renal loss of Ca2+
how does estrogen build bone (2)
- increase osteblast activity
2. decrease osteoclast activity
what is the main indicator of ventillation
PaCO2 (inversely related)
bc CO2 -> perfusion limited, equilibrates FAST
(high conc gradient)
O2 is also perfusion limited, but does not equilibrate as fast as CO2
when see low CO2, think..
hyperventilation
determinant of PaCO2 =
basal metabolic rate / alveolar ventillation
normal BMR: 0.8 CO2 produced for every O2
decreased PaO2 & PaCO2
PaCO2 = indicator of ventilation.
likely hyperventilation (blowing off CO2) but not sufficient to oxygenate blood
due to PE or pneumonia
blood oxygen state after PE or pneumonia
hypoxemia causes peripheral arterial chemoreceptors to send neural impulses to CNS respiratory centers, to increase respiratory drive
—> hypocapnia
but, hypoxemia continues –> have increased alveolar-arterial oxygen gradient.
(can correct w/ more oxygen)
significant upper airway obstruction on blood gases
increase PaCO2, decrease PaO2
hyperventilation does not correct this
significant respiratory muscle fatigue on blood gases
// decreased chest wall compliance
increase PaCO2
blood CO2 determined by (2)
- respiratory rate
2. tidal volume
blood O2 determined by (1)
available alveoli
alveolar ventilation status determined by..
arterial PaCO2
“floating” ribs vs “false” ribs
floating ribs: 11 & 12, not bound anteriorly to rib cage by cartilage
false ribs: bound to anterior rib cage by cartilage 8, 9, 10
which ribs overlie spleen?
ribs 9, 10, 11
which ribs overlie kidney?
rib 12
rib 12 can lacerate..
displace into retroperitoneum * lacterate kidney
which posterior ribs overlie liver?
8, 9, 10, 11
at rest: inferior margin of left lung along midscap line?
during max inhalation
rest: 10th rib
max inhalation: 12th rib
what vertebral level does pancreas overlie?
L2
describe important structures at
T12, L1, L2, L3, L4
T12: esophagus enters, celiac branch
L1: SMA
L2: pancreas
L3: IMA
L4: bifurcation of abdominal. aorta
perfusion limited gases
CO2, N2O
equilibrates FAST (early along capillary).
ventilation determines PaCO2
(when have poor perfusion i.e. w/ PE, hyperventillation can still blow off CO2
diffusion limited gases
CO
gas does not equilibrate by the end of capillary
oxygen in normal health is.. (perfusion/diffusion limited)
in fibrosis, emphysema? exercise
normal health: perfusion limited (will equilibrate by end of capillary, though not as fast as CO2
exercise: blood flows fast, but will still equilibrate by end
fibrosis: diffusion limited now (never diffusion limited for CO2)
thyroid arterial supply
- superior thyroid artery (branch of external carotid)
2. inferior thyroid artery (branch of subclavian)
ligation of inferior thyroid artery can…
injury recurrent laryngeal n (CNX)
–> hoarseness
unilateral damage to recurrent laryngeal n. causes?
bilateral damage?
recurrent laryngeal n (CN X) feeds all muscles of larynx (except cricothyroid) & sensory below vocal folds
unilateral: hoarseness
bilateral: airway obstruction by immobile vocal folds
ligation of superior thyroid artery can..
injury to external branch of superior laryngeal n (CNX)
paralysis of cricothyroid m.
impaired ability to produce pitch –> monotone
branches of superior laryngeal n.
external: supplies cricothyroid (muscle of larynx)
internal: sensory from epiglottis to vocal folds
(below vocal folds -> recurrent laryngeal)
ansa cervicalis
C1, C2, C3 cervical plexus
courses deep to CNS, loop around IJV
feeds: sternohyoid, sternothyroid, omohyoid
“strap muscles”
hypoglossal n (CNXII)
exists cranium via hypoglossal canal
innervates all intrinsic muscles of tongue, except palatoglossus
spinal accessory N (CNXI)
exists via jugular foramen, courses atop levator scapsular –> SCM and trapezius
recurrent laryngeal n (CN X)
feeds all muscle of larynx (except cricothyroid) & sensory below vocal folds
(above vocal folds: internal branch of superior laryngeal n.)
where does a horseshoe kidney get stuck
inferior pole by IMA
risk for urinary tract obstruction & development of hydronephrosis
fetal metanephros initially in sacral region, ascent to T12-L3
what vertebral levels are kidneys?
