test #12 3.31 Flashcards
epithelium of ovary
simple cuboidal. also known as germinal epithelium. transitions to peritoneum at broad ligament of uterus
epithelium of fallopian tube
simple columnar: ciliated cells, help transport egg/embryo. peg cells: secrete nutrients
epithelium of uterus
simple (psuedostratified) columnar. contains tubular glands. divided into fxnal and basal layers
epithlium of cervix
endo: simple columnar. ecto: stratified squamous. contains cervical glands.
epithelium of vagina
stratified squamous. non keratinized. contains glycogen
acute hemolytic transfusion reaction
chills, shortness of breath, fever, hypotension, DIC, renal failure, hemoglobinuria. think: blood transfusion after MVA: ABO incompatibility: type II hypersensitivity Ab mediated –> activate COMPLEMENT
TNF-alpha released in response to..
bacterial endotoxin– SHOCK
kartagener inheritence and presentation
autosomal recessive: immotile cilia (microtubular defect): male infertility, recurrent sinusitis, bronchiectasis. situs inversus.
activation of trypsinogen to trypsin
trypsinogen secreted by pancreas –> enterokinase in duodenal lumen –> trypsin
2 protective mechanisms to limit amount of trypsinogen that becomes prematurely activated in pancreas
(1) SPINK1: serine peptidase inhibitor Kazal type I: secreted by pancreatic acinar cells: fxns as trypsin inhibitor. (2) trypsin cleaves other trypsin molecules (its own inhibitor)
hereditary pancreatitis
rare disorder: mutations in trypsinogen or SPINK1 genes. most common mutation: trypsinogen that is not susceptible to inactivating cleavage by trypsin.
helicobacter pylori is commonly associated w/
(1) peptic ulcer disease (2) gastric adenocarcinoma
treatment of choice for gestational diabetes?
INSULIN. diet and activity modifications alone are efficacious too.
why are oral hypoglycemic mediations avoided in gestational diabetes?
risk of fetal insulinemia and hypoglycemia
most effective motion sickness prevention meds work on…
(1) antimuscarinics or (2) antihistamines w/ antimuscarinic action
pathophysiology of motion sickness? rx?
muscarinic M1 and histaminic H1 pathways stimulated –> nausea and vomiting. first-generation antihistaminic drugs (meclizine and dimenhydrinate) scopolamine –> only anti muscarinic, also effective
H1 receptor blockers fxn by?
increasing proportion of inactive H1 receptors: REVERSE BLOCKADE utimate decreases the activity of H1 receptor
patients w/ amino acids in urine may have…
disorders of amino acid resoprtion: fanconi or hartnup
adult vs. infant botulism
ADULT botulism: consumed preformed TOXIN.
INFANT: consume c. botulinum SPORE
which cells directly mediate the vascular response to endothelial and intimal injury (leading to intimal hyperplasia // fibrosis)
reactive smooth muscle cells! injured endothelial cells secrete factors, (PDGF, FGF, endothelin-1) –> promote SMC migration, proliferation from media to intima & produce new connective tissue. macrophages help.
von Hippel-Lindau
rare, autosomal dominant condition characterized by (1) presence of capillary hemangioblastomas in retina/cerebellum, (2) congenital cysts/neoplasms in kidney, liver, pancreas. increased risk for (3) renal cell carcinoma (can be bilateral)
von Reckinghausen’s disease
NF1 (chromosome 12, 12 letters) inherited PERIPHERAL nervous system tumor. neurofibromas, optic nerve gliomas, lisch nodules (pigmented nodules of iris), cafe-au-lait (hyperpigmented cutaneous macules)
NF2
autosomal dominant nervous system tumor. bilateral cranial n VIII schwannomas & mult meningiomas
Sturge Weber (encephalotrigeminal angiomatosis)
rare congenital neurocutaneous disorder: cutaneous facial angiomas (port-wine stain) and leptomeningieal angiomas. skin: usu V1 or V2. mental retardation, seizures, hemiplegia, skull radiopacities: tram-track calcifications
tuberous sclerosis
cortical and subependymal HAMARTOMAS. cutaneous angiofibromas (adenoma sebaceum), visceral cysts (i.e. kidney, liver, pancreatic), renal angiomyolipoma and cardiac rhabdomyoma. SZ. other hamartomas too.
