Will's random shit Flashcards
Baker Cyst
Site is at popliteal artery (Associated with arthritis) = outpouch swelling behind knee of synovial pouch/fluid
Most common peripheral artery aneurism
popliteal artery at popliteal fossa
Winter’s Formula What is it used for? what is the formula?
Used to evaluate respiratory compensation during metabolic acidosis. Answers the question, is there a concurrent respiratory alkalosis/acidosis? PaCO2= (1.5xbicarb) + 8 +- 2
Superior gluteal nerve damage cause s.s
cause: L4-S1; posterior hip dislocation or polio Innervates gluteus medius, minimus, and tensor fascia lata Trendelenburg sign; while walking patient hip will drop to unaffected side cannot abduct thigh
Obturator nerve damage Cause s/s
L2-4, anterior hip dislocation Innervates medial thigh. Will have troble with thigh adduction and medial skin sensory
Femoral nerve damage Cause S/s
L2-4; pelvic fracture Supplies muscles to anterior thigh and skin (some medial leg) Damage: cannot flex thigh to body or extend leg from knee. -absent patellar reflex
Common peroneal vs tibial nerve cause s/s
Both supplied by sciatic (posterior thigh splits into peroneal and tibial) dmg:lateral leg fibular dmg PED: Peroneal, Everts, Dorsiflexes -> Dmg = foot dropPED dmg: knee/tibial trauma TIP: Tibial, Inverts, Plantar flex -> Dmg = cannot stand on TIPtoe
Inferior gluteal cause s/s
posterior hip dislocation cant jump, climb stairs, rise from seat…. can’t push down
serratus anterior damage and innervation
innervated by long thoracic nerve attatched lateral ribs 1-8 and medial border of scapula dmg -> winging of scapula; holds it in place in order to abduct arm
cancellous bone =?
cancellous = spongiosa/spongy bone = trabecular bone
cortical bone
hard, supporting bone, most of the peripheral limb bones
osteopetrosis
normal bone marrow is filled with spongy bone, bones are harder but more brittle
HLA subtype associated with disease HLA-A3
Hemochromatosis HLE gene assoc with C282Y chromosome 6
HLA subtype associated with disease HLA-B27 (4)
Psoriasis, Ankylosing spondylitis, Inflammatory Bowel Disease, Reiter’s sundrome(reactive arthritis)
PAIR: seronegative spondyloarthropathies
HLA subtype associated with disease HLA-DQ2/DQ8
Celiac disease
HLA-DR2 (4)
MS, hay fever, SLE, goodpastures, UC
HLA subtype associated with disease HLA-DR3 (2)
DM I, Graves disease
HLA-DR4 (2)
RA, DM I
HLA-DR5
Pernicious anemia Hashimoto’s thyroiditis
HELLP syndrome associations and acronym
Hemolysis (microangiopathic) Elevated Liver enzymes (likely as above) Low Platelets (part of activated coag cascade) -associated with pre-eclampsia
Pre-eclampsia risk factors (4) and definition
DFN: HTN, Proteinuria, edema post 20wks up to 6 wks after delivery (occurs in 7% of women) RISKS: HTN, DM, CKD, Autoimmune problems Tx; delivery, bed rest, tx htn, Iv mag if seizures
Gardeners syndrome
FAP (chrom 5q, Aut Dom, tumor suppressor) + with osteomas and soft tissue tumors, congenital hypertrophy of retinal pigment
Turcot’s Syndrome
FAP + malignant CNS tumors (medulloblastoma/glial cell) Turcot = Turban
Trisomy 18
Edwards Syndrome (Election age at 18) 2nd most common trisomy in LIVE births S/S low set ears, clenched fist, prominent brow, microcephally (and basically any neural tube defect), rocker bottom feet, (E)dwards has low Estradiol **death in a year
Trisomy 13
Patau’s syndrome (Puberty at 13) S/S prosencephally, polydactyly, omphalocele, NUCHAL TRANSLUCENCY **DOES NOT HAVE clenched hands/overlapping fingers ***Death in a year
47 XXX
typically clinically silent
Congenital microdeletion of 5p
Cri-du-chat chr5 short arm deletion, S/S microcephaly, mental retardation, high pitch cry/mewing, VSD
Williams syndrome
Chr.7 deletion (includes elastin S/S elven facies, intellectual disability, hypercalcemia (increased Vit D sensitivity), well developed verbal skills, too friendly with others. CVD problems
Tumor marker PSA
Follow prostate carcinoma. may be elevated in BPH. Questionable as screening tool
Tumor marker Prostatic acid phosphatase
Prostate carcinoma. remember that tumor markers shold not be used as primary tool for diagnosis. Have to do histology
Tumor marker CEA
nonspecific, but produced by 70% colorectal and pancreatic CA may also be in gastric, breast, medullary thyroid carcinoma
Tumor marker alpha fetoprotein
hepatocellular carcinoma nonseminomatous germ cell tumors (yolk sac)
Tumor marker b-hcg
hyadidiform mole choriocarcinoma
Tumor marker ca-125
Ovarian cancer
Tumor marker s-100
melanoma, neural tumors, schwannoma
alk phosphatase
metastases to bone, liver, pagets disease of bone
bombesin
neuroblastoma, lung, gastric cancer
TRAP
hairy cell B cell leukemia
CA 19-9
pancreatic adenocarcinoma
calcitonin
medullary carcinoma of the thyroid (c cells)
Charcot-Bouchard microaneurysm What are they? Where?
Small < 1mm diameter aneurisms in basal ganglia, internal capsule, thalamus Associated with long standing HTN. **They’re intrparenchymal
Multiple intraparenchymal hemorrhages in an elderly person Cause?
B-Amyloid cerebral angiopathy. Not associated with systemic amyloidosis or alzheimers.
Berry aneurysm/saccular aneurysm
Occurs at bifercations of circle of willis (most commonly ACA). -> subarrachnoid hemorrhage RISK: ADPKD, ehlers danlos, marfan, smoking, htn
end plate potential
The voltage change at the site of NMJ interaction (the immediate response to acetylcholine binding)
CD31
PECAM-1: expressed on endothelial cells. Helps migration/diapedesis. ** Can be used to differentiate tumor origin
CD 16
Fc receptor
CD18
Integrin
CD 14
LPS PAMP on macrophages
munro microabscesses = ?
Neutrophils in stratum corneum in psoriasis
parakeratosis
hyperkeratosis with retention of keratinocyte nuclei in stratum corneum (psoriasis)
psoriasis also causes acanthosis (stratum spinosum hyperplasia)
specialized vs generalized transduction
Lysogenic cycle: virus just chilling specialized is when bacterial gen ends up in viral capsid what was close to the viral insertion point in the DNA Lytic cycle: virus kills cell Generalized is when the cell bursts and random DNA is incorportated during cell death
Melanoma common mutation? Tx?
Common BRAF kinase mutation Tx; excision 2nd vemurafenib (BRAF kinase inhib) if BRAF +
Achondroplasia mutation inheritance
mutation is activation of FGFR3 which inhibits chondrocytes inherited AD, but usually sporatic mutation, associated with advanced PATERNAL age
Osteogenesis Imperfecta Inheritance how blue sclera?
AD usually collagen type I Blue sclera from thin sclera, you can see the choroidal veins (which are part of the vascular network btw the sclera and retina
Osteomyelitis seeding children? adults?
Children bacteria seed the metaphysis Adults the epiphysis is most commonly seeded
Causes of aseptic necrosis of bone
Trauma/fx (most common) #steroids #Caisson disease (decompression sickenss with nitrogen occluding bone vasculature
Osteomyelitis causes (6)
Staph aureus; most common (90%) N gonnorrhoeae- sex Salmonella- sickle cell pseudomonas- diabetics/drug users Mycobacterium tb- pott’s disease (vertebrae)
invasive gastroenteritis organisms
salmonella, shigella, campylobacter, EIEC, + enameoba histolytica
suprachiasmic nucleus
hypothalamic nuclei: regulates sleep
what’s the most commonly injured ankle ligament
from INVERSION injury and tear of ATFL, anterior talofibular ligament “always tear first ligament” 2nd: calcaneofibular ligament 3rd: posterior talofibular ligament
What is the medial ankle ligament?
deltoid ligament
dorsal interosseous muscles do what? palmar interosseous muscles do what?
DAB: Dorsal abduction PAD: palmar adduction
Tumors that like to metastasize to bone
Prostate -> blastic lesions*** Renal Cell Carcinoma Testicular/Thyroid Lung -> lytic lesions Breast -> lytic/blastic “Permanently Relocated Tumors Like Bone” ***most are lytic except prostate
Tuberous Sclerosis findings
HAMARTOMAS Hamartoma’s of CNS and skin
Adenoma sebaceum (cutaneous angiofibromas)
Mitral regurgitation
Ash-leaf spots
Rhabdomyoma (cardiac, benign)
Tuberous sclerosis dOminant (autosomal)
Mental retardation
Angiomyolipoma (renal)
Seizures variabille expressivity, incomplete penetrance hamartin or tuberin protein mutation
Pseudogout What deposition and where Diagnosis Tx
Deposition of calcium pyrophosphate in joint space usually of larger joints (knee)
Basophilic thomboid crystal weak positive birefringence blue on parallel light (vs gout which is yellow on parallel light)
Tx; NSAIDS, steroids, colchicine
Actinic keratosis
precursor to squamous cell carcinoma (dysplastic)
keratoacanthoma
Squamous cell carcinoma that grows rapidly (4-6 weeks) and may regress spontaneously. characterized by keratin cup filling the center.
What is the most common cancer from immunosuppressive therapy?
Squamous Cell carcinoma
Which type of sunlight is the worst for cancer dmg? Which type is responsible for sunburns? How about tanning
UVB -> cancer and sunburns
UVA -> less cancer, tanning
What enzyme in the kidney inactivates 25-dihydroxy vitamin D?
24-hydroxylase in the kidney may inactivate it -> 24,25-dihydroxy vitamin D
What are the two ligands for osteoclast differentiation? Where do they come from? What cell lineage do osteoclasts come from?
RANKL and M-CSF (macrophage colony stimulating factor), comes from osteoblasts, the lineage is from mononuclear cells
osteoblast cell lineage? chondrocyte cell lineage?