T12-L3
right is slightly lower
4 fates of vitelline duct abnormalities?
- persistent vitelline duct (full connection from midgut -> umbillicus
- meckel diverticulum: outpouch of midgut (umbillicus part -> fibrosis
- vitelline sinus: outpouch of umbillicus (midgut part -> fibrosis
- vitelline duct cyst (enterocyst) -> pouch between the two, fibrosed on either side.
pronephros
develops in week 4, then degenerates
mesonephros
serves as interim kidney in 1st trimester, later contributes to male genital system
(female) paramesonephros
metanephros
permanent. appears week 5, nephrogenesis from 32-36 wks of gestation
origin of the collecting system of kidney (ureter, pelvises, calyces, collecting ducts
ureteric bud, from caudal end of mesonephros
origin of glomerulus to collecting duct of kidney
metanephros
describe renal development
ureteric bud (from caudal end of mesonephros)
forms ureter, pelvises, calyces, collecting ducts
canalize by week 10
induces differentiation & formation of glomerulus through DCT (metanephros)
what is the last region of the kidney to canalize?
uteropelvic junction.
most common side of obstruction in fetus (hydronephrosis)
blood flow through kidney
renal artery -> segmental artery -> interlobular artery -> arcuate artery -> radial artery -> afferent arteriole -> glomerular capillaries -> efferent arteriole -> peritubular capillaries -> interlobar vein.
on RPF & FF.
moderate efferent constriction causes? severe?
FF = GFR/RPF
moderate efferent arteriole constriction increases GFR & reduces plasma flow –> increases FF
severe efferent constriction will increase capillary oncotic pressure (due to filtration of plasma & increased concentration of non-filterable plasma proteins), which will cause an OVERAL DECREASE in GFR (though filtration fraction will still be up)
afferent arteriole constriction on FF and GFR?
reduce RPF, will equally decrease GFR, so no net change in FF. /
asked for the probabililty that at least 1 false positive test will result in 8 negs (given 95% specificity)?
- caculate probability that all independently correctly false (0.95^8)
- at least 1 means..
1-probabilty all negative (1-0.95^8)
(accounts for situation where all are false + or at least 1 is)
if events are independent, probability that all events turn out same is product of separate probabilities for each event.
probability of at least 1 event turning out differently is 1-probability all same.
linkage disequilibrium
pair of alleles from two loci are inherited together in the same gamete (haplotype) more or less often would be expected by random change alone given corresponding allele frequency
what can cause linkage disequilibrium?
physical proximity of allelic loci, but not always!
can be due to mutations, genetic drift, migration, selection pressure, and non-random mating
Hardy-Weinberg principle
if p & q are frequency of separate alleles (SAME LOCI)
p^2 + 2pq + q^2 = 1
and p+q = 1
p^2 = frequency of homozygosity for allele p
2pq = carrier frequency / frequency of heterozygosity
q^2 = frequency of heterozygosity for allele q
Hardy-weinberg assumptions (4)
- no mutation in locus
- natural selection not occurring
- completely random mating
- no net migration
Hardy-weinberg: frequency of X-linked recessive disease in male? in females?
male = q female = q^2
how do we estimate the probability of two alleles appearing together if distinct loci? same loci (in hardy-weinberg)
distinct loci: multiple occurance rate –> ‘haplotype freq’
same loci: 2pq
antibodies to PRP (polyribitol ribose phosphate) suggests..
h. influenza type B capsule
presentation of epiglottitis
abrupt onset of obstructive laryngeal edema
acute fever, inspiratory stridor, drooling, osynophagia, positive “thumb” sign on lateral cervical x-ray (edematous epiglottis)
positive “thumb” sign on lateral cervical x-ray?
edematous epiglottis
epiglottitis, prob H. flu type B
malignant pustule (painless ulcer w/ black eschar & local edema)
b. anthracis
capsule of D-glutamate
what can we expect after replenishing Fe2+ after Fe2+ deficient anemia?
increased hgb 2g/dl per week for 1st 3 weeks
enhanced erythropoesis & accelerated release of both mature RBC and reticulocytes
reticulocyte is..
immature RBC. slightly larger & bluer.
lacks nucleus but retains basophillic, reticular, mesh-like network of residual ribosomal RNA.
after wright-giemsa stain
rate of reticulocyte in blood stream
will mature into RBC, which will live for 120 days
adenomyosis
presence of endometrial glands in the myometrium
present: menorrhagia & dysmenorrhea
why is uterus enlarged w/ adenomyosis?