osler-weber-rendu
hereditary hemorrhagic telangiectasia. autosomal DOMINANT. rupture –> epistaxis, GI bleed, hematuria. cysts not common
two common scenarios where antibiotics are prescribed but not needed
(1) VIRAL URI (2) acute otitis media (which resolves spontaneously often)
cutaneous lateral aspect of leg? medial aspect of leg
lateral: common peroneal (L4-S2). medial: femoral (L2-L4)
formula for number needed to treat
1/ARR. ARR (event rate in placebo - event rate in treatment)
rare disease assumption
approximate odds ratio and relative risk when studying rare diseases
how does mannitol reduce cerebral edema but increase pulmonary edema?
retain plasma // tubular fluid osmolality – extract water from interstitial space into vascular space // tubular lumen. brain: redistribute of water from tissue into plasma. but this causes increase hydrostatic pressure in vasculature –> can cause pulmonary edema
mechanism of morphine
mu opiod g-protein coupled receptor –> one pathway: (1) increased K+ conductance (efflux) –> hyperpolarize and decrease pain transmission. ALSO, inhibit adenylyl cyclase, (2) inhibit Ca2++ conductance (less NTX release
silent GERD presentation
no heartburn; dysphagia, nocturnal cough, sore throat
histological findings in GERD (3)
basal zone hyperplasia, elongation of laina propria papillae, inflammatory cells (eosinophils, neutrophils, lymphocytes)
pill-induced esophagitis seen w/ (3)
(1) tetracyclines (2) KCl (3) bisphosphonates
most common cause of infectious esophagitis
candida albicans. herpes simplex is other.
achalasia
(1) impaired relaxation of LES (2) impaired peristalasis of esophagus
absent esophageal peristaltic movt in (2)
achalasia and scleroderma
posterior & anterior urethra
posterior: prostatic segment & membranous segment (above bulb of penis.
anterior: bulbous segment & penile segment (within bulb and remainder of corpus spongiosum)
which part of urethra is most susceptible to damage from trauma?
membranous segment of posterior urethra. unsupported & weak.
falling on crossbar of bicycle or top of a fence, ‘straddle injury’ in male?
crushing injury to bulbous urethral segment
cuneate vs. lingual gyrus of striate cortex
cuneate – superior lobe, inferior visual field. lingual – inferior lobe, superior visual field.
Wallenberg syndrome
contralateral loss of pain and temp. ipsilateral loss of CN V, VIII, IX, X, XI, and horner’s syndrome
rightward shift of venous return curve
increased MAP
acute and chronic arteriovenous fistula
acute: decreased TPR (increased cardiac output, increased venous return). overtime: sympathetics and kidney compensates for fistula by increased CO, vascular tone, and circulating blood volume. this results in increased cardiac function curve, and increased mean systemic pressure (rightward shift of venous return curve)
acute GI bleed (on venous return curve)
decreased MAP: leftward shift
phenylephrine on cardiac output / venous return curve
increased sympathetic tone (vasoconstriction) decrease both CO and venous return
MI on cardiac output / venous return curve
isolated decrease in CO, no change in blood volume / venous return
anaphylaxis on cardiac output / venous return curve
widespread venous / arteriolar dilation. increased capillary permeability – 3rd spacing on fliud. DROP in venous return
GH stimulates linear growth of long bones via..