Both come from mesenchymal stem cells
What are you thinking if you have a fat tumor with lipoblasts?
lipoblasts= Liposarcoma (most common malignant soft tissue tumor in adults), vs lipoma which is most common benign.
What is most common malignant soft tissue tumor in children?
Rhabdomyosarcoma classic site is vagina in female (grape like protrusion)
Dermatomyositis S/S Labs associations tx;
proximal muscle weakness with skin symptoms (malar rash, gottron’s papules (papules on nuckles), heliotrope rash (eyelids). “mechanic hands, shawl and face rash” CD4+ t cell perimysial inflammation and atrophy. Labs: Increased CK, positive ANA, positive anti-jo-1 *associated with malignancy (often gastric) Tx; steroids **This condition is in contrast to polymyositis that’s endomysial, increased MHC I, no skin involvement. Similar labs and Tx. Not associated with malignancy
What is urushiol?
a small substance that acts as a hapten (must attach to random protein to become allergenic) -poison oak, sumac, and Ivy all have urushiol type Iv
What does Alpha 1 antitrypsin stain?
Stains purple with PAS (periodic acid schiff) Smoking makes the disease worse by oxidizing and inactivating the antitrypsin at a methionine residue
3 causes of HIV esophagitis
1) candida 2) HSV-1 vesicles -> punched out erosions 3) CMV linear ulcer/erosions
HLA DR1
Chrohn’s predisposition
femoral neck fracture most commonly injures which vessel
the medial circumflex femoral bc it supplies the majority of the blood supply to head and neck (injury = avascular necrosis)
What artery supplies the SA and AV nodes?
RCA
If you have increased AFP in serum/amniotic fluid, what’s a helpful confirmatory test for neural tube defect?
Elevated AChE **these elevations are from failure of neural tube(spinal canal) to close and a persistent connection with the amniotic cavity.
signs of anencephaly risks
increased AFP, AChE, polyhydramnios (lost swallowing center in brain) –brain develops normally but acidic amniotic fluid destroys it RISKS: maternal DM I, and low folate
Risks of holoprosencephaly
patau’s (trisomy 13), fetal alcohol syndrome Sonic Hedgehog mutations
GFAP
astrocyte marker (intermediate filament) used to ID tumors ie: glioblastoma benign pilocytic astrocytoma
Microglia response to HIV infection in cns
become multinucleated giant cells
Large clear fired egg appearance found in (3)
oligodendrocytes koilocytes of HPV infection Seminoma
guillan-Barre S/S Damage to what? Risks
S/S ascending bilateral plegia/paresis/paresthesia (hands and feet) Damage to schwann cells Risk: campylobacter or CMV infection
Bilateral acoustic neuroma
Neoplasm of schwann cells NF-2
Who does reactive gliosis?
Astrocytes (the support cells with fibroblast like scar tissue repair)
what embryologic origin are ependymal cells derived from?
Neural ectoderm
wallerian degeneration
dmg to axon with proximal retraction and distal degeneration
Fenestrated regions of BBB
area postrema -> vomiting esp after chemo) OVLT- osmotic sensing (organum vasculosum of the lamina terminalis) hypothalamic input and output permeat BBB such as part of neurosecretory product: ADH, oxytocin
location of NE production in brain what lvls associated with anxiety and depression?
locus ceruleus (pons) increased in anxiety decreased in depression
location of dopamine production in brain lvls assoc with schizo, parkinsons, depression
ventral tegmentum in midbrain (-> cortex or -> limbic)
SNc -> neostriatum
schizo is increased dopamine mesolimbic (positive symptoms) vs decreased mesocortical (negative symptoms),
parkinsons is decreased,
depression is decreased
Serotonin location and association with anxiety and depression
raphe nucleus (pons) decreased in anxiety and depression
ACh CNS location and assoc with alzheimers, huntingtons, REM sleep
ACh is basal nucleus of meynert alzheimers decreased (meynert degeneration) huntingtons decreased REM sleep increased
GABA location and assoc with anxiety and huntingtons
Nucleus accumbens (reward center), decreased in anxiety and huntingtons (causes choreoform from excess muscle excitation)
Glycine neurotransmitter
main inhibitor in spinal cord GABA is main in CNS
Reticular Activating System does what?
mediates attentiveness and consciousness
its in midbrain and above
Schizophrenia dopamine issues
you have increased dopamine in limbic system -> positive symptoms you have decreased dopamine in cortex -> negative symptoms
What is the bundle of bilateral nerves that link broca’s area in the frontal cortex to wernicke’s area in the temporal lobe?
Arcuate fascicles
Where does the vagus nerve run in the neck?
Within the carotid sheath with the common carotid and internal jugular vein
blood supply to brain stem and cerebellum?
basalar artery (also pontine aa supply pons) and vertebral arteries,
Conduction aphasia
poor repetition (cannot repeat no ifs ands or buts) can comprehend and speak fluently dmg; arcuate fasciculus
global aphasia
nonfluent aphasia with impaired comprehension. Broca(nonfluent) and wernicke’s(fluent) fucked up
Dysprosody dmg result
damage is non dominant hemisphere brocas: cannot express emotions/inflection wernicke’s: can’t understand emotion/inflection
Gerstmann syndrome
lesion to dominant angular gyrus (left sided parietal lobe) -agraphia (inability to write) -acalculia (bad math) -R/L disorientation -finger agnosia (can’t tell difference)
Hemispatial neglect
lesion to nondominant parietal lobe (draw clock on one side, don’t shave)… usually right sided
Frontal cortex lesion
disinhibition, poor judgement, primitive reflexes
prefrontal cortex
poor executive function
Frontal eye field lesion (which is in cortex/controls eye movement)
lesion wil deviate eyes ipsilateral to lesion
PPRF lesion: paramedian pontine reticular formation pontine area
eyes will deviate contralateral to lesion it’s in the medial pons near MLF
Superior colliculus lesion (parinaud’s syndrome) in brainstem
paralysis of upward gaze (they look downward)
can occur from pineal gland germ cell tumor or stroke
RAS damage
stupor and coma
hippocampus lesion bilaterally limbic system
anterograde amnesia (cannot make new memories)
mamimillary body lesion limbic system
wenicke korsakoff: eyes, lies capsize confusion, confabulation, ataxia, memory loss (anterogrand and retrograde amnesia) Don’t give glucose without B1 to B1 deficient patient (may precipitate condition
amygdala limbic system
bilateral amygdala lesions kluver bucy syndrome: hyperorality (likes putting things in mouth), hypersexual, disinhibited behavior (not afraid), docile, extreme curiosity HSV 1 association
Hemiballismus
lesion of subthalamic nucleus lesion involuntary flailing of one arm
what cerebellar lesion could produce dysarthria?
cerebellar vermis lesion
Nuclei locations of CN’s
1 2 forebrain 34 midbrain 5678 pons “5 6 7 8 cheer with pom pons” 9 10 12 medulla 11 spinal cord
homonymous hemianopsia
lesion of optic tract (not nerve) with one sided visual loss
lesion of center of visual field
lesion of macula (ie macular degeneration)
homonymous hemianopsia with macular sparing
lesion of posterior cerebral artery. Macula is spared bc it gets collateral from middle cerebral (its important)
myopia
near sighted, predispose to retinal detatchement. retinal detatch also associated with diabetic traction and inflammatory effusions
What conditions can cause a facial nerve palsy?
ipsilateral FULL FACIAL paralysis vs motor cortex contralateral lesion of just lower face “Lovely Bella Had An STD” -Lyme disease -Bells palsy = idiopathic -HSV and zoster (likely termed idiopathic) -AIDS -sarcoidosis -tumors -diabetes
The second arch contributes to what in the human?
facial nerve muscles (muscles of facial expression) and cnVII
Describe motor cortex lesion of face (like in a stroke)
motor cortex contralateral lesion of just lower face bc lower facial muscle is just innervated by contralateral side. Upper face is innervated by both sides of motor cortex So in acute presentation of face check eyebrows!!! if can move it’s probably a stroke, if not, likely facial nerve palsy
CN V (trigeminal) exit from skull
“Standing Room Only” -superior orbital fissure (w/3,4, 5, 6 -Rotundum -ovale
VII-XII exit
In posterior cranial fossa (temporal or occipital bones) VII-VIII internal auditory meatus IX,X,XI through jugular foramen XII hypoglossal canal
vagus nerve damage, uvula will deviate which direction?
To the opposite side of damage. Because the vagus elevates the soft papate
Nucleus Ambiguous innervation
aMbiguous: MOTOR innervation to pharynx, larynx, upper esophagus. SWALLOW AND SPEECH vaGUS from ambiGUUS IX, X cortical lesions affect both sides, no deviation
For hypoglossal lesion, what is the deficit?
CN XII is intrinsic tongue movement. tongue licks the lesion. deviate toward lesion cortical lesions affect both sides, no deviation
gag reflex test
CN IX, X IX is afferent, X efferent
cavernous sinus lesions
CN III, IV, VI pass through (opthalmoplasia with double vision) + V1 -> pain upper opthalmic branch V2 also passes through going down and medial: 3,4,V(1),V(2),6 internal carotid and postganglionic sympathetics also present there
Tongue sensation and movement
movement: XII somatosensation: trigeminal mandibular branch along with gums (anterior 2/3), post 1/3 is glossopharyngeal taste: ant 2/3 facial, post 1/3 glossopharyngeal, very back vagus
Nucleus Solitarius
A vagal nuclei VII, IX, X Sensory: taste, baroreceptors (carotid IX, aortic X), gut distension
where do the dorsal columns decussate?
The medulla, becoming the medial lemniscus
Vagal Dorsal motor nucleus
X sends parasympathetic to heart, lungs, upper GI
Where is the inferior olivary nucleus?
medulla
what artery supplies antero-medial part of medulla?
anterior spinal
what artery supplies the nucleus ambiguus?
PICA
Z = what for the 95% CI and 99% CI
Z= 1.96 Z= 2.58
what is the corticobulbar/corticonuclear tract?
brings motor from cortex to brainstem, carrying the non-oculomotor CNervs
What does the posterior internal capsule carry?
