test #16 4.4 Flashcards
why does infxn w/ neisseria gonorrhoeae not result in lasting immunity?
modify outer membrane proteins by antigenic variation. Abs made in infxn – specific for single specific antigenic epitope.
kawasaki disease
vasculitis of medium-sized arteries
most serious complication of kawasaki disease?
coronary artery aneurysm.
symptoms of kawasaki
(1) persistent FEVER (2) bilateral CONJUNCTIVITIS (3) LYMPHADENOPATHY (4) CUTANEOUS involvement: (a) oropharyngeal: erythema of palatine mucosa, fissured erythematous lips, “strawberry” tongue (b) peripheral extremities: edema of hands * feet, erythema of palms and soles, desquamation of fingertips (periungual). (c) generalized rash: polymorphous (usu urticarial) erythemtaous rash beginning on extremities and moving to trunk (centripetal speed).
serious complication: coronary artery aneursym
which vasculitides are associated w/ mononeuritis multiplex (peripheral neuropathy of multiple individual nerves)
(1) granulomatosis w/ polyangiitis (2) polyarteritis nodosa
caudal regression syndrome. associated w/ & (3) signs
uncontrolled maternal diabetes. babies w/ agenesis of sacrum & occasionally lumbar spine –> (1) flaccid paralysis of legs, (2) dorsiflexed contractures of feet, (3) urinary incontenience
range of caudal regression syndrome
isolated anal atresia to sirenomelia (mermaid syndrome)
sirenomelia
mermaid syndrome, can result from caudal regression syndrome. legs fused together
cocaine on pregnancy
vasoconstriction: insufficient blood flow to developing fetus –> spontaneous abortion, intrauterine growth retardation, placental abruption, and/or prematurity
an URI that can negatively impact baby (gestation)
rubella (TORCHES). transmitted respiratroy. MR and congenital heart defects.
vitamin A overdose in pregnancy results in…
craniofacial abnormalities, posterior fossa CNS, auditory defects, abnormalities of great vessels (similar to DiGeorge)
vitamin A overdose in pregnancy in baby mimics?
DiGeorge
strict vegetarians (esp vegans) are at risk for which nutritional defeciencies?
(1) iron and (2) B12
tramadol
(1) very weak opiod agonist; also inhibits 5-HT and NE reuptake (2) (SNRI). mult ntx: tram it all w/ tramadol. use for chronic pain
positive predictive value
of those two test positive, how many are true positives.
a/a+b
validity of a test measured by
specificity and sensitivity
95% of gas gangrene caused by.. how?
Clostridium perfringes. toxin: phospholipase, cell death –> tissue damage, necrosis, reduction of blood supply. organism metabolizes carbohydrates –> generate gas.
clostridium perfinges causes (2)
(1) gas gangrene w/ penetration (2) transient watery diarrhea LATE-onset food poisoning, ingestion of spores in reheated meat dishes. late bc spores must germinate
early onset food poisoning (2) vs. late onset (1)
early-onset: preformed toxin (1) s. aureus (2) b. cereus.
late onset: c. perfringes (must germinate)
(2) bacteria associated w/ polyarthritis
(1) septic arthritis: gonorrhea (2) Group A strep
culture agar for cornybacterium diptheriae (2)?
(1) cysteine-tellurite agar, dark BLACK, slightly iridescent. (2) Loffler’s medium – cytoplawsmic metachomatic granules after stain w/ aniline dye.
how does maconkey prevent the growth of gram positives?
bile salts
colistin / polymyxin kills what? spares?
kills most gram negatives, but spares neisseria.
blood agar w/ bile & hypertonic saline used to..
differentiate enterococci (e. faecalis, e. facium; can grow in both) from nonenterococci group D strep (strep bovis / equinus)
Nonenterococcal group D strep grows in..
BILE but not hypertonic saline
Bordet-Gengou medium for…
Bordetella pertusus (whooping cough)
mental status exam testing: comprehension
follow multistep command
mental status exam testing: concentration
months of year backward; serial 7s, world backwards
mental status exam testing: visual-spatial
draw a clock face
score of 24 or < on mini-mental state exam
dementia
acute opioid tolerance mediated by?
uncertain, but phosphorylation of opioid receptors by protein kinase
chronic opioid tolerance?
increased adenylyl cyclase activity or NO levels
morphine tolerance?
glutamate mediated! NMDA receptor activation –> increased phosphorylation of opioid receptors & NO levels. (ketamine & dextromethorphan can block opiod tolerance)
what is required for the binding of glutamate to NMDA receptors?