IGF-1 secreted from LIVER
Laron dwarfism
decreased linear growth due to defective growth hormone receptors –> serum levels of growth hormone high w/ low levels of circulating IGF-1
mechanism underlying hypoxic pulmonary vasoconstrictoin
direct hypoxemia-induced increase in smooth muscle cytosolic Ca2++, w/ Ca2++ sensitization factor
when does hypoxemia cause arteriolar dilation in cerebral circulation
PaO2 < 50mmHg
length constant // space constant
how far along an axon an electrical impulse can propagate. specifically: distance at which originating potential decreases to 37% of its original amplitude. decreased w/ demyelination.
time constant
time it takes for a change in membrane potential to achieve 63% of the new value. related to membrane capacitance. myelination DECREASES membrane capacitance (decreases time constant). low time constant, quicker change in membrane potential, increase axonal conduction speed.
PRPP synthetase
enzyme responsible for synthesis of activated ribose, which is needed for de novo purine/pyrimidine synthesis. increased purine production –> hyperuricemia –>
glucose-6-phosphatase deficiency
von Gierke disease
acid maltase deficiency
Pompe disease
negatively birefringent crystal under polarized light
monosodium urate crystals: gout
cell responsible for intense inflammatory response in acute gout?
neutropils – phagocytose monosodium urate crystals.
colchicine
acute management of gouty arthritis: reduce inflammatory response by interfering w/ adhesion molecules and microtubules (neutrophil chemotaxis) and decreasing tyrosine phosphorylation in response to monosodium urate crystals (decreased neutrophil activation)
starvation for 16-24 hours causes..
peripheral tissue shift to rely on lipid-derived fuels (free fatty acis & ketones) instead of glucose for energy.
beta oxidation
within mitochondria of the liver. yields significantly more energy per carbon atom than carbohydrate.
each round of fatty acid beta-oxidation produces
1 NADH, 1 FADH2, 1 acetyl-CoA. acetyl-CoA –> TCA cycle: 3 NADH, 1 FADH, 1 GTP. rapid beta-oxidation overwhelms TCA, shunt to ketone production.
failure to produce ketone bodies when fasting suggests
impaired beta oxidation. most commonly due to defects in first enzyme in pathway: acyl-CoA dehydrogenase
acetyl-CoA carboxylase
first step in fatty acid synthesis.
glycogen phosphorylase
mediates glycogenolysis. removes single glucose residues form alpha-1,4-linkages within glycogen molecules.
deficiency in muscle glycogen phosphorylase
muscle cramping and fatigue w/ exercise, McArdle’s glycogen storage disease type V
intracellular breakdown of glycogen
most: by cytosolic phosphorylase. some by lysosomal enzyme alpha-1,4-glucosidase (acid maltase).
pompe disease (glycogen storage disease II
deficiency of alpha-1,4-glucosidase (lyososmal enzyme) glycogen accumulation in lyososmes. cardiomegaly, hypotonia, occasional hypoglycemia, early demise
most common predisposing factor to native valve bacterial endocarditis
mitral valve prolapse: platelet and fibrin deposition spontaneously occur, causing nonbacterial thrombotic endocarditis. then, colonized by microorganisms. rheumatic valvular disease is a potential, but less common cause of NVBE
degenerative mitral annual calcification
can result in mitral regurg due to loss of sphincteric action of annulus. can predispose to bacterial endocarditis. most common in females over 60 with prior history of myxomatous degeneration of valve and in pts w/ chronically elevated left ventricular pressure
when in gestation does differentiation and development of external genitalia occur
8-15 wks.
fate of urogenital folds in female vs. male
female: urogenital folds do NOT fuse; labia minora. male: urogenital folds fuse to form ventral aspect of penis and penile raphe.
genital tubercle goes on to become what in female vs. male?
clitoris or penis
bifid scrotum occurs when..
malunion of labioscrotal folds.
de Quervain’s thyroiditis also known as..
subacute granulomatous thyroiditis. mixed cellular infiltrate w/ occasional multinucleate giant cells.
thyrotoxicosis in subacute granulomatous thyroiditis caused by..