Most of corticospinal tracts and somatic sensory, visual, and auditory fibers
what does the anterior internal capsule carry?
some of the thalamocortical fibers
where is the substantia nigra?
midbrain ventral tegmentum is there too (midline midbrain assoc with reward pathways)
http://what-when-how.com/wp-content/uploads/2012/04/tmp15F10_thumb.jpg
dopamine is increased or decreased in reward pathways?
It’s increased (as in drugs of abuse) in the mesolimbic pathway (same area of positive symptoms of psychosis)
Leber hereditary optic neuropathy
A mitochondrial inherited disease (heteroplasmy) leads to bilateral vision loss
Myoclonic epilepsy with ragged red fibers
Heteroplasmy inherited: myoclonic seizures and myopathy associated with excercise. Skeletal muscle biopsy shows ragged red fibers
Mitochondrial encephalopathy with lactic acidosis and stroke like epilepsy (MELAS)
Heteroplasmy: stroke like episodes, muscle weakness, increased serum lactate post exercise and at rest
UC difference in crc from sporatic
1) progress from flat nonpolypoid dysplasia 2) early p53 mutation 3) proximal colon involvement 4) mucinous w/signet ring 5) multifocal 6) affect younger pts
thymoma differential
1) pure red cell aplasia (or parvo or some lymphocytic leukemia’s) autoantibodies 2) myasthenia gravis
Rule of 4’s
1) 4 medial structures with M -motor (corticospinal) -> contralateral motor -medial lemniscus -> contralateral sensory -medial longitudinal fasciculus (MLF) -> ipsilater internuclear opthalmogplegia -motor cranial nerves (as below) 2) 4 lateral with S -spinocerebellar (coordinates movement ipsilateral) -> ips ataxia -spinothalamic tract (pain/sense) -> contralateral affected -sensory nucleus CN V -> ipsilateral pain/temp on face -sympathetic pathway -> ipsilateral horners 3) 12 34 5678 9,10,12 11 4) The medial motor CN nuclei divide into 12: 3,4,6,12
Wallenberg syndrome
PICA syndrome Lateral medullary lesion: 9 10 12 (some of V) spinothalamic: contralateral pain/temp trigeminal nucleus (huge) : ipsilateral face pain/temp Nucleus ambiguous: difficulty swallowing/hoarse voice descending sympathetic: ipsilateral horners vestibular nucleus: vertigo/nystagmus inferior peduncle (spinocerebellar tract) -> ataxia
What does PICA supply?
Lateral medulla
What does AICA supply?
Lateral pons
What does anterior spinal artery supply in brainstem?
middle medulla
Basal artery supplies?
middle pons; , more specifically the paramedian branches of basalar artery
MLF syndrome causes (2)
located in pons, helps eyes track adducting medial rectus palsy in ipsilateral MLF & contralateral abduction lateral gaze nystagmus cause: medial pontine stroke and MS
Locked in syndrome causes
only move eyes # stroke of medial pons # central pontine myelinolysis with rapid hyponatremia Na correction => find increased signal intensity in pons
Weber syndrome
anterior midbrain stroke from occlusion of paramedian branches of posterior cerebral artery infarct peduncles (corticospinal and corticobulbar tracts) -may affect CN III
What AA are modified in golgi? and in RER lysosome trafficking?
Golgi: O-oligosaccharides SERINE THREONINE +asparagine: N-oligosaccharides RER: N-oligosaccharides Asparagine glutamine: Lysosome trafficking from golgi of mannose-6-phosphate. DEFECT = I cell disease
Limbic system control
“primitive” part of brain + learning 5 Fs Feeding, fleeing, fighting, feeling, fucking
anterior hypothalamus nuclei
A/C = anterior cooling -> thermoregulation Damage => hyperthermia
suprachiasmatic nuclei
in hypothalamus regulates circadian rhythm “need sleep to be charasmatic”
Preoptic area
hypothalamus: secrete GnRH
supraoptic nucleus
anterior hypothalamus water balance: ADH damage: central DI
paraventricular nucleus
In anterior hypothalamus oxytocin: oxys= quick, tocos = birth +CRH, TRH
posterior hypothalamus
if you zap it you become a poikilotherm = cold-blooded, no heat production
lateral hypothalamic nucleus
hunger. destruction -> anorexia (shrink laterally). Inhibited by leptin
ventromedial hypothalamic nucleus
satiety. stimulated by leptin. damage=obesity. (grow ventrally) also savage behavior if damaged
melatonin secretion? derived from?
pineal gland secretes melatonin from seratonin follows circadian rhythm inhibits sex drive
kluver bucy syndrome
bilateral amygdala lesions kluver bucy syndrome: hyperorality (likes putting things in mouth), hypersexual, disinhibited behavior (not afraid), docile, extreme curiosity
psuedotumor cerebri
RISK: young obese women, ppl using vitamin A daily
pulsatile headache,
-retrooccular pain worse on movement
N/V
papilledema (increased ICP) but no hydrocephalus)
vision loss
NO TUMOR
NO dilation of VENTRICLES
LP -> ICP elevated
Tx; weight loss, acetazolamide, serial LP,
CSF generation where?
choroid plexus in the ventricles reabsorbed by arachnoid granulation
Normal pressure hydrocephalus vs hydrocephalus ex vacuo
Normal pressure has dilated ventricles that compress corona radiata -> wacky wobbly wet Hydrocephalus ex vacuo no increased ICP, just apparent bc of brain atrophy (alzheimers, HIV, Pick’s disease)
NORMAL PRESSURE HYDROCEPHALUS IS REVERSIBLE
elevated ICP usually damages what CN?
CN III -> palsy -> down and out eye presentation
spinal cord ends
L1-2
LP
L3/4 or 4/5 in children L4/5 L5/S1 L4 vertebra at iliac crest
intraventricular hemorrhage of newborn
most common in premature < 32wks and low birthweight neonates. occurs in first 72hrs of life originates in subgerminal matrix subependymal all newborns < 32 weeks should be screened by US for this
thrombolytic cutoff
4.5 hrs (max 6)
carotid sinus carotid body what monitor? what nerve?
carotid sinus = baroreceptor carotid body = chemosensation CNIX watches these
sturge weber syndrome
underlying vascular problems with Port wine stain in opthalmic V1 distribution
glaucoma, seizures, hemiparesis, intellectual disability
AVM from ipsilateral leptomeningeal angiomatosis
STURGE
stain, sporatic, unilateral portwine stain, glaucoma/GNAQ inactivation, epilepsy
what controls the parasympathetic system? sympathetic?
anterior hypothalamus -> parasympathetic
posterior hypothalamus - > sympathetic
Tx tension headache
NSAIDS: naproxen
Bilateral, nonpulsatile, over 30 minutes, steady pain without photophobia or phonophobia
Tx migraine headaches
-triptans sumatriptan
Unilateral, pulsating, +-aura, photophobia and/or phonophobia, made worse by foods with tyramine
increased risk stroke
-triptan
MOA
USE
SE
serotonin agonist
cause vasoconstriction modulate trigeminal nerve neurotransmission
USED: take as soon as start/aura migraine (PO) ,
2ndline cluster(IV)
SE: contraindicated CAD, prinzmetal, pregnancy
Tx cluster headache
100% O2 NRB: may abort in 5min, use for 15min
2nd line triptan
*nerve block, steroids
**more common in men, unilateral, ptosis, miosis, smokers
What conditions will tyramine make worse?
Cause a HTN crisis in MAOi takers
migraines
Where are VLCFA broken down?
In peroxisomes. Vs in the mitochnodria with LCFA and MCFA. branched chain FA are also broken down here (alpha oxidation)
calcified cystic mass in brain?
craniopharyngioma, often filled with brown fluid with cholesterol. lined by stratified squamous epithelium. Rathke’s pouch origin
length constant of neurons?
how far along an axon an electrical impulse can travel
time constant of neurons?
how long it takes for neurons to depolarize, myelin decreases time constant
Hageman factor actions?
Factor XII: proinflammatory protein produced by liver 1) Activated upon exposure to subendothelial/tissue collagen which leads to -coagulation cascade -complement activation (through kinin system) -XII @ kallikrein (kinin) -> @bradykinin -> pain and vasodilation, some vascular permeability
what is a population study?
an ecological study; vs a cross sectional study would use a disease and collect data at a PARTICULAR POINT IN TIME
what optic radiation goes through meyers loop?
Meyers loop passes through the temporal lobe and will give you a contralateral upper field defect (goes to lower part of occipital lobe)
calcarine fissure
divides visual fields in occipital lobe (upside down and R/L reversed
Metastatic cancers to brain location
multiple well circumscribed at grey-white junction Many TOP: Lung, Breast, Kidney
meningioma cell
more in adults (female) arachnoid cell, often present with seizure, compress but doesn’t invade whorled cells EXPRESSES ER receptor
glioblastoma multiforme cell
astrocyte, butterfly glioma, very malignant, GFAP positive with pseudopallisading located cerebral hemisphere
Pilocytic asrocytoma
benign tumor of astrocytes in children (most common tumor in children) “nodule growing on cyst wall” GFAP positive
Medullaroblastoma cells
malignant, most commonly in children, arising from neuroectoderm
salivation from parotid gland
Glossopharyngeal nerve IX
brain tumors adults
Metastasis 50% Glioblastoma (astrocytes) Meningioma (arachnoid) Schwannoma + Oligodendroglioma (frontal lobe usually) MGM StudiOs arranged in most common
homer wright rosette in what CA
medulloblastoma
Perivascular pseudorosette in what cancer
ependymoma
Brain tumors pediatrics
pilocytic Astrocytoma (GFAP_ medulloblastoma (high grade benign neuroectoderm) ependymoma (ependymal) AME arranged in most common
uncal herniation symptoms
CN III compression, outside: parasympathetic dmg -> mydriasis inside: motor dmg -> down and out -contralateral homonymous hemianopsia
what is ApoE4 associated with?
Late onset alzheimers chr.19
3 mutations associated with early onset alzheimers = <60y/o
APP chr21 Presenilin 1 chr 14 Presenilin 2 chr 1
What is ApoE2 associated with?
protective against alzheimers chr.19
Ebstein’s anomaly
atrialized right ventricle from downward displacement of tricuspid valve. from lithium ingestion early in pregnancy
sciatic nerve roots
L4-S3 branches into common peroneal and tibial
subluxation
is the incomplete/partial dislocation of a joint
ristociton
the test for vWF deficiency. causes vwf to clot platelets (unless you dont have any)
somatomedin C is what?