glycine – co-agonist for glutamate. NECESSARY
pheochromocytoma rule of 10 (4)
10% occur as a part of hereditary syndrome (MEN2A and B, VHL). 10% bilateral. 10% malignant. 10% extraadrenal
involuntary head bobbing
sign of widened pulse pressure (peak systolic - end diastolic pulse pressure)
piriform recess
small cavities that lie on either side of laryngeal orifice. bounded medially by aryepiglottic folds. laterally by thyroid cartilage and thyrohyoid membrane. lead food into esophagus.
diversion of food from tracheal during swallowing
food diverted by epiglottis laterally through piriform recesses into esophagus
what n. courses superficially (under mucosa) in piriform recess?
internal laryngeal n (branch of superior laryngeal n CN X). afferent limb of cough reflex (sensation form mucosa superior to vocal cords)
recurrent laryngeal n & external laryngeal n? internal laryngeal?
recurrent & external: carry motor fibers involved in vocal cord fxn. internal: only sensory to larynx & epiglotis
fish bone / chicken lodged in piriformis. what n at risk? what reflex?
internal laryngeal (branch of superior laryngeal CN X). impair cough reflex
does irritation of larynx / epiglottis cause cough or gag?
COUGH
cough reflex
induced by upper respiratory tract irritation. afferent: X. efferent: X. afferent: internal branch of superior laryngeal. efferent: recurrent / external branch of superior.
gag reflex
afferent: glossopharyngeal CN IX. efferent limb: vagus CN X.
glossopharyngeal n. salivation pathway.
parasympathetics from glossopharyngeal onto otic ganglion. postganglioncs travel via auricotemporal n. to parotid.
therapeutic radiation initiates cell death by (2)
(1) DNA double strand breakage (2) formation of free radicals (from ionization of water – cause cellular and DNA damage). particularly hurts rapidly dividing cells
DNA crosslinking caused by (chemo)..
alkylating agents
DNA damage from exposure to UV radiation?
pyrimidine-pyrimidine dimers
among drugs of abuse, which is most likely to induce violent behavior?
PCP
fatalities associated w/ PCP abuse usu associated w..
TRAUMA, not from intoxication itself.
PCP causes.. (4)
(1) belligerence (2) loss of coordination (3) NYSTAGMUS (4) acute brain syndrome: disorientation, poor judgement, memory loss). can cause seizures too. DIE FROM TRAUMA
cocaine intoxication can cause
MI
seizures and strokes are common neurologic sequelae
cocaine & amphetamines
bath salts
amphetamines
statin side effects
myopathy and hepatitis. associated w/ liver function test abnormalities. monitor LFTs!
monitoring LFT w/ statin guidelines
LFT before starting. no need for routine monitoring unless signs of liver dysfxn develop (fatigue, malaise, anorexia). hepatotoxicity usu 3 months of starting statin therapy.
statins ought be used w/ caution in..
patients on other adrenal enzyme inhibitors (ketoconazole, aminoglutethimide)
sign of hepatoxicity on statins
fatigue, malaise, anorexia
3 portacaval anastomoses. clinical manifestation: portal circulation –> systemic circulation
(1) esophageal varices: left gastric vein –> esophageal vein (2) hemorrhoids: superior rectal vein –> middle/inferior rectal veins (3) caput medusae: paraumbilical veins –> superior & inferior epigastric veins
TIPs procedure
transjugular intrahepatic portosystemic shunt. shunt portal vein to hepatic vein percutaneously.
middle colic vein
drains transverse colon
right gastroepiploic vein
drains venous blood from lower parts of the anterosuperior and posteroinferior surface of stomach. runs from left to right along greater curvature of stomach
portal vein =
splenic vein + superior mesenteric vein
toxins produced by pseudomonas
(1) endotoxin (fever, shock) and (2) exotoxin A (inactivates EF-2)
antipseudomonal antibodiotics
- aminoglycosides (gentamicin, tobramycin, amikacin)
- antipseudomonal penicillins (ticarcillin and piperacillin)
- 3rd and 4th generation cephalosporins (ceftazidime, cefepime)
- quinolones (cipro)
- monobactams (azetreonam)
- carbapenems (imipenem, meropenem)
malignant otitis external infxn? demographic? characteristic finding? what can it lead to?
frequently caused by pseudomonas aeruginosa in elderly (non lactose fermenting, oxidase +, motile gram neg rod. exquisite ear pain & drainage.