released of STORED thyroid hormones secondary to inflammation. NOT excess production (iodine uptake is decreased). followed by hypothyroid state for few months
recent viral illness, increased ESR, markedly reduced radioactive iodine intake, thyrotoxicosis, tender thyroid
de Quervain (subacute granulomatous thyroiditis)
ground-glass nucleus w/ intranuclear grooving (orphan annie eyes)
papillary thyroid cancer
chronic lymphocytic thyroiditis
hashimoto’s thyroiditis: formation of germinal centers – diffuse mononuclear infiltration. normal ESR, nontender thyroid, high antithyroid peroxidase (anti-TPO antibody)
anti-TPO
hashimoto’s thyroiditis
phenytoin, carbamazepine, and valproic acid…
inhibit neuronal high-frequency firing by reducing ability of voltage-gated Na+ channels from recovering from inactivation.
differential media vs. selective media
differential: differeniate organsims based on metabolic / biochemical properties. selective: kills all else
thayer-martin VCN
Neisseria specific. vancomycin kills gram positives. colistin kills gram negs other than neisseria. nystatin kills fungi.
side effect of opiods
BILIARY COLIC. contraction of smooth muscles in sphincter of Oddi –> increased pressure in bile duct & gallbladder.
intestinal malrotation
cecum found in right upper quadrant, fixed w/ fibrous bands (Ladd’s bands) to second aspect of duodenum. entire midgut fixed to SMA. INTESTINAL obstruction –> due to adhesive bands compressing duodenum –> bilious vomiting. can have midgut volvulus – twisting of gut around SMA, decreasing perfusion –> intestinal gangrene and performation
normal rotation in GI development
6th wk: midgut herniates through umbilical ring. returns at 10th wk, completing 270 degree counterclockwise rotation around SMA. allows for proper placement and fixation of intestine in abdominal cavity.
pancreatic divisum
failure of ventral and dorsal pancreatic buds to fuse during 8th wk of embryonic life. incidental.
omphalomesenteric duct. failure to obliterate?
connects lumen of midgut to yolk sac. failure to obliterate –> vitelline fistula (connection between ileum and outside body at umbilicus. partial failure –> Meckel diverticulum
hindgut descent
along IMA after midgut returns to abdominal cavity.
two main manifestations of intestinal malrotation
(1) intestinal obstruction – compression via adhesive bands (2) midgut volvulus – intestinal ischemia due to twisting around blood vessels
pili
hair-like protein polymers projecting from surface of cell. involved in attachment of organism to mucosal surfaces. HIGH antigenic variation (developing vaccine against gonococcal pilus –> challenging)
calcineurin
protein phosphatase –> dephosphorylates NFAT (nuclear factor of activated T cells), allows it to enter nucleus and bind to IL-2 promoter (stimulate growth & differentiation of T cells)
inhibition of calceneurin (2)
cyclosporin and tacrolimus
low back pain & morning stiffness in young man suggest…
ankylosing spondylitis (chronic inflammatory condition). most commonly affects: sacroiliac and apophyseal joints of spine. progressive exacerbation / remission. mild-moderate disease w/o permanent disability.
HLA-B27
seronegative spondyloarthropathies PAIR: psoriasis, ankylosing spondylitis, inflammatory bowel disease, reiter syndrome. NO rheumatoid factor
ankylosing spondylitis involves which 4 systems. in what way?
(1) musculoskeletal: peripheral enthesitis: calcaneus, tibial tuberosity, patella, trochanters, distal ulna most common. (2) pulmonary involvement due to enthesopathy of costovertebral & costosternal junctions –> hypoventilation. TEST CHEST EXPANSION. (3) cardiovascular: ascending aortitis –> dilatation of aortic ring and aortic insufficiency. (4) eye: anterior uveitis – blurred vision, photophobia, conjunctival erythema
most common benign vascular tumor
cherry hemangioma / angioma. small, bright-red, papular lesion. appear in 3rd-4th decade of life. do not regress spontaneously & number increases w/ age –> ‘senile hemangiomas’. always cutaneous, not on mucosa / deep tissue. histologically: sharply circumscribed areas of congested capillaries and post-capillary venules in papillary dermis.