IGF-1
most common cause of aseptic meningitis?
1 is cocksackie virus enteroviruses (picornoviruses) = + sense ssRNA, naked PERCH: polio, echovirus, rhinovirus, cocksackie A (handfootmouth,B (pericarditis), hep A
Werdnig-hoffman disease
AR: Inherited degeneration of anterior motor horn. *SPINAL MUSCLULAR ATROPHY -Presents as floppy baby, death occurs within a few years
Differentiation btw ALS and syringomyelia
syringomyelia will involve the spinothalamic (pain and temperature) ALS is only LMN UMN
ALS occurance
Mostly sporatic Familial= Zinc-copper SOD mutation with free radical injury to neurons.
degeneration of cerebellum and spinal cord tracts with hypertrophic cardiomyopathy
mutation in Frataxin (essential for mitochondrial iron regulation -> free radical damage)
Friedreich’s Ataxia
Expansion GAA
- cerebellar degen - > ataxia
- multiple spinal tract degeneration -> sensation/vibration losses, muscle weakness, loss DTR.
- presents in childhood -> wheelchair bound within a few years
**Associated with hypertrophic cardiomyopathy
How does meningitis cause hydrocephalus, hearing loss, seizures?
All through healing and scarring process, can occlude CSF drainage (like arachnoid granulations), can affect nerve, may cause disturbance in conduction pathways through scarring.
Ratio of CSF to Blood glucose
0.6 (2/3)
cortical laminar necrosis
A type of global ischemia/infarction of vulnerable regions of pyramidal neurons of cortex 3,5,6,
vulnerable areas from global ischemia
cortical layers 3,5,6 hypocampus(temporal lobe): learning long term purkinje layer of cerebellum: integrates sensory perception with motor control
embolic vs thrombotic stroke macroscopic histology
thrombotic will be pale stroke (bc thrombus isn’t lysed) embolic will be hemorrhagic bc the clot will eventually be lysed
ischemic lacunar stroke locations
typically from lenticulostriate vessels coming off of MCA internal capsule (pure motor) thalamus (pure sensory) RISKS of HTN, DM vs basal ganglia for charcot bouchard (can be more diffuse)
earliest change in stroke
Red Neurons (12 hrs)
xanthochromia and blood on inferior brain
Subarachnoid hemorrhage. yellow is from heme breakdown
why is berry aneurism caused so easily?
It’s at branch point and lacks media layer (which is present before and after branch point)
uncal herniation s/s
compression CN III (down and out) # compression posterior cerebral artery (contralateral homonymous hemianopsia) #rupture of paramedian (pontine) arteries -> duret brainstem hemorrhage.. They basically get torn off **uncus is involved with olfaction and memory of smells
arylsulfatase A deficiency
lysosomal storage disease central/peripheral demyelination -> ataxia/dementia
Krabbe’s disease
lysosomal storage disease galactocerebrosidase deficiency #peripheral neuropathy, developmental delay, optic atrophy, GLOBOID CELLS
oligoclonal IgG bands, lymphocytes, myelin basic protein on LP
MS “very high elevation of proteins in CNS”
may see lipid laden macrophages that ate the myelin
JC virus infection in immunocompromised
PML: progressive multifocal leukoencephalopathy #rapidly progressive neurological signs leading to death
Progressive, debilitating encephalitis leading to death. from virus in infancy
Subacute sclerosing panencephalitis from measles -viral inclusions in gray and white matter
striatum
putamen (motor) + caudate (cognitive)
lentiform
putamen (motor) + globus pallidus
subthalamic nucleus does what?
inhibits movement (stimulates GPi)
depigmentation of substantia nigra
lewy body accumulation (alpha synuclean eosinophilic intracellular inclusions) with decrease in dopamine and melanin production. melanin as part of that pathway
meperidine
demerol (opioid) MPTP -> MPP(from MAO metabolism) byproduct causes parkinsons through dmg SN from inhibition complex I ETC
CD80/86
B7 on dendritic cells
what supplies anterior spinal artery?
the aortic artery
Amyloid plaque
Called a neuritic plaque
seen in alzheimers disease.
Is an extracellular accumulation of ABeta amyloid with entangled neuritic processes
neurofibrillary tangle
intracellular phosphorylated tau protein = insoluble cytoskeleton (microtubule organizer); they correlate with degree of dementia
Alzheimers
Picks disease
picks picks the frontal and temporal
early behavioral and language problems
findings of ROUND tau protein in neurons that stain with SILVER, they don’t survive neuronal death
lewy body dementia
EARLY dementia with Parkinsonian features. The alpha synuclein eosinophilic lewy bodies are in the cortex (vs SNpc in Parkinsons)
-parkinsonism with dementia and HALLUCINATIONS and possibly repeated syncope
corona radiata stretching is classic to
normal pressure hydrocephalus
wacky wobbly wet
increased CSF without increased ICP
spike wave complex on EEG
Creutzfeldt jakob disease (prion)
also assoc with rapid dementia (death within year), startle myoclonus, ataxia
familial fatal insomnia
inherited prion disease with startle reflex and insomnia
cowdry type A inclusion
HSV encephalitis
lewy bodies stain with what?
show up as alpha synuclein stained by PAS and ubiquitin (intracellular in parkinsons)
pseudodementia
dementia (memory problems) associated with depression
The patient often KNOWS they’re having difficulty with memory (vs a patient with true dementia)
magnetic gait
normal pressure hydrocephalus
Screens to rule in dementia
RPR (for syphillis)
HIV
TSH (hypothyroid)
Vitamin B12
MRI brain (multiple infarcts/NPH)
most common causes of delerium
drugs (esp think about acetylcholine antagonists)
UTI
lesch nyhan enzyme deficiency
hypoxanthine-guanine phosphoribosyltransferase
tx; Allopurinol (xanthine oxidase inhibitor)
s/s spasticity, choreathetoid movements, self mutilation
does uremia cause exudative or transudative pleural effusions?
exudative
GGT
serum gamma-glutamyltransferase
specific indicator of liver damage, sensitive in alcohol use
hypocretin 1
neuropeptie only produced in lateral hypothalamus that is low/undetectable in narcolepsy
cataplexy
brief loss of muscle tone preceded by strong emotion
jaundice occurs at what bilirubin lvl?
>2.5mg/dL
kernicterus bilirubin build up where?
basal ganglia
what is required for de novo pyrimidine production?
aspartate and glutamine
cori cycle
the glucose -> pyruvate -> lactate
to
lactate -> pyruvate -> glucose
cycle in muscle/rbc -> liver
alanine cycle
the alanine - pyruvate -> glucose cycle to recycle ammonia
ITP
what is it?
where is the Ab produced?
autoimmune destruction of platelets
Ig aimed at GpIIbIIIa
Ab is produced in spleen, macrophages eat platelets in spleen.
tx; steroids, IVIG, splenectomy as last resort
Undercooked beef will classically give you…
E Coli O157H7
-> HUS, especially in children
verotoxin damages endothelial cells and possibly also ADAMSTS13
what does uremia do to clotting?
disrupts adhesion (gpIb) and aggregation (gpIIbIIIa and fibrinogen) of platelets
3 steps to activate coagulation (not adhesion/aggregation)
1- activating substance (collagen/thromboplastin)
2- calcium
3-phospholipid membranes
most common inherited coag disorder
VWB disease
autosomal dominant
vwb stabilizes factor VIII
abnormal ristocetin
PTT changes but no real problems with secondary hemostasis (coagulation
ristocetin
aggregates platelets that requires vwf
if vwb disease, will not aggregate (unknown mechanisms), but if add vwf (plasma mixing) -> platelets will aggregate
vs
bernard soulier syndrome, mixing will NOT improve aggregation
cryoprecipitate
given in DIC
contains
fibrinogem , VWF, factor VIII and XIII
where is tPA?
in endothelial cells
though kallikrein can also activate plasmin (through hageman factor)
plasmin action
destroys fibrin and fibrinogen
destroys coag factors
blocks platelet aggregation
**alpha 2 antiplasmin inactivates plasmin
disorders of increased plasmin -> bleeding
urokinase in radical prostatectomy
liver cirrhosis; reduced production of alpha 2 antiplasmin
no d-dimer, normal platelets
d-dimer = split fibrin, not fibrinogen
Tx; aminocaproic acid (blocks plasmin)
lines of zahn
present in thrombus that was present before death in area of higher blood flow
characterized by lines of fibrin alternating with RBC’s
can help determine cause of death
most common inherited hypercoagulable state
factor V leiden: protein C cannot cleave it
prothrombin 2010a
point mutation in prothrombin 3’ UTR -> increased gene expression x2
if you give heparin and PTT doesn’t rise, what’s the problem?
deficiency in ATIII
2,7,9,10,11,12
dyspnea, neurologic abnormalities (AMS,seizures), and petechiae over skin, especially the chest,head,neck,axilla
fat embolus in pulm vasculature
after bone fx or orthopedic procedure
may see retinal fat globules
acute intermittent porphyria
s/s
deficiency
tx
5p’s Autosomal Dominant
port wine urine: darkens on exposure to air/light bc of oxidation
painful abdnomen
precip by drugs (p450 inducers)
psych disturbances
polyneuropathy
def; porphobilinogen deaminase (hydroxybmethylbilane synthase)
tx; glucose and heme to inhibit ALAS
alkaptonuria
s/s
deficiency
aut recessive benign
defect in homogentisic acid oxidase which tyrosine -> fumurate
s/s dark connective tissue, brown pigmented sclera, urine turns BLACK on prolonged exposure to air
may have arthralgias
binding sites
HIV
EBV
Parvovirus B19
HIV: CD4 gp120
EBV CD21 gp350 (the c3d complement receptor)
Parvo -> erythrocyte P antigen (globoside)
iron deficiency anemia findings
anemia, koilonychia, pica
koionychia is spoon shaped nails
increased FEP: free erythrocye protoporphyrin
and then all the basics
RBC should = nucleus of lymphocyte
hepcidin
sequesters iron in storage sites (enterocytes, liver, macrophages)
AND
decreases EPO
parietal cells
pink (chief cells are more blue)
assoc with pernicious anemia
proton pump
tongue in megaloblastic anemia
glossitis (poor turnover)
but remember in plummer vinson it can also have glossitis (iron deficiency, glossitis, esoph webs)
reticu count in anemia with proper nutrients and capacity
corrected >3%
but have to correct for total RBC
correct with retic% x Hct/45
*45 being a normal hct
reticular endothelial system
spleen, liver, lymph nodes
13q deletion
associated with CLL
abnormal 5 maleimide binding test
hereditary spherocytosis
autosomal dominant
LDH in hemolytic anemia
increased; duh RBC’s use a lot of that
can macrophages activate naive T cells?
no, only mature active effectors and memory t cells, and then, only if the macrophages have been induced to (prob with IFN-gamma)
gardos (calcium dependent) channel blocker
prevents erythrocyte dehydration by blocking potassium/water efflux from cells
this prevents sickling in HbSS
CO affect on cells
(carboxyhemoglobin)
- binds to hgb and prevents O2 from binding
- prevents o2 release (left shift of dissoc curve)
- inhibits complex 4 of ETC (which cyanid does too)
carbaminohemoglobin is what?