endometrial glands in myometrium
mostly: uterine smooth muscle hypertrophy & hyperplasia in response to ectopic endometrial gland tissue.
physical exam of adenomyosis vs. leiomyoma
adenomyosis: uniformly enlarged
leiomyoma: IRREGULARLY enlarged uterus or mass
most common gynecological malignancy?
endometrial (adenocarcinoma)
size of uterus w/ ectopic pregnancy?
uterus is NOT enlarged, but will
(on biopsy: uterine wall will have decidualized stroma bc hormona changes still occur!
a unique tRNA exists for every..
mRNA codon sequence
though mult diff codon seq might get the same amino acid
t arm of tRNA (thymine, pseudouridine, cytosine)
only RNA sequence w/ thymine
binds to ribosome
‘touch’ ribosome
D arm of tRNA
dihydrouracil residue
helps tRNA recognition by correct aminoacyl tRNA synthetase
‘determine’ synthetase
what codon sequence is on tRNA 3’ end
3’ -> CCA
‘can catch amino acid’
site for amino acid binding
carnitine deficiency will result in…
acetoacetate
what is carnitine important for..
B-oxidation of fatty acids
take fatty acyl-CoA from cytoplasm into mitochondrial matrix
describe fatty acid metabolism
fatty acid –> acyl-CoA
-via acyl-CoA synthetase
carnitine + aceyl-CoA –> acyl-carnitine CoA
-via CAT1
go through mitochondrial membrane
acyl-carnitine CoA –> carnitine + acyl-CoA
-via CAT 2
then B-oxidation w/
FADH2 + acyl-CoA dehydrogenase
what are CAT 1 and CAT 2
carnitine-acyl transferase 1:
combines carnitine + acyl-CoA to enter mitochondrial membrane
carnitine-acyl transferase 2:
inside mitochondria, releases carnitine + aceyl-CoA
describe process of beta-oxidation
like ETC, takes off some e- and moves from FAD/FADH2 and NAD/NADH w/ an ATP synthetase
carnitine deficiency
or: myopathic CAT deficiency
unable to bring fatty acid from cell into mitochondria to break down
in skeletal muscle
myoglobinemia
weakness following exercise
hypoketonia
MCAD deficiency (medium chain acyl-CoA dehydrogenase
medium chain = 8-10
present:
- fasting hypoglycemia (no energy from b-ox to fuel gluconeogenesis)
- no ketone in blood, see c8-c10 in blood (not enough acetyl-CoA)
- vomitting
peroxisomes will do w-oxidation, will see
- dicarboxylic acids
- & C8-10 in blood
link between gluconeogenesis & b-oxidation
need beta-oxidation energy to FUEL gluconeopgenesis!
differentiate McArdle from carnitine deficiency?
McArdle: increased glycogen in muscle
carnitine deficiency: increased fatty acid / triglycerides
bc: when play -> epinephrine increase hormone sensitive lipase, increase FA, enter muscle for energy, but can’t bind to carnitine –> accumulate!
ketogenic amino acids
leucine & lysine
major stimulus for ketogenesis in prolonged starvation & diabetic ketoacidosis? in alcoholics?
prolonged starvation: oxaloacetate consumed in gluconeogenesis
alcoholics: oxaloacetate -> malate
both build up acetyl-CoA, which shunts glucose & fatty acids to ketogenesis
hexokinase vs. glucokinase
hexokinase all tissue
glucokinase in liver
glucokinase only kicks in when glucose is HIGH
2 general pathways for apoptosis
- intrinsic mitochondrial
2. extrinsic death receptor
intrinsic path for apoptosis
- cessation of survival signals/ stress
anti-apoptotic Bcl-2 & Bcl-x in mitochondrial membrane replaced w/ Bak, Bax, Bim
allow for increased mitochondrial permeability
release caspase-activating substances (like cytochrome c)
release of cytochrome c from mitochondria..
pro-apoptotic protein, activate caspase for apoptosis
2 types of extrinsic apoptosis
- death receptor on cell surface [TNF-R1 and Fas]
2. immune cell: perforin/granzyme release
2 major death receptors
TNF-R1 and Fas (CD95)
how does Bcl-2 block apoptosis
Bcl-2 prevents cytochrome c release from mitochondria.
