Flashcards in test #34 4.22 Deck (113)
3 determinants of malignant potential of an adenomatous polyp
1. size (> 4cm have 40% risk of malignancy
2. histology: villous more prone to be malignant than tubular
3. degree of dysplasia
bell curve: what %age of population falls in 1 standard deviation? 2? 3?
1 standard deviation = 68%
2: 95% (2.5 below, 2.5 above)
where is CCK made
I cells of duodenum and jejuneum.
increase pancreatic enzyme secretion and gallbladder contraction
decrease gastric emptying
where is vasoactive intestinal peptide made?
pancreas & parasympathetic ganglia
stimulates intestinal water secretion, counteracts gastrin, promotes bicarb secretion for pancreas
classic galactosemia is inherited as..
lack galactose-1-phosphate uridyltransferase
3 steps of deglutition (swallowing)
1. oral: voluntary
food bolus collected at back of mouth, lifted upwards to posterior wall of pharynx
2. pharyngeal, involuntary
pharyngeal muscle contractions propel food bolus to esophagus
3. esophageal phase
- enters & stretches walls. peristalsis begins above site of distention and moves food down.
difficulty swallowing "felt at the throat"
cricopharyngeal muscle dysfunction. diminished relaxation of pharyngeal muscles during swallowing.
how does cricopharyngeal muscle dysfunction lead to zenker diverticulum?
diminshed relaxation of pharyngeal muscles during swallowing demands more force to move food bolus down.
more intense contraction of pharyngeal muscles --> increase oropharyngeal intraluminal pressure.
eventually, pharyngeal mucosa herniate through muscle fibers in zone of weakness (posterior hypopharynx).
only mucosa --> FALSE / pulsion (as opposed to all walls of organ --> true / traction)\
can lead to aspiration of food -- bc food stuck in diverticulum high up
can be palpated as lateral neck mass
mediastinal lymphadenitis (TB, fungal) can lead to what esophagus problem
scarring & traction --> true diverticula, mid portion of esophagus
hemoglobin synthesis in fetus (4)
yolk sac, liver, spleen, bone marrow.
liver begins HbF 10-12 wks of gestation --> spleen --> bone marrow.
when does HbF transition to HgA?
HbF (a2y2) --> HbA (a2b2) during first 6 months.
normal variant of human hemoglobin. 2-5% of adult hemoglobin
hemoglobin gower (z2e2)
earliest hemoglobin in fetus.
synthesized in yolk sac, replaced by hemoglobin portland --> hemoglobin gower 2 --> hemoglobin F (10-12 wks)
no alpha made.
high affinity for oxygen, never gives it up, get hydrops fetalis
muscles that attach to clavicle
-pec major (inferomedial)
-sternocleidomastoid (superior medial aspect)
where does sternocleidomastoid articulate
manubrium, medial clavicle, and mastoid
rhomboid muscle articulation
vertebral bodies to medial border of scapula
pec minor articultation
3-4th rib, insert on coracoid process
1-8th rib, insert on medial border of scapula
originates on 1st rib, inserts on inferolateral aspect of clavicle
floor of anatomical snuff box
scaphoid and trapezium
benign, slowly progressive fibroproliferative disease of palmar fascia.
as scarring progresses, nodules form on palmar fascia, fingers gradually loose flexibility, eventually resulting in CONTRACTURE that draws fingers in FLEXION
celiac comes out at what vertebral level? SMA & renal artery? IMA?
SMA & renal: L1
transverse duodenum lies at what vertebral level?
L3, between aorta and SMA (can be compressed)
ligament of treitz
suspensory ligament of duodenum (connect right crus of diaphragm to duodenal jejunal flexure)
what can be compressed when mesenteric fat is lost between SMA and aorta?
left renal vein & transverse duodenum
also occurs w/ pronounced lordosis, or surgical correction of scoliosis
filtration fraction =
usu = .2 (1/5th of RPF is filtered)
how much of renal plasma flow is filtered
how does RPF, GFR, and FF change in SEVERE dehydration
RPF falls a lot
GFR falls less (efferent arteriole constricts to maintain some GFR)
FF goes UP
end up compensating to filter a larger amount of the little incoming renal plasma
what forms erythema migrans of ixodes bite? how does it look
erythematous macule that enlarges w/ advancing erythematous borders as BACTERIA MIGRATE slowly through skin outward from inoculation site
classically has central clearing, but NOT ALWAYS!