CO2 on hgb
metabisulfate
will sickle any cells with HgbS, even in trait
hemosiderinuria
occurs days after intravascular hemolysis
What are PNH patients at risk of?
10% dvlp AML
also iron deficiency anemia
stain for heinz bodies with heinz preparation
confirmatory test?
shows precipitated hgb
to do enzyme conirmatory test, must wait until after the acute episode bc all the current cells will have g6pd
cold agglutinin infectious disease causes
Infectious mononucleosus
mycoplasma pneumonia
basophilia
associated with CML
lymphocytic leukocytosis
viral
bordetella pertussis: lymphocytosis promoting factor(blocks lymphs from entering lymph node)
leukemia
>20% blasts
large, low cytoplasm, high nuclear
punched out nucleolus
tdt +
lymphoblast
ALL
t or b
MPO+
myeloblast
tdt is absent: tdt is a dna polymerase only present in immature lymphocytes
cd10
present on B cells
think B-ALL
B-ALL translocation
Age <15y/o: peripheral blood and bone marrow involved
t12 21
t9;22 less common, poor prognosis (usually that’s the translocation in CML)
tdt+, CALLA +
GOOD PROGNOSIS, responsive to therapy
down syndrome > 5y/o
acute monocytic leukemia
an AML that lacks MPO and involves gums of patient ->bleeding gums
CLL markers
CD5 and CD20 (CD 5 is usually only on t cells, but here its’ on B)
smudge cells
-> SLL if lymph node involved
may transform to large B cell lymphoma -> present with enlarging spleen or lymph node
LAP (leukocyte alkaline phosphate)
negative
positive
negative in CML
positive in leukemoid rxn
lots of platelets in blood
differential
essential thrombocythemia (a type of myeloproliferative disorder)
OR
iron deficiency anemia
acute megakaryoblastic leukemia vs myelodysplastic syndrome vs myelofibrosis vs essential thrombocythemia
myelodysplastic syndrome: precursor to AML, characterized by <20% blasts in blood
acute megakaryoblastic leukemia: an AML disorder, proliferation of megakaryoblasts. arises in down syndrom often before age of 5
myelofibrosis: myeloproliferative disorder with mostly megakaryocytes, JAK2 assoc, PDGF -> marrow fibrosis
essential thrombocythemia: a myeloprolif disorder JAK2 assoc, but pretty much a bunch of platelets
sponataneous hemarthroses in vwf disease
DOES NOT OCCUR despite increased PTT
shine delgarno
kozac sequence
shine delgarno is prokaryotic translation start sequence
kozac is sequence assoc with eukaryotic translation starting. requires purine (A or G) 3 base paires up from AUG to work well
Birbeck granule
tennis racket on EM of pt with langerhans cell histiocytosis
also have S-100
reed sternberg cell
CD15 and 30
multilobed nuclei
prominent nucleoli
a B cell, but not CD20+
hodgkins often has abundant IL5 and eosinophils
what monoclonal antibody does multiple myeloma make?
ie M spike
usually IgG
can be IgA
monoclonal IgM macroglobullnemia
B-cell lymphoma
Waldenstrom Macroglobulinemia
visual and neurologic problems: stroke, retinal bleeding
increased risk of bleeding/thrombosis
henoch schonlein purpura vs churg strauss
henoch schonlein:
IgA deposition following URI: palpable purpura, arthralgia, GI symptoms/bleeding. Self limited.
churg strauss
IgE, eosinophils, granulomas, pANCA
heart, lung kidney invovement
has asthma, sinusitis, palpable purpura, peripheral neuropathy
renal artery stenosis in young female
fibromuscular dysplasia
-> HTN
branchial cleft, arch, pouch
cleft is ectoderm
arch is mesoderm
pouch is endoderm
4 branchial pouches
ears, tonsils, bottom to top
1st pouch: endoderm of middle ear and proximal
2nd pouch: epithelial tonsils
3rd pouch: bottom parathyroids and thymus
4th pouch: superior parathyroid
1st arch
Muscles of Mastication
Maxillary/Mandibular V nerve
Maxillary artery
2nd arch
Stapedial artery
Smile with CN VII
Facial expression
3rd arch
Common Carotid
don’t Choke with CNIX
stylopharyngeus
4th/6th arch
CN X
swallow and speak
cartilage and shit of neck
developmental Clefts
1st = external auditory meatus
2,3,4 obliterated
if persistant = branchial cleft cyst in lateral neck (doesn’t move with swallowing like a thyroid cyst)
embryo
vitelline veins
cardinal veins
umbilical veins
vitelline -> portal system
cardinal veins -> systemic veins
umbilical veins -> degenerate to round ligament as part of falciform of liver
plaque formation
1) endothelial damage (toxins, HTN) -> increased permeability
2) lipid deposition
3) macrophage entry
4) platelet, endothelial, macrophage PDGF
combined PDGF (GF for fibroblasts, smooth muscle, endothelium)
5) TGF from platelets -> fibroblast growth factor
6) battle btw macrophage collagenase and collagen from smooth muscle/fibroblasts
7) plaque rupture/thrombosis via coag
TGF-alpha
TGF Beta
PDGF
Fibroblast growth factor (FGF)
VEGF
TGF-A: epithelial and fibroblast growth
TGF-B: fibroblast growth
PDGF: GF for endothelium, smooth muscle, fibroblasts
FBF: angiogenesis
VEGF angiogenesis
Fick’s principle
CO = rate of O2 consumption/ arterial O2 content - venous O2 content
laplace law for heart wall tension
wall tension: Pressure x r / (2xwallthickness)
papillary muscle rupture
anterior
posterior
anterolateral is less common bc it is supplied by LAD and circumflex
posterior is supplied by PAD (usually from RCA)
dressler syndrome
antibody to pericardium -> pericarditis
arises 1-2months after MI
most common congenital heart defect
and often why?
VSD
fetal alcohol syndrome
most common ASD
most common with down syndrome
most common = osteum secondum
down syndrome = osteum primum
PDA associated with congenital infecions
Rubella
boot shaped heart
tetralogy of fallot
transposition of the great vessels risk factor
maternal diabetes
what does glucose do to the lac operon
It decreases cAMP -> decreases promotor activity on lac operon
the regulator makes a repressor for the operator, lactose binds to and releases the reperssor
NO vs adenosine
artery vs arteriole dilation
coronary artery responsive to NO, arteriole more to adenosine
what auscultative finding correlates with severity of mitral regurge?
An S3
bc the murmer may be less with larger regurge orifice and louder with a smaller orifice, but not always and is variable
ejection click =
aortic stenosis with crescendo decrescendo systolic ejection a littl after S1
midsystolic click
mitral valve prolapse, with crescendo murmur loudest right before S2
Opening snap
mitral stenosis abrupt halt in leaflet motion. delayed rumbling late diastolic murmer (a little bit after you hearS2)
roth’s spot
white spot on retina surrounded by hemorrhage
associated with bacterial endocarditis
janeway lesions
small, painless, erythematous lesions on palms and soles.
associated with bacterial endocarditis septic emboli
Vs Osler’s are painful and raised lesions
anti-DNAse titer
used to diagnose strep pyogenes infection
also not ASO as well
aschoff bodies with anitchkow cells
Occur in rheumatic fever around myocytes of heart
Aschoff body is granuloma with giant cells
anitschkow are wavy looking activated histiocytes
Myocarditis is what kills people in acute phase of rheumatic fever
S4 in older adult
sign of less compliance, not always pathological.
In younger adult it is ALWAYS pathalogical
S3 sound
in younger adults S3 can be normal.
In older adults S3 is basically always pathological
hyperplastic arteriolosclerosis cause
malignant hypertension
onion skinning of small arteries.
Different from fibromuscular dysplasia in women
most common heart tumor?
in adults?
in kids?