Bcl-2 inhibits Apaf-1. Apaf-1 usu activates caspases.
receptor-mediated extrinsic apoptosis
death receptor: [TNF-R1 and Fas]
- receptor cross-link w/ ligand
- form a binding site for FADD (death domain containing adapter protein)
- caspases flock to FADD & activation is induced
physiologic example of intrinsic apoptosis
loss of IL-2 stimulation of T cells –> apoptosis
physiologic example of extrinsic apoptosis
Fas/Fas-L in thymic medullary negative selection
what type of physiologic apoptosis is impt for autoimmunity
Fas/Fas-L
important for negative selection in thymus medulla
succinate dehydrogenase
mitochondrial enzyme in ETC.
oxidizing succinate to fumarate & reducing FAD to FADH2.
superoxide dismutase
reduce superoxide to hydrogen peroxide
TTP vs. HUS
on a spectrum
both have pentad:
- fever, neuro manifestation, acute renal failure, thrombocytopenia, microangiopathic hemolytic anemia.
TTP:
usu adults, more neuro
HUS:
more kids, mostly renal
isolated activation of platelets (usu don’t bleed) normal PT, PTT, fibrinogen)
syrup of ipecac
emetic treatment.
used immediately after injection of toxin
cryoprecipitant contains
factor VIII, factor XIII, vWF, fibrinogen
good for hemophilia A, vwd, hypofibrinoginemia
side effects of SNRIs (duloxetine and venlafaxine)
high BP
also: stimulant effects, sedation, naseua
major side effects of TCA? one’s impt for drug intxn?
serious 3 C’s: cardiotoxicity, coma, convulsions
consider:
- a1-blocking effects: postural hypotension
- anticholingeric: tachycardia, urinary retention, dry mouth, hyperthermia
- block NE & 5-HT reuptake: tremor, insomnia
- block fast-acting Na+ channels: conduction defect, arrythmia, hypotension
- H1 antaognist: sedation
which TCA has most anticholinergic effects?
amitryptyline
list TCA’s
amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine
use for diabetic neuropathy? (2)
TCA: amityrptyline (also very anticholinergic!)
SNRI: duloxetine
TCA (esp amitryptyline) in patient w/ BPH
worry about urinary retention bc of anticholinergic effects
mechanism of neuroleptic malignant syndrome
specific to anti-D2 effects
block central dopaminergic systems involved in thermoregulation & regulation of muscle tone and movt
distinguish serotonin syndrome from neuroleptic malignant syndrome
serotonin syndrome: myoclonus
neuroleptic malignant syndrome: rigidity
rx for neuroleptic malignant syndrome?
- bromocriptine: Dopamine agonist
- amantidine: increase Dopine efflux
- dantrolene, stop rigidity
vision problems, dry skin, generalized pruitis
suggests prolonged biliary obstruction resulting in..
- vit A deficiency : vision & dry skin!
most common cause of night blindness
hereditary retinitis pigmentosa
5 signs of vitamin A deficiency
- nyctalopia: night blindness
- xerosis cutis: dry, scaly skin
- keratomalacia: corneal degeneration
- alopecia
- immunosuppression
4 differential diagnosis for acquired nyctalopia
- toxic retinopathy (phenothiazine & chloroquine
- vitamin A deficiency
- congenital rubella, syph..
- diabetic retinopathy
light tapping on chin induces masseter muscle spasm..
variant of chvostek sign; hyperactive jaw jerk
sign of hypoparathyroidism
Chvostek sign
facial muscle contraction elicited by tapping on the facial n. just anterior to ear
sign of hypoparathyroidism
(neuromuscular hyperexicitability)
Trousseau sign
occlusion of brachial artery w/ BP cuff –> carpal spasm
sign of hypoparathyroidism
(neuromuscular hyperexcitability)
2 exam signs of hypoparathyroidism
Chvostek sign
-tap on cheek, near ear -> facial muscle spasm
Trousseau sign
-BP cuff –> carpal spasm
(neuromuscular hyperexcitability)
at what Ca2+ levels do neuromuscular excitability manifest?
<7mg/dl
complication of thyroid surgery –> neuromuscular hyperexcitability
accidentally take out parathyroid!
improper fusion of maxillary prominence w/ medial nasal prominence results in..
cleft lip (primary palate)
improper fusion of lateral palatine process
or
improper fusion of lateral palatine process w/ nasal septum / median palatine process
cleft palate (secondary palate
inheritance of cleft lip/cleft palate
distinct etiology, but often occur together
MULTIFACTORIAL inheritance
[not associated w/ digeorge!]
when do lip / palate form
6th wk of embryonic development
midline intermaxillary segment forms..
philtrum of upper lip, four medial maxillary teeth, primary palate
choanal atresia
bone maldevelopment in fetus, causes obstruction of one or both nasal passage –> respiratory distress & cyanosis
how is ammonium from muscle disposed of?