caused by mycobacterium scrofulaceum.
found in and around environmental water sources.
characterized by lymphadenitis (usu cervical) in kids
leptospirosis & weil's disease
exposure to animal urine.
no cutaneous manifestation
usu asymptomatic, self limited
progression to weil's:
jaundice, renal dysfunction, thrombocytopenia, bleeding
fructose and glucose
galactose and glucose
glucose and glucose
which two dissacharides are in breast milk
maltose and galactose
what is starch made of..
major carbohydrate in plants
only glucose molecules:
what is cellulose made of..
linear polysach of glucose, mainly present in cell wall of plants.
not digested by GI enzymes.
composes one form of non-soluble dietary fiber --> bulk of fecal matter.
aldolase B deficiency
hypoglycemia after fructose ingestion due to phosphate trapping by fructose-6-phosphate.
essential fructosuria & galactokinase deficiency are..
fructose intolerance & classic galactosemia are..
violaceous discoloration of upper eyelids & raised violaceous scaling eruption on kuckles
heliotrope rash & grotton's sign.
(w/ proximal muscle weakness)
usu elevated cpk
2 main diff between pemphigus vulgaris & bullous pemphigoid
pemphigus vulgaris 1. affects oral mucosa 2. ruptures easily
mutation in ALS?
copper zinc superoxide dismutase (SOD1)
rx for ALS
riluzole, decreases glutamate release
macroscopic changes in ALS
thin anterior roots, atrophy of precentral gyrus
PKU that does not alleviate w. phenylalanine restriction / tyrosine supplementation
dihydrobiopterin reductase deficiency.
needed for both
1. phenylalanine -> tyrosine
(via phenylalanine hydroxylase)
2. tyrosine -> DOPA
(via tyrosine hydroxylase)
"atypical" or "malignant" phenylketonuria
problems w/ dihydropterin reductase deficiency
inability to convert phenylalanine -> tyrosine, tyrosine -> dopa.
tetrahydrobiopterin is impt for tyrosine, DOPA, 5-HT and NO synthesis.
present w/ high prolactin bc can't make dopamine in tuberoinfundibular system
deficiency in homogentisic acid
(break down homogentistic acid, which is a toxic tyrosine byproduct, harmful to bone & cartilage)
convert NE -> E
need SAM (s-adenosyl-methionine) as cofactor --> s-adenosylhomocysteine
how does WPW present (2)
accessory pathway bypassing bundle of kent
(1) pre-excitation: first impulse through accessory path, then shortly thereafter via AV node.
(2) allows for recurrent, temporary tachyarrhythmias due to atrioventricular re-entry circuit involving AV node & accessory path
WPW pre-excitation on EKG
shortened PR interval ( makes for wider QRS
delta wave goes away in re-entrant tachyarrhythmia bc no longer pre-excitation
what can trigger malignant hyperthermia?
inhaled anesthetics (esp halothane)
why does malignant hyperthermia happen?
skeletal muscles hypersensitive to inhalation anesthetics (esp halothane) & succinylcholine.
defect on ryanodine receptors of sarcoplasmic reticulum. release too much Ca2+, stimulating ATP-dependent reuptake of Ca2+ into SR. excessive ATP consumption --> generate lots of heat
loss of ATP + heat --> muscle damage --> rhabdomyolysis --> release K+, myoglobin, creatinine kinase
dantrolene: prevent Ca2+ release from ryanodine receptors
phentolamine & phenoxybenzamine
which drug causes increased triglyceride levels as side effect
cholestyramine (bile acid resins)
bile acid production increases, but so does hepatic production of TG and VLDL.
cholestyramine side effects (3)
bile acid resin:
- GI upset
- impaired nutrient absorption & drugs
- elevated triglycerides
- also increase cholesterol content of bile --> stones
niacin on triglycerides
reduces serum TGs
also decreases VLDL conversion to LDL (less LDL)
B6-deficiency related anemia
needed for hemoglobin synthesis. can cause hypochromic microcytic pyridoxine responsive sideroblastic anemia
segmental granulomatous large vessel arteritis
when can hepatitis D virus cause infection?
when encapsulated with HBsAg.
hepatitis D is replication defective RNA.