Most common is metastasis
primary Adult = myxoma: tumor of mesenchyme, presents with syncope bc ball and valve obstruction
primary kid = rhabdomyoma
Hypertrophic cardiomyopathy inheritance
autosomal dominant
sarcomere protein
usually B myosin heavy chain
also assoc with friedreich’s ataxia mutation (not inherited)
loeffler syndrome
eosinophillic infiltrate with endomyocardial fibrosis. Often in setting of parasitic invasion
lymph node drainage
upper rectum
lower rectum above pectinate line
below pectinate line
upper rectum- pararectal nodes
lower rectum above pectinate line- internal iliac
below pectinate line- superficial iliac
normal vital capacity volume
normal tidal volume
normal total lung capacity
normal residual capacity
4.2 L
500mL
6L
1.2L
Dead space equation
this is the Bohr equation
V(dead space) = Tidal volume x (PaCO2 - PexpiredCO2)/PaCO2
“the volume of inspired air that does not take part in gas exchange”
**As PeCO2 approaches PaCO2 -> less dead space
what is the pressure of the airway/alveoli at FRC
pressure is 0
intrapleural pressure is negative
compliance change in emphysema/normal aging
compliance change in pulm fibrosis/pneumonia/edema
C= V/P
compliance increases with emphysema and normal aging
decrease with pulm fibrosis/pneumonia/edema
Diffusion equation for lungs (and whatever else i guesS)
Vgas diffusion = Area/thickness x diffusionconstant(P1-P2)
A decreases in emphysema (but emphysema is more a V/Qmm… increased blood flow for decreased area it encounters)
T increases in pulmonary fibrosis
Both lead to less diffusion => make O2 diffusion limited (partial shunt)
pulm HTN diagnosis
>25mmHg or >35 during excercise
alveolar gas equation
PAO2 = PIO2 - PaCO2/R
Or
PAO2 = 150 - PaCO2/0.8
A-a gradient = PAO2 - PaO2 = 10-15 normal
Cause of increased Aa: shunt, V/Qmm, diffusion
Causes of hypoxemia (
normal A-a gradient
increased A-a gradient >15
Normal A-a: high altitude, hypoventilation
Increased A-a:
V/Qmm (PE)
diffusion limitation (fibrosis/emphysema)
R/L shunt (VSD/pulm edema/asthma)
Haldane effect
Haldane has halitosis (lung effect)
In lungs, oxygenation of Hb dissociates H+ from Hb. All that bicarb that you’ve transported is split into H20 and CO2. CO2 is released.
aka shifts equilibrium toward CO2 formation
Bohr Effect
The H+ from metabolism (glycolysis mostly as well as conversion of CO2 with H20 to bicarb) shifts dissociation curve to right -> unload oxygen
Tx of methemoglobinemia
methylene blue and Vitamin C acutely
Cimetidine (H2 blocker) can be used chronically in a patient that must be on a methgbemia type drug like dapsone
normal PaO2/FiO2
300-500
less than 300 indicates gas exchange problem
hypoxia causes
ischemia (low blood flow from low cardiac output, impeded arterial flow, reduced venous drainage, shock, embolis)
hypoxemia (low inspired O2, hypoventilation, V/Q mismatch, Diffusion problem, R/L shunt)
Decreased O2 carrying capacity (CO poison, anemia)
Floppy baby with congenital anterior horn degeneration (LMN)
Werdnig Hoffman disease
Autosomal Recessive. Median death at 7months
what will hypocapnia cause?
low CO2 -> bronchoconstriction
low CO2 in the blood will cause vasodilation in pulmonary vessels
type II pneumocyte lamellar body
is the membrane bound intracellular inclusions of cell membrane material loaded with dipalmitoyl phosphatidylcholine
hyperammonemia
what diseases?
MOA of ammonia damage?
S/S
tx
diseases: liver disease or hereditary (urea cycle def)
MOA:
- excess NH4 -> depletes ketoglutarate -> inhibtion of TCA cycle
- NH4 damages lipids (encephalopathy)
- and others
S/S: tremor (asterixis), slurring speech, blurred vision, lethargy -> seizure -> coma->death
Tx; benzoate or phenylbutyrate bind amino acids -> secretion
OR
lactulose (nondigestable sugar) to acidify GI tract and trap NH4 bc bacteria ferment it and broduce lactate
Down syndrome quad screen
AFP, B-hCG, Estriol, Inhibin A
Decreased AFP
increased B-hCG
decreased inhibin A -> decreased Estriol (through lower FSH)
+increased nuchal translucency in first trimester
Edward syndrome quad screen
AFP, B-hCG, Estriol, Inhibin A
AFP decreased, B - hCGH decreased, estriol decreased, NORMAL inhibin A
trisomy 18 (election age)
clenched hands
Patau’s syndrome
quad screen
B-hCG, PAPP-A, nuchal translucency
low B-hCG, decreased PAPP, increasewd nuchal translucency
trisomy 13 (puberty)
polydactyly, holoprosencephally
Myxoma S/S, why?
S/S syncope, positional dyspnea. bc of ball and valve issues.
emboli (from easily friable materia)
mid diastolic rumble (mitral stenosis type, but the problem is the ball rolling around and causing turbulence during atrial emptying)
IL-6 production -> constitutional symptoms
radial nerve damage
fracture of spiral groove of humerous
radial nerve extends arm and provides dorsal skin innervation
C7 mostly
nasal polyp differential
repeated bouts of rhinitis
cystic fibrosis
aspirin intolerant asthma
angiofibroma vs nasopharyngeal carcinoma
angiofibroma is recurrent epistaxis, benign tumor of nasal mucosa
nasopharyngeal carcinoma: assoc with EBV, biopsy with keratin positive epithelial cells poorly differentiated on background of lymphocytes
laryngeopapilloma in adults and children
both from HPV 6,11
adults = single papilloma
children = multiple nodules
HPV high risk serotypes
why?
16,18,31, 33,45 ect
E2 normally suppresses E6/7
E6 suppresses p53
E7 suppresses Rb
E2 is not active in high risk serotypes
these are EARLY (E) expressed proteins by HPV
phases of lobar pneumonia
1) congesion
2) red hepatization: exudate, neutrophils, hemorrhage
3) gray hepatization: degredation of red cells
4) resolution:
coxiella burnetti infection
vets and farmers
atypical pneumonia caused by spores deposited by ticks on cattle and cattle placenta
Q fever (high fever, vs atypicals are often low fever)
It is a rickettsial organism but is different in that it causes pneumonia, doesnt cause rash, and doesnt need arthropod vector
mycoplasma pneumonia
most common cause atypical pneumonia
IgM cold hemolytic anemia
erythema multiforme
no cell wall
ghon focus
often just below the pleural lining -> subpleural
tb focus of fibrosis and calcification
miliary tb
widespread in lungs and diseeminated tb
when tb involves meninges, where is it classically?
base of the brain
alpha 1 antitrypsin deficiency
codominant; if homozygous -> cirrosis from accumulation in RER of liver.
more severe in lower lobe vs upper lobe in smokers
panacinar vs centriacinar in smoker
charcot leyden crystals
show up in asthma = eosinophil production of major basic protein
curschmann spirals
Curschmann’s spirals refers to a finding in the sputum of asthmatics which are spiral shaped mucus plugs from subepithelial mucous gland ducts or bronchiole
bronchiectasis
what is it?
who gets it?
s/s
Occurs from necrotizing inflammation/infection of the broncioles/bronchi -> increased dead space
Who gets it: CF, kartageners, tumor, necrotizing infection, allergic bronchopulmonary aspergillous (chronic inflammatory dmg)
s/s cough, dyspnea, foul smelling sputum (poor ciliated function, inflammatory crap, necrotic and rotting)
complication = hypoxemia with cor pumonale and scondary amyloidosis (from inflammation)
IT IS AN OBSTRUCTIVE DISEASE
allergic bronchopulmonary aspergillosis
what does it cause?
who gets it?
leads to bronchiectasis from chronic allergic inflammation with eosinophil involvement
found in pts with asthma or cystic fibrosis
caplan syndrome
pneumoconiosis + rheumatoid arthritis
the pneumoconiosis (coal, silica, asbestos) increases risk of RA
Anthracosis
Pneumoconiosis = restrictive lung disease, risk of cor pulmonale and caplan syndrome
anthracosis is coal laden macrophages
coal miners lung
affects upper lobes
silicosis
Pneumoconiosis = restrictive lung disease, risk of cor pulmonale and caplan syndrome
sandblasting and mines
upper lung (think TB)
silica disrupts phagolysosome -> increased susceptability to TB (ONLY ONE) and to getting bronchogenic carcinoma
eggshell calcifications of hilar lymph nodes
asbestosis
Pneumoconiosis = restrictive lung disease, risk of cor pulmonale and caplan syndrome
Ivory white pleural plaques and asbestos fibers (golden brown fusiform rods look like dumbells, have iron on them)
Affects lower lobes
associated with bronchogenic carcinoma > mesothelioma
“plaque of lung, plaque of pleura, cancer of lung, cancer of pleura”
asteroid body
characteristic of sarcoidosis (granuloma of lung, hilar lymph nodes, other tissues of body), it’s within the granuloma
sarcoidosis can also give uveitis, skin nodules and erythema nodosum, can look like sjogren’s. can be in any tissue
increased ACE, increased Vit D 1alpha hyrdocylase -> calcium
tx with steroids
uvea layers
iris: opening of pupil
ciliary body : controls shape of lense and aquous humor production
choroid: vascular layer of eye
hypersensitivity pneumonitis
cheese washer, composter, coffee grinder ,pigeon breeders lung, there are others
granulomatous inflammation due to hypersensitivity (high eosinophils)
presents fever, cough, dyspnea hours after exposure, resolves if taken away from exposure
chronically can produce intersitial pneumonitis
plexiform lesion
a consequence of pulmonary htn = grouping of blood vessels
Other associations; hypertrophied smooth muscle, some intersitial fibrosis, RVH
ARDS mechanism and complication on recovery
underlying theme is neutrophilic activation and free radical damage destroying type I and II pneumocytes
MANY CAUSES
end up with fluid, neutrophils, hyaline membrane, alveolar collapse
Recovery may be complicated by intersitial fibrosis bc stem cell (type II pneumocyte) has been knocked out
NRDS associated with 3 syndromes
prematurity, c section, maternal diabetes (insulin inhibits lecithin production)
attributable risk percent
ARP = 1-RR/RR
calcitriol
1,25 hydroxyvitamin D
1,25 hydroxycholecalciferol
ergocalciferol
D2 ingested from plants
cholcalciferol
Vit D3
urinary acid buffers
NH3-> NH4+
HPO4 (2-) -> H2PO4 (-)
both are used to keep the pH from dropping too much in the urine
adenocarcinoma of the lung
Peripheral mostly
most common cancer of nonsmokers and females (smoker or not)
K-ras mutation
bronchioalveolar subtype (not assoc with smoking, good prognosis, grows along alveola septa (thickening of walls)
Squamous cell carcinoma
of lung
Central
cigarettes (most common lung tumor for male smoker)
Hilar mass
cavitation
hyperCalcemia (PTHrP) production
Keratin pearls and intercellular bridges
small cell (oat) carcinoma
Central (male smokers)
undifferentiated -> VERY aggressive
may produce: ACTH, ADH, Antibodies (lambert eaton). Amplification of myc oncogens
inoperable (all the others generally are)
This is a NEUROENDOCRINE TUMOR. kulchitsky cells = small dark blue cells
chromogrannin +
large cell carcinoma
Peripheral
highly anaplastic and undifferentiated
poor prognosis
Large cell is the name given if the tumor doesnt have keratin pearls/mucinous glands/ intercellular bridges
surgical removal.