alanine shuttle all transamination, req B6 in MUSCLE: -amino acids a-ketoacids -alpha-ketoglutatate glutamate
amino group from amino acids transferred to make glutamate
- glutamate a-ketoglutarate
- alanine pyruvate
amino group from glutamate passed to pyruvate to make alanine
alanine can travel in blood to LIVER
- alanine pyruvate
- alpha-ketoglutarate glutamate
NH3 released from glutamate via glutamate dehydrogenase, converted to urea & excreted
how is ammonia excreted from most other tissues (not muscle / liver?)
glutamine is released into blood
in kidney:
glutamine —> glutamate
via glutaminase
which releases NH3, converted to NH4+ and released in urine.
alanine cycle
alanine form muscle brought to liver, converted into pyruvate (NH3 transferred to make glutamate), pyruvate-> glucose, which goes back to muscle.
in muscle, glucose –> pyruvate –> alanine, all over again
cori cycle
pyruvate -> lactate, which goes to liver and is converted to pyruvate -> glucose, which goes back to muscle, makes pyruvate, etc
important nitrogen transporters in body
alanine & glutamine
pathogenesis of porcelain gallbladder
Ca2+ salts deposit intramurally secondary to chronic irritation // component of natural progression of chronic inflammation
usu asymptomatic, can comlpain of RUQ pain w/ firm nontender mass
prognosis of porcelain gallbladder
11-33% will develop gallbladder carcinoma
clearance of digoxin
primarily renal exretion
half-life 2.5 days (40hrs)
elderly pt w/ digoxin toxicity..
likely related to age-related renal insufficiency!
consideration w/ meds for all elderly?
reduce doses of renally-cleared medications to prevent toxicity
enzyme deficiency in von gierke’s
glucose-6-phosphatase
2 roles of debranching enzyme
- cleave 3 of the 4 limit dextrans (1,4 glucosidase) and put them to the main alpha 1,4 chain
- cleaves the last alpha-1,6-glycosidic bond to release free glucose
liver findings in Cori disease
lack of debranching enzyme
hypoglycemia, ketoacidosis, hepatomegaly
accumulation of dextrin-like structures in cytosol of hepatocytes in abscence of histopathlogical fatty liver infiltration
affects both muscle and liver cells
organ affected in von girke’s
only liver, bc enzyme glucose 6-phosphatase not in muscles
manifestation: hypoglycemia, lactic acidosis, hyperlipidemia, hyperuricemia
hepatic steatosis –> CARDINAL MANIFESTATION
why can muscle fxn without glucose 6-phosphatase?
bc uses glucose 6-phosphate for gluconeogenesis! isn’t trying to release glucose into circulation
cause of tabes dorsalis in tertiary syphillis. presentation
damage DORSAL ROOTS, leading to secondary demyelination & loss of axons in DORSAL COLUMN
present w/ lancinating pain, paresthesia, and loss of vibratory & position sense
can also have (1) areflexia & (2) loss of bladder fxn
maternal presentation of measles
postauricular lymphadenopathy, rash, arthralgia
malformed teeth: hutchinson’s incisors & mulberry molars think..
congenital syphillis
NF-kB is important for..
transcription factor for cytokine production
possible pathogenesis of crohn’s
increased activity of nf-kb (impt for cyotkine production)
appropriate response to intracellular microbes is blunted, microbe persist and produce chronic inflammation in GI tract
main CSF difference in viral / bacterial meningitis
- cell differential
bacterial: neutrophil
viral: lymphocyte - glucose & protein
bacterial:
glucose < 150mg/dl - gram stain/culture
bacteria: often +, not always
viral: no organism identified
most common viral cause of meningitis
echovirus
usu enteroviruses (coxsackie, echo, polio, enterovirus)
most common cause of bacterial meningitis
s. pneumo
2nd most common cause of bacterial meningitis
n. meningitidis
most common causes of common cold
coronavirus, rhinovirus, adenovirus
graves vs. hyperthyroidism
graves = hyperthyroidism AND..