characteristic finding: granulation tissue seen within the ear canal, w/ intact tympanic membrane. infxn progression can lead to (1) osteomyelitis of skull base and (2) cranial n damage.
comma-shaped rod, oxidase +, gram negative, that can grow on alkaline media?
vibrio cholerae
frequent cause of otitis media: (inflamed, erythematous, bulging, immobile tympanic membrane) in children and adults?
nontypable (unencapsulated) H. influenza. gram negative, rod shaped bacterium that requires factor X (hematin) and factor V (NAD+)
nitroprusside is a..
short acting balanced venous & arterial vasodilator. decreases LV PRELOAD and AFTERLOAD –> allows cardiac output to be delivered at a lower LV end diastolic volume. lower LVEDP (preload), lower mean systolic intraventricular pressure (afterload), without changing stroke volume.
LVEDP =
preload
primary cause of iron deficiency anemia
blood loss
variation in peak bone mass among individuals is largely accounted for by..
80% of variation due to GENETIC FACTORS (environmental factors like Ca++, vitamin D, physical activity play a lesser role,
human placental lactogen
secreted from syncitiotrophoblast. has structural and biologic properties similar to prolactin and growth hormone.
increases maternal insulin resistance (decreases maternal glucose utilization and increases blood glucose levels –> shunt to fetus)
hPL also increases maternal lipolysis and proteolysis, increasing free fatty acids and ketones –> energy to mother (freeing more glucose for fetus)
how do hPL levels change throughout gestation
levels rise w/ increasing gestational age & plateau at term (reflecting increased energy requirements of growing fetus)
maternal insulin resistance (during pregnancy) caused by..
human placental lactogen. also: placental production of growth hormone, estrogen, progesterone, glucocorticoids..
what chemical ensures baby gets enough glucose during prengnancy
human placental lactogen. causes maternal insulin resistance. more glucose for baby.
gestational diabetes mellitus
results when a woman’s pancreatic function is not sufficient to overcome this pregnancy-related increase in insulin resistance.
oxytocin plays a role in (2)
(1) uterine contraction (2) milk letdown reflex
how does pregnancy affect total T3 and T4 levels?
pregnancy increases levels of thyroid-binding globulin, increasing the total circulating T3 and T4, but free thyroid hormone = normal
3 fxns of human placental lactogen (hPL)
(1) increase insulin resistance in mom (2) stimulate proteolysis and lipolysis (3) inhibits gluconeogenesis.
to make medical decisions, does husband (i.e. next of kin to child/wife) need paper work
NO
in an emergency situation (i.e. pt is incompetent and perhaps next of kin do not understand gravity of situation (i.e. jehovah’s witness & blood transfusion). default is..
give blood / treat accordingly. only stop if there is a clear understanding that pt/kin knows they will die w/o the blood.
duodenal villi are covered w/?
simple columnar epithelium w/ brush border interspersed w/ goblet cells and APUD (amine precursor uptake and decarboxylation) cells.
deeper within lamina propria of duodenum lies..?
crypts of Lieberkuhn. simple tubular glands that rest immediately atop the muscular mucosae. deliver secretions into intervillar space.
deep to the muscular mucosae (submucosa) lies..?
compound tubular brunner’s glands. unique to duodenum. secrete alkaline mucous into ducts that track upward through muscularis mucosae and into the crypts of Liberkuhn for release into the lumen.
histology of stomach fundus?
numerous gastric pits lined by simple columnar epithelium. base of gastric pits are 2-4 fundic glands, primarily contain parietal cells and chief cells. below glands = muscularis mucosae
compare villi of jejunum & villi of duodenum
villi of jejunum contain more goblet cells. crypts of Liberkuhn persist in jejunem. heavy lymphocytic infiltration of lamina propria is common here/
compare histology of jejunum to ileum
ileum similar to jejunum, but ileum has more lymphatic nodules (peyer’s patches) immediately adjacent to villi and crypts
colon histology
crypts of Liberkuhn persist and heavily populated by mucus-producing goblet cells. NO pits or villi.
brunner’s glands specific to…? peyer’s patches specific to…?crypts of liberkuhn specific to…? gastric pits specific to..?
brunner’s glands = duodenum. peyer’s patches = ileum. crypts of liberkuhn = small & large bowel. gastric pits = stomach
name 3 alpha 1 blockers
(BPH and HTN)
doxazosin, terazosin, prazosin
thiazides are contraindicated in which 3 patient populations
diabetics, gout, hypercalcemia (causes increate reabsorption of glucose, uric acid, and Ca++)
calcium channel blockers for HTN (i.e. amlodipine, nifedipine) particularly good for (2)
patients w/ vasospasm: Raynaud, Prinzmetal
patients w/ coronary artery disease & HTN benefit from.