- acute coinfection w/ hep B (hep B established to provide HBsAg) or superinfection of a chronic HBV carrier
common extrahepatic disease in chronic hep C infection (2)
(1) membranous glomerulonephropathy
(2) mixed cryoglobulinemia
2 forms of chronic gastritis?
type A: autoimmune (fundus/body)
type B: h. pylori bacteria (antrum)
disruption of mucosal barrier
(stress, NSAID, alcohol, uremia, burns (curling ulcer), brain injury (cushing ulcer), chemo, shock..
autoimmune type A chronic gastritis
autoantibodies to parietal cells / intrinsic factor, results in
2. anemia (no b12)
also increased risk of gastric adenocarcinoma
type B gastritis is associated w/ increased risk of
Maltoma & gastric adenocarcinoma
what's one way acute gastritis can be differentiated from chronic gastritis?
acute: neutrophil predominant
chronic: lymphocyte & plasma cell
what kind of reaction does a foreign body cause? how does this happen.
takes several days/wks. antigen that cannot be eradicated by usu mechanism
activated Th1 CD4+ cells secrete IFN-gamma, activates macrophages. macrophage secrete THF-alpha, which forms granuloma.
aggressive, ulcerating squamous cell carcinoma.
presents in an area of previously traumatized, chronically inflammed, or scarred skin.
malignant transformation occurs long after initial trauma, usu > 10yrs later.
time frame of wound healing
1. inflammatory (immediate):
- clot & clean
2. proliferative (2-3 d later):
- granulation & contrature
3. remodeling (1wk later):
- type III -> type I
which class III antiarrhythmics is not associated w/ Tdp
amiodarone (silver lining!)
which class I antiarrhythmics predispose to Tdp?
class IA (have class III properties too)
adenosine on EKG
expect it to prolong PR, but cleared so quickly (t1/2: <10seconds)
digoxin 2 fxn
1. increase vagal tone of AV: antiarrhythmic
2. increase contractility
characterestics of glioblastoma multiforme
necrosis and vascular proliferation
prognosis of glioblastoma
highly malignant. will die within 1-2 years
cyst formation & rare mitosis in brain suggests?
colloid cyst -- pathologically benign tumor, usu in 3rd ventricle. can cause lethal obstructive hydrocephalus
reticulin deposits and chronic inflammatory infiltrate in brain suggests?
variant of astrocytoma, can progress to GBM
what causes congenital pyloric stenosis? acquired?
congenital: smooth muscle hypertrophy of pyloric muscularis mucosae
acquired: associated w/ gastritis, peptic ulcer in pylorus, neoplasm
transverse processes & lateral aspect of T12 through L5 vertebrae --> down across pelvic brim anterior to hip joint capsule & deep to inguinal ligament to insert into the lesser trochanter (shared tendon w/ iliacus)
psoas abscess forms from..
direct spread of infection from adjacent structure (vertebral bodies, appendix, hip joint)
or hematogenous / lymphatic seeding from distant site
movement that causes psoas muscle to be stretched/extended.
associated w/ appendicitis
coarses posterior to psoas muscle. connects 12th rib & upper lumbar vertebra to iliac crest --> extension & lateral flexion of vertebral column
rx for warfarin reversal
fresh frozen plasma
(vit K would help, but takes time bc need to resynthesize clotting factors)
antifibrinolytic agent -- inhibit plasminogen activators
heparin reversal, binds/inactivates heparin
what's contained in cryoprecipitate vs. fresh frozen plasma
fresh frozen plasma: all coagulation factors
cryoprecipitate: only cold soluble proteins: factor VIII, fibrinogen, vWF, and vitronectin
serum vs plasma
serum = plasma w/o clotting factor
desmopressin in heme
increases factor VIII activity (in pts w/ hemophilia A & vWD)
most common cause of overdose related deaths?
prescription opiod pain relievers
(exceeds heroin + cocaine combined)
due to increase in prescribing w/o adequate drug monitoring.
potency of inhaled anesthetic depends on..
inversely related to minimal alveolar concentration
when inhaled anesthetic administered at constant rate over prolonged period, its partial pressure in brain = partial pressure in other compartments.