- infiltrative opthalmopathy
- exopathalmos (GAG deposit)
- myositis of extraocular musc. - pretibial myxedema
[last 2 caused NOT by hyperthyroidism, but by autoimmune response to anti-TSH receptor, which is located also on fibroblasts & adipocytes]
causes of hyperthyroidism (4)
- graves disease (most common)
- toxic adenoma
- toxic multinodular goiter
- thyroiditis
describe pretibial myxedema
late manifestation of grave’s
NON-PITTING edema that is sometimes scaly in appearance (classically resembling an orange peel)
lower leg skin thickening & induration
which is the first factor to go in alcoholic cirrhosis of liver?
the one w/ shortest half-life, factor VII
why does thrombocytopenia develop in alcoholic cirrhosis of liver
hypersplenism – sequestered
what is barret’s esophagus a risk factor for
esophageal adenocarcinoma
will be clinically silent until it obstructs esophageal lumen
achalasia is caused by
loss of myenteric ganglion cells of the LES –> can’t relax
leads to high LES opening pressure & uncoordinated peristalisis
major risk factors for squamous carcinoma of the esophagus
- smoking
2. alcohol use
squamous vs. adenocarcinoma of the esophagus location? lymph spread?
squamous: upper 2/3
adeno: lower 1/3
upper 1/3: cervical nodes
middle 1/3: mediastinal/tracheobrachial
lower 1/3: celiac & gastric
most common risk factors squamous carcinoma
anything that causes irritation
alcohol & cigarette smoking (both)
important side effects of carbamazepine
- bone marrow suppression: anemia, agranulocytosis, thrombocytopenia
- hepatoxotic: monitor LFT
- SIADH
simple vs. complex seizure
simple: no impairment of consciousness during or after
complex: loss of memory during event / post-ictal state
important prognosticfactor in poststreptococcal glomerulonephritis
AGE
95% of children recover completely w/ conservative therapy
only 60% of cases in adults will result, rest become RPGN or chronic glomerulonephritis
pathogenesis of peripheral neuropathy in diabetes
- diabetic microangiopathy of endoneural arterioles:
nonenzymatic glycosylation of proteins leading to increased thickness, hyalinization, and narrowing of artery walls
- intracellular hyperglycemia in periphreal nerves, converted to sorbitol via aldose reductase. osmotic damage to axons & schwann cells
diabetic neuropathy sensation
paresthesia (tingling, numbness)
intense BURNING pain
types of neuropathy in diabetes
- distal symmetric polyneuropathy: “stocking and glove” distribution
- autonomic polyneuropathy: constipation, orthostatic hypotension, incontinence, erectile abnormalities
- mononeuropathy: cranial n (i.e. oculomotor, facial, optic), median n, etc
histology of cystic medial degeneration
fragmentation of elastic fibers in media –> “basket-weave” appearance.
space filled in by amorphous matrix
–> see MYXOMATOUS changes
myxomatous changes in media of large artery
cystic medial degeneration, related to aortic aneursym
which collagen disorder is associated w/ berry aneursym
type IV ehlers danlos
false aneursym
result of a breach in the continuity of all three layers of blood vessel (or heart)
leading to blood leakage / hematoma formation OUTSIDE vascular wall –> in connective tissue surrounding point of arterial wall rupture.
often: leaks at anastamosis sites of vascular grafts, postinfarction myocardial rupture contained by pericardial adhesions
where does mycobacterium leprae like to act
likes cool temperatures, so infects skin & superficial nerves.
“glove & stocking” loss of sensation
leprosy resevoir in US
armadillos
2 forms of Hansen’s disease
- lepromatous: diffusely over skin, lion like face, communicable.
low cell-mediated immunity w/ a humoral Th2 response
- tuberculoid (milder): limited to a few hypoesthetic, hairless skin plaques.
HIGH cell mediated immunity; largely Th1 type immune mediated
immune response to lepromatous vs. tuberculoid forms of hansen (leprosy)
- lepromatous: weak cell-mediated immunity w/ a humoral Th2 response
- tuberculoid: strong cell-mediated immunity. CD4+ Th1 immune response.
locally anesthesized hypopigmented spots
consider tuberculoid leprosy
lepromin skin test
m. leprae antigen injected intradermally.
+ test -> indurated nodule at site.
POSITIVE in patients w/ TUBERCULOID leprosy bc strong CD4+ Th1 cell-mediated immune response. –> activates macrophages to kill organism.
NEGATIVE in patients w/ LEPROMATOUS form. weak cell-mediated immunity.
which has a strong cell mediated component: tuberculoid or lepromatous form of leprosy?
tuberculoid has strong cell-mediated. [think: TB]
lepromatous: look like lepers w/ lion-face, loss of fingers / toes bc can’t feel anymore –> weak cell mediated.
skin biopsy of tuberculoid leprosy patient?
dominance of CD4+ T lymphocytes in skin lesions