strawberry (infantile/capillary) hemangioma
appear during first weeks of life. intially grow rapidly, then frequently regress by 5-8 years. bright red when near epidermis, violaceous when deeper.
spider angiomas
bright red central papule surrounded by several outwardly radiating vesselse that blanch w/ pressure & refill centrifugally on release. dilitation of central arteriole & superficial capillary network. ESTROGEN dependent
cavernous hemangiomas
dilated vascular spaces w/ thin-walled endothelial cells. present as soft BLUE, compressible mass (few cm in size). appear on skin, mucosa, deep tissue, viscera. when on skin – usu based in dermis. less likely to regress spontaneously. when in brain & viscera, associated w/ VHL
cystic hygroma
lymphatic cysts, lined by thin endothelium. present at birth, most commonly on neck / lateral chest wall. neonates w/ turner / down syndrome
differential cyanosis (cyanosis in lower extremity, not in upper)
reduced arterial oxygen in aorta distal to left subclavian. patent PDA which transforms into right-to-left shunt due to pulmonary HTN. note: eisenmenger & tetrology of fallot would cause cyanosis in upper & lower equally
fantasy vs. denial defense mechanism
fantasy: substituting imaginary scenarios. denial: behaving as if an aspect of reality doesn’t exist (refusing to acknowledge)
defense mechanism
means of protecting oneself from painful awareness of feelings
what antiseizure med causes generalized lymphadenopathy?
phenytoin. also causes undesirable cosmetic effects (hirsutism, coarsening of facial features, acneiform skin rash, gingival hypertrophy)
most feared complication of carbamazepine
agranulocytosis
complication from valproic acid
severe hepatoxicity
features of type II pompe’s disease
deficiency of lysosomal alpha-glucosidase: NORMAL blood sugar level, severe cardiomegaly, GLYCOGEN ACCUM in LYSOSOMES, normal glycogen structure, hepatomegaly, macroglossia, hypotonia. mental retardation
feature of type V mcArdle’s disease
deficiency of glycogen phosphorylase deficiency: weakness and fatigue w/ exercise, little/no rise in blood lactate w/ exercise, high levels of glycogen in muscles
features of type I von Gierke’s disease
deficiency on glucose-6-phosphatase in liver: hepatomegaly, fasting hypoglycemia, lactic acidosis, hyperuricemia and hyperlipidemia, increased glycogen storage but normal strxr
releasing glucose from glycogen
cytosolic glycogen phosphorylase shorts glycogen chains by cleaving alpha 1,4 glycosidic linkages. until 4 residues left before branching point. branching enzyme (1) transferase cleaves outer three residues and transfers to non-releasing end of other strand. (2) alpha 1,6 glucosidase releases free glucose. glycogen phosphorylase makes glucose-1-phosphate. converted to glucose-6-phosphate by phosphoglucomutase. in liver, glucose-6-phosphotase converts to glucose. small amounts of glycogen broken down by lysosomal enzyme alpha-1,4-glucosidase (acid maltase). deficiency –> pompe disease.
debranching enzyme deficiency
Cori or Forbes disease. childhood hepatomegaly, growth retardation, hypoglycemia, hyperlipidemia. muscle weakness.
galactokinase deficiency
normally: catalyzes phosphorylation of galactose in presence of ATP. cataracts is predominant manifestation of deficiency.
pyruvate kinase deficiency
chronic hemolytic anemia, splenomegaly, poor exercise inolerance
clinical manifestation of left vs. right side colorectal carcinoma
left: infiltrate intestinal wall, encircle lumen: symptoms of partial intestinal obstruction –> change in stool caliber, constipation, cramping abdominal pain, abdominal distension, nausea. vomiting.
right: exophytic mass. usu not obstructive bc larger caliber lumen, usu iron deficiency anemia (fatigue, pallor) due to ongoing blood loss. nonspecifc symptoms of anorexia, malaise, weight loss.
tenesmus & thin stool suggest
space occupying lesion of rectum, i.e. rectal adenocarcinoma.