Pleomorphic giant cells
Bronchial carcinoid tumor
excellent prognosis, low metastatic rate.
Symptoms from mass effect or occasionally seratonin syndrome.
these are neuroendocrine cells chromogranin positive
coin lesion in lung differential
lung cancer
granuloma (Tb, sarcoidosis, histoplasma)
bronchial hamartoma (often calcified, with lung parenchyma AND cartilage)
bronchioalveolar subtype
bronchioalveolar subtype (not assoc with smoking, good prognosis, grows along alveola septa (thickening of walls), starts in small airways
arises from clara cells
pneumonia like consolidation
UNIQUE site of lung metastasis
adrenal gland
ziehl-neelsen
carbolfuchsin stain
(aniline dye)
this is the acid fast stain of mycobacterium and nocardia
silver stain
stains fungi, legionella, helicobacter
india ink stain
stains cryptococcus neoformans
crystal violet dye
gram stains things positive
safranin or fucshin (not carbolfuchsin)
counterstain for gram negatives
giemsa
Certain Bugs Really Try my Patience
Chlamydia, Borrelia, Rickettsiae, Trypanosomes, Plasmodium
dihydrorhodamine flow cytometry
another way other than nitroblue tetrazolium to test for NADPH oxidase deficiency
will flouresce green
CGD is X linked
cystic fibrosis inheritance
Autosomal recessive
mallory body
damaged intermediate filament inclusions in liver
these would be in hepatitis diseases
councilman bodies
an apoptotic eosinophillic swelling hepatocyte from viral hepatitis
eosin is acidic and stains basic things that are acidophillic
haematoxylin is basic and stains acid structures that are basophillic
minute ventilation
minute ventilation = tidal volume x RR
reid index
normal mucus glands <40% wall thickness
Bronchitis is >50%
obstruction is caused by lumenal narrowing because of increased thickness, and mucus production
dysplastic kidney
noninherited with renal parenchyma composed of cysts and abnormal tissue (like cartilage)
can be unilateral (most common) or bilateral
Sue to abnormal interaction btw ureteric bud and metanephric mesenchyme
medullary cystic kidney disease
inherited autosomal dominant cysts in kidney
bilateral
cysts are MEDULLARY, vs PKD wich is CORTEX AND MEDULLA
infant with worsening renal failure, htn, portal hypertension
autosomal recessive PKD with hepatic fibrosis
in general PKD causes cysts in kidneys, liver, brain (berry aneurisms)
acute interstitial nephritis
intrarenal azotemia
causes: NSAIDs, PCN, diuretics
s/s: oliguria, fever, rash, eosinophilic infiltrate (HSR)
renal pallillary necrosis
**can become chronic, but is often still reversible
horseshoe kidney
location
association
located about L3 under IMA vs normal L1/L2
associated with Turner Syndrome (XO)
predisposed to renal stenosis, uretopelvic junction(last plce to fuse), hydronephrosis
occurs 1/500 autopsies
what barrier is lost in nephrotic syndrome?
the charge barrier -> leak of proteins normally repelled
filtration fraction
GFR/RPF
RPF usuing PAH clearance
filtered load
GFR x Px
excreted load = filtered - reabsorbed or filtered + excreted
excretion rate = V x Ux
glucosuria begins at ?
Saturation at?
max absorption/min?
glucosuria begins at
160mg/dL BGL
saturated transporters (Tm)
350mg/ddL
max absorption = 200mg/min @Tm
hartnup disease
deficiency of neutral amino acid reabsorption (tryptophan)
-> pellagra (diarrhea, dementia, dermatitis)
tryptophan -> B3 with B6 help
cystic bone spaces filled with brown firbous tissue with bone pain
osteitis fibrosa cystica = stones, groans, bones
due to primary hyperparathyroidism
neurofibromatosis type I
s/s
s/s cafe au lait spots, lisch nodules (hamartoma of iris with pigmentation), neurofibroma of skin
optic glioma, pheochromocytoma,
Autosomal dominant
100% penetrant, variable expression
Mutated NF1 gene
RPF
Using PAH usually
RPF = RBF x (1-hct)
metabolic alkalosis differential
resp alkalosis (low PCO2)
-hyperventilation, salicylates (early)
Metabolic
- loop diuretics, thiazides (saline responsive)* high urine chloride
- antacid
- vomiting (saline responsive)* low urine chloride
- hyperaldosteronism (not saline responsive): high urine chloride
**ones that correct with saline bc of volume loss
increasing renal afferent resistance on GFR
initially increases until the point where reduced volume due to hydrostatic pressure -> leads to increased oncotic pressure within the capillary. NO more increase GFR
ANP
BNP
secreted by atria and ventricles respectively in response to stretch/volume overload
increase GFR without increasing Na resorption => net loss of sodium and water
shifts of potassium
digitalis
hyper/hypoosmolity
insulin
cell lysis
acidosis
B adrenergic agonist/antagonist
Dig= K out of cell (block Na/K) = hyperkalemia
K follows water = hyperosm -> hyperK
Insulin increases Na/K= K into cell = hypokalemia
Lysis - K out of cell = hyperkalemia
Acidosis: H/K exchange: hyperkalemia
B agonist: increase Na/Katpase = hypokalemia
hypercalcemia
stones(kidney), bones (pain), groans (abd pain), psych overtones(AMS, anxiety)
hypermagnesemia
decreased DTR, bradycardia, hypotension, cadiac arrest, hypocalcemia
=> hyperpolarize cell
RBC cast
glomerulonephritis, ischemia, malignant htn
wbc casts
tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
fatty casts
oval fat bodies
nephrotic syndrome
granular “muddy brown” casts
acute tubular necrosis
etiology: renal ischemia (shock, sepsis), crush injury (myoglobinuria), drugs, toxins (lead, aminoglyosides
waxy casts
advanced renal disease, chronic renal failure
hyaline casts
nonspecific. can be normal, esp in dehdrated patients
Focal segmental glomerulosclerosis
A “worse” minimal change disease
EM effacement of foot process, LM sclerosis/hyalinosis.
NO IF
Most common nephrotic syndrome of (esp.hispanics/AAmerican)
HIV, heroin, CKD, sickle cell
membranous nephropathy
LM
EM
IF
LM: diffuse thickening of CAPILLARY AND GBM
EM: spike and dome
IF granular subepithelial deposits
most common in caucasian adults
“bugs drugs tumors rheum”
idiopathic, NSAIDS, infections, SLE, tumor
minimal change disease
most common in kids
LM normal
EM foot process effacement
Loss of ONLY albumin, not globulins
Triggered often by recent infection,immunization, atopic disorders… or “immune stimulus.” Responds to corticosteroids. Associated with cytokines and Hodgkin’s lymphoma
only nephrotic syndrome with excellent response to steroids
minimal change disease
every membranous nephrotic syndrome IF
will be granular with IC deposition
spike and dome vs lumpy bumpy renal problem
spike and dome = membranous nephropathy, granular IF, subepithelial deposits
lumpy bumpy = nephritis, PSGN, subepithelial deposits
tram track appearance
membranoPROLIFERATIVE glomerulonephritis type I (subendothelial) or II (intramembranous)
C3 nephritic factor association
Type II (intramembranous) membranoproliferative glomerulonephritis
C3 nephritic factor stabilized C3 convertase –> inflammation
disease is IC deposits
decreased C3
alport syndrome
Mutation type IV collagen, x linked
-> split basement membrane (don’t confuse with membranous glomerulonephritis)
*glomerulonephritis, deafness, ocular disturbances
goodpastures syndrome
type II hypersensitivity
antibodies against GBM and alveolar BM
linear IF
**inflammation, C3 deposition, and fibrinoid necrosis occurs with fibrin leaking through into GMB and bowmen’s capsule => RPGN with cresents made up of macrophages and fibrin (not collagen!)
ceruloplasm
the copper binding agent that is often low in Wilson’s disease
Note that wilson also can’t secrete copper in bile
Aurosomal recessive chr.13q mutation ATP7B
**liver and neuropsychiatric problems
*renal tubular acidosis (proximal bicarb handling)
ceramide trihexoside accuulation
Fabry’s disease. Peripheral burning sensation of hands/feet (acroparesthesia)
angiokeratomas (dark nonblanching papules/macules btw knee and umbilicus)
cardiovascular/renal disease
hypohidrosis (diminished sweating)
Enzyme deficiency = alpha galactosidase (X-recessive)
may treat with enzyme replacement therapy
renal plasma flow stays normal over what ranges (due to autoregulation)
100-200mmHg
scarring of cortex in upper and lower poles
characteristic of cesicoureteral reflux and chronic pyelonephritis with scarring and fibrosis
thyroidization of kidney
atrophic tubules with eosinophillic proteinaceous materia looks like colloid of thyroid
SEEN IN chronic pyelonephritis/VUR
waxy casts too
calcium oxalate stone association to disease
crohns! increased resorption of oxalate
two stones that precipitate in alkalinized urine
calcium phosphate
ammonium magnesium phosphate
radioluscent kidney stone
Uric acid stone
UUUUric acid stone is radioLUUUUUcent
staghorn calculi
in adult
in kid
adult: urease +: proteus or klebsiella
kid: cystinuria (failure to resorb cysteine)
osteomalacia
when you don’t mineralize new osteoid layed down by osteoblasts
cysts in shrunken kidney risk of cancer
increased risk of renal cell carcinoma in patients with renal failure on dialysis.