since concentration in brain directly proportion to partial pressure, it is a measure of potency
intrinsic property of anesthetic, does not depend on surgery, duration, sex/height/weight.
anesthetics arteriovenous concentration gradient is a measure of
measure of solubility in tissue.
high = increased time for blood to be saturated = slow time of onset
blood/gas partition coefficient is a measure of
solubility in blood --
high blood/gas partition = very soluble in blood = slower onset of action
steepness of arterial tension curve of inhaled anesthetic measures..
depends on solubility of anesthetic in blood.
partial pressure rises steeply when less soluble
2 fxn of von willebrand factor
1. protect factor VIII from degradation
2. connects collagen to platelets (via GpIb)
what activates protein C
von Gierke disease
type 1 glycogen storage disease
deficiency glycogen phosphorylase
cannot do: glycogen -> glucose 1-phosphate
via glycogen phosphorylase, breaks alpha (1,4) glucosidase link
severe fasting hypoglycemia, increased glycogen in liver, increased blood lactate.
NOTE: in muscle
[glycogen-> glucose 1-phosphate]
btw: glucose 1-phosphate --> glucose 6-phosphate (via phosphoglucomutase) and then...
glucose 6-phosphate -> glucose
via glucose phosphorylase
synthesis of glycogen
glucose 6-phosphate --> glucose 1-phosphate
glucose 1-phosphate --> UDP glucose
via: UDP-glucose pyrophosphorylase
UDP-glucose -> glycogen
via: glycogen synthase
(stimulated by insulin, inhibited by PKA)
branches made via branching enzyme
type 2 glycogen storage disease
deficient in lysosomal alpha 1,4-glucosidase (aka acid maltase)
[limited amount in lysosomes]
trashes the pump --> cardiomyopathy, liver, and muscle problems
type 3 glycogen storage disease
alpha 1,6 glucosidase
milder than type 1, normal blood lactate
type 5 glycogen storage disease
can't use glycogen in muscle
cannot do: glycogen -> glucose 1-phosphate
[note, in muscle glucose 1-phosphate -> glucose 6-phosphate via phosphoglucomutase]
glucose 6-phosphate is used as is! no glucose phosphorylase, bc don't want to release glucose into circulation
symptoms: decreased exercise tolerance, myoglobinuria, muscle pain w/ activity
relieved w/ exogenous glucose
breakdown of glycogen requires 4 enzymes (in liver).. [3 in muscle]
1. glycogen phosphorylase
glycogen -> glucose 1-phosphate
2. debranching enzyme
glycogen -> glucose 6-phosphate
glucose 1-phosphate -> glucose 6-phosphate
MUSCLE just uses glucose 6-phosphate
4. glucose 6-phosphatase (only in liver)
glucose 6-phosphate -> glucose
when there are 4 residues on a glycogen branch (glycogen phosphorylase already did its thing)
first: 4-alpha-D-glucanotransferase takes off 3 glucose 1-phosphates
second: alpha 1,6-glucosidase takes off 1 glucose 1-phosphate
how does HBV allow hepatitis D virus?
hep D = 35nm double-shelled particle.
HDAg + short ssRNA
needs to be COATED w/ HBsAg.
acute coinfection or superinfection of chronic HBV carrier.
only w/ HBsAg can it: penetrate hepatocyte, survive in cell, replicate viral RNA, and translate genome
constitutional symptoms, mid-diastolic rumbling murmur at apex, positional dyspnea, large pedunculated mass in left atrium suggests..
make lots of IL-6, constitutional symptoms
most common primary cardiac neoplasm.
approx 80% arise in left atrium
histology of atrial myxoma
scattered cells within a mucopolysaccharide stroma, abnormal blood vessels (lots of VEGF), and hemorrhaging (hemosiderin depositions)
drug-induced acute interstitial nephritis characterized by..
eosinophilia [serum & urine]
drug acts as hapten, hypersensitivity
down syndrome, ataxia-teleangiectasia, and NF-1 associated w. increased risk of..
cleavage during 0-4 days (from zygote to morula)
cleavage during 4-8 days (from morula to blastocoele)
cleavage during 8-12 days
(from blastocoele to embryonic disc)
cleavage from 13+ days
does NOT EXIST
chorion = outer cover