s/s renal cell carcinoma
pathogenesis
triad: hematuria (most common), flank pain, palpable mass
can be associated with paraneoplastic symptoms: EPO, renin, ACTH, PTHrH
fever and weight loss
patho: VHL loss (tumor suppressor)
beckwith wiedmann syndrome
wilms tumor (most common in children)
neonatal hypoglycemia
muscular hemihypertrophy
organomegaly (esp tongue)
another syndrome is WAGR: wilms tumor, aniridia (absence of iris), genital abnormalities, mental/motor Retardation
aniridia
aniridia = absence of iris = WAGR syndrome
wilms tumor, aniridia, genital abnormalities, mental/growth Retardation
adenocarcinoma of bladder
only really occurs from urachal (allantois) remnant on the superior aspect of bladder (dome)
or bladder extrophy with exposure of bladder to outside world
often occurs with epispadius
or metaplasia from longstanding inflammation
aldosterone secretion control
1) ATII
2) hyperkalemia
3) ACTH (a little)
RPGN
3 types
1) Goodpastures with IgG and C3 deposits
2) “lumpy bumpy:” PSGN, SLE, IgA nephropathy += Henoch Schonlein purpura
3) pauci immune: wegeners,
and maybe churg strauss, microscopic polyangiitis
characterized by macrophage infiltrate, fibrin leak, fibroblast proliferation, and parietal cell proliferation
immune complex deposition activation of complement
the alternative pathway is activated, which spares C1 and C4 => low C3 but higher C1/C4
hereditary angioedema
sporatic attacks of swelling
lack c1 esterase inhibitor
so c1 esterase breaks down C4 and activates compliment
Autosomal Dominant
pyrogenic exotoxin 3
antigen implicated in PSGN from strep pyogenes
verrucae
warts
caused by HPV
condyloma acuminatum
condyloma “knuckle” refers to genitals
condyloma acuminatum = genital warts
dermatitis herpetiformis
IgA deposits at the tips of dermal papillae cause herpetic type vesicles
associated with celiac disease, from epidermal tissue transglutaminase
erythema multiforme
targets with multiple rings and dusky center
associations
HSV, mycoplasma pneumonia, drugs (sufas), lupus
steven johnson syndrome
s/s
associations
seperation of DERMAL/EPIDERMAl junction
fever, bulla formation, necrosis, sloughing of skin, HIGH MORTALITY RATE
may appear as erythema multiforme but progress
if >30% skin = toxic epidermal necrolysis
association with medication rxn (lamotragine and others)
lymph drainage
below pectinate line
above pectinate line
sigmoid colon
lower 1/3 vagina
upper 2/3 vagina
below = superficial inguinal
lower rectum above pectinate= internal iliac
sigmoid colon = colic -> IMA
lower 1/3 vagina -> superficial inguinal
upper 2/3 -> internal iliac
invasive cervical cancer death through?
will often block ureters -> renal failure
bores through anterior uterine wall -> bladder
pap smear great for scc, not adenocarcinom
quadravalent vaccine only lasts 5 yrs: still need pap smear
lichen sclerosis
thinning of epidermis,
fibrosis of underlying dermis
leukoplakia (white patch) that’s parchment like
benign but small risk of scc, post-menoposal
lichen simplex chronicus
leukoplakia that is thick/leatherlike hyperplasia of squamous epithelium
CHRONIC irritation and scratching
benign (NO INCREASED RISK SCC)
vulvar leukoplakia differential
lichen simplex chronicus
lichen sclerosis
vulvar carcinoma (HPV or lichen sclerosis related)
paget’s vs melanoma
pagets (mamillary or vulva)
PAS+, keratin+, S100-
melanoma (may be vulva)
PAS-, keratin-, S100+
**Both these are intraepithelial, random cells in the epithelium
Adenosis
persistance of columnar epithelium in vagina
happened with DES (diethylstilbestrol),
leads to clear cell adenocarcinoma of vagina
-> also related to ectopic pregnancies in DES daughter (smooth muscle problems)
thalidomide
used for morning sickness, caused limb malformation (phocomelia)
p21
cdk inhibitor upregulated by p53
HPV high risk infection
smoking and immunodeficiency
asherman syndrome
2nd amenorrha from basalis destruction
from overaggressive DnC
Asher
chronic endometritis characteristic cell
plasma cell must be present for dx
chocolate cyst
endometriosis in ovary (most common site)
accumulation of multiple cycles grow/shed
in soft tissue = gunpowder lesion
adenomyosis
presence of endometrium in myometrium
endometrioid carcinoma
arises from unopposed estrogen and endometrial hyperplasia (> 50s)
in contrast to sporatic (p53 mutation) serous papillary endometrial carcinoma arrising from atrophic endometrium ( >70y/o ==> psammoma bodies
psammoma bodies
papillary carcinoma of thyroid
meningioma
papillary serous carcinoma
mesotheliom
multiple defined white whorly masses
leiomyoma = fibroids
premenopausal (usually asymptomatic but may lead to bleeding)
vs leiomyosarcoma: single, often hemorrhage/necrosis, postmenopausal… ARISES DENOVO. NOT FROM Leiomyoma’s
ovarian follicle
PCOS
LH:FSH
LH:FSH >2
3:1 = diagnostic
lots of LH, less FSH
high androgen (theca cells)
high estrogen (fat aromatization)
estrogen feedback inhibits LH & FSH
increased AFP
schiller duval bodies (resemble glomeruli)
germ cell tumor
yolk sac tumor
endodermal sinus tumor
increased hCG
increased LDH
associated with turner syndrome
dysgerminoma (ovarian germ cell tumor)
equivalent to male seminoma
increased hCG
early hematogenous spread
NO chorionic villi
choriocarcinoma, malignancy of trophoblastic tissue
90% of germ cell tumors
mature and immature
teratoma: females generally benign
mature = teeth/hair ect = mostly benign
immature: atypical cells, malignant
struma ovarii
a teratoma with functional thyroid tissue -> hyperthyroidism
normal histology
endometrium
fallopian tube
ovary
endocervix
endometrium - endometrial cells
fallopian - serous columnar
ovary- cuboidal from coelomic epithelium
endocervix- mucinous columnar
**surface epithelial tumors are most common (more than germ cell)
endometial tumor is MOST COMMON
benign teratoma in women
mature teratoma has to have ALL mature tissue.
can have somatic malignancy within mature tissue. most commonly squamous cell
immature teratoma (such as containing neuroectoderm is malignant)
cystic teratoma is most common germ cell tumor
classic BRCA1 ovarian tumor
SEROUS cystadenocarcinoma
**also at risk for breast cancer and fallopian tube
brenner tumor
contains urothelium
benign and bilateral
most common germ cell tumor women
cystic teratoma
dysgerminoma is most common malignant germ cell tumor
reinke crystals
sertoli-leydig cell tumor: androgen production
reinke crystals in leydig cells
meig’s syndrome
ovarian fibromas, pleural effusions, ascites
intraperitoneal accumulation of mucous (jelly belly)
pseudomyxoma peritonea
can be from ovarian or appendiceal tumor, likely a metastasis from appendix
placenta accreta
placental invasion into myometrium -> diffiulty delivering placenta after birth -> hysterextomy
choriocarcinoma
gestational vs sporatic
response to chemo
gestational responds well (will have chorionic villi): will melt away
sporatic does not (no chorionic villi) will be in ovary (germ cell tumor)
urogenital folds make?
male urethra/ventral shaft
female labia minora
labioscrotal swelling make?
scrotum or labia majora
prostate comes from what ?
urogenital sinus (also makes the male glands of cowper
and
female bartholin/skene glands
genital tubercle makes what?
male: glans penis, corpus cavernosum (fill with blood baby) and spongiosum(around urethra)
female: glans clitoris and vestibular bulbs (erectile tissue of vestibule)
vessels in suspensory ligament
suspensory ligaments of the ovaries
ovarian vessels (ligate when ovarian removal)
also contains lymphatics and nerves
vessels in cardinal ligament (transverse ligament)
Uterin vessels
care for ureter injury (goes under uterine vessels)
mesosalpinx
broad ligament covering everything
round ligament of uterus
contains artery of sampson -> travels through inguinal canal
estriol is a marker of what?
it increases 1000fold in pregnancy, indicates fetal well being
produced by the placenta
best test for menopause
way increased FSH
moderately (and later) increase in LH
increased GnRH
how does menopause lead to osteoporosis
estrogen inhibits osteoclasts. when low -> osteoclast haven
quellung test
positive capsule swells when specific anticapsular antisera is added along with methylene blue to make it swell
halo appears
the SHiNE SKiS are positive
red on mucicarmine stain
cryptococcus neoformans
cord factor = mycoside
correlates with virulence of mycobacterium tuberculosis
If lacking they don’t cause disease
appearance of serpentine cords on growth medium is diagnostic
sulfatides from mycobacteria
inhibit phagosome fusion with lysosomes in macrophages
virulence feature of mycobacterium tb
what bacteria have IgA protease?
H. Flu, Neisseria meningitis, Strep pneumonia
where do DNA viruses replicate?
exception?
nucleus (except pox); they need the cells polymerases (except pox and HBV.. and HBV is still in nucleus)
Where do RNA viruses replicate?
exception?
cytoplasm (use of ribosomes)
-except influenze and retroviruses(bc it integrates, duh)
where does herpes virus get it’s unique phospholipid envelope?
The nucleus of the cell
(all the herpes viruses)
naked viruses
Give a PAPP and CPR to naked Hepe
PAPP CPR Hepe
Parvo
adeno
polyoma (JC)
papilloma
RNA: calici (noro), picorno, reo(rota), hepe (HEV)
only dsRNA
reovirus = rotavirus
linear dsRNA
paramyxovidiridae
enveloped, ss -, nonsegmented
parainfluenza - croup,
rsv- bronchiolitis (no H or N)
measles, mumps
klebsiella
enteric
non-motile gram negative urease positive, lactose fermenting, catalase negative
nosocomial sepsis
BAD lobar pnemonia (of sick and alcoholics)
vaccines
attenuated
inactivated
adjuvant
conjugant
attenuated: live; small yellow chickens, MMR sabin, IN influenza + typhoid and BCGtb
inactivated: heat/chemical killed
adjuvant: PAMP added to increase immune system response
conjugate: covalent link of protein to promote IgG class switch
23 valent vs 13 valent pneumococcal vaccine
23 valent( PPSV23) is only polysaccharide
only B cell IgM response
13 valent is conjugated to diptheria => IgG response/memory
**neisseria meningitis and H flu also have polysaccharide (not conjugated) vaccines
where is the site of most lipid absorption?
jejunum