beta-blockers
alkaptonuria presentation
relatively benign childhood disorder that matures into arthritis in adult life. autosomal recessive. deficiency in homogentisic acid oxidase (normally metabolizes homogentisic acid into maleylacetoacetate). urine black on standing (homogentisic acid is oxidized)
accumulation of homogentisic acid
in adulthood, deposit in sclera and ear cartilage. also, large joints and spine (ankylosis and motion restriction)
how is melanin synthesized?
from tyrosine via tyrosinase
oseltamavir
sialic acid analogue inhibitor of influenza A and B virus neuraminidase
Tensilon (edrophonium) test
short-acting cholinesterase inhibitor. if improve symptoms –> myasthenia gravis, increase DOSE. if does not work, but has myasthenia, might be in CHOLINERGIC CRISIS (excessive stimulation of skeletal muscles caused refractory period)
pralidoxime rx? mechanism
used in organophosphate poisoning. regenerates cholinesterase in neuromuscular jxn.
enzyme deficiency in classic homocystinuria?
cystathione beta-synthase
clinical characterization of homocystinuria?
ectopia lentis, mental retardation, mafanoid habitus, osteoporosis, vascular problems
parental imprinting
preferential transcription of genes from one or another homologous pair of chromosomes depending on the parental origin of the chromosome
which is the only inhalation anesthetic that is not a respiratory depressant?
nitrous oxide. others: decrease tidal volume and minute ventilation –> hypercapnia
which inhalation anesthetic is good for asthma patients?
halothane & sevooflurane – bronchodilation properties. usu inhaled anesthetics inhibit mucociliary elevator, so must be catious
how do fluorinated anesthetics increase cerebral blood flow?
reduce vascular resistance in brain, increase ICP
characterize renal fxn in general anesthesia
decreased GFR and decrease in renal plasma flow.
APC mutations (chrom 5) found in (2)
(1) most cases of sporadic colon cancer (2) all familial polyposis syndromes
MSH2 gene
one gene responsible for DNA mismatch repair. implicated in HNPCC, or lynch syndrome
parvovirus B19 associated w. (3)
(1) erythema infectiosum “fifths disease” (2) aplastic anemia (3) hydrops fetalis if infxn before 20wks
major viral causes of acute hepatitis (5)
picornaviridae, hepadnaviridae, flaviviridae, deltaviridae, hepeviridae
major viruses responsible for bronchitis/bronchiolitis
influenza A (orthomyxoviridae), RSV (paramyxoviridae), coronavirus. all RNA
rubella (german measles)
togavirus
which patients depend on efferent arteriole constriction to maintain renal perfusion (and thus, ACE inhibitors are contraindicated)
renal artery stenosis, decompensated heart failure, chronic kidney disease, volume depletion
heroin and pamidronate can cause what nephropathy (drug induced glomerular disease)
focal sclerosing glomerular sclerosis
most common agents causing drug-induced (drug induced tubular necrosis) (5)
aminoglycosides, radiocontrast media, cisplatin, amphotericin B, fosacarnet
which drugs can precipitate in renal tubules (4)? drug-induced tubular obstruction
sulfonamides, methotrexate, IV acyclovir, triamterene
drug-induced renal interstitial nephritis (8).
most common: METHICILLIN. cephalosporins, acetazolamide, allopurinol, sulfonamides, NSAIDs. lithium & cyclosporine – cause chronic interstitial nephritis
mechanism of warfarin
inhibits vitamin K-dependent carboxylation of glutamic acid residues of clotting fators II, VI, IX, and X. makes dysfxnl coag factors
characterize polyarteritis nodosa. what vasculature is unaffected
segmental, transmural, necrotizing inflammation. medium to small sized. usu KIDNEY, heart, liver, GI. SPARES pulmonary arteries (& rarely involves bronchial arteries). inflammation results in ischemia, infarction, hemorrhage. bead-like aneursym formation, esp in mesenteric circulation. 1/3 experience livedo retiucarlis & palpable purpura
livedo reticularis
seen w/ PAN. purplish network-patterned discoloration.
erythroid precusror cells in the liver & spleen indicates.. most frequently caused by..
extramedullary hematopoesis. most frequent caused by extravascular hemolysis (like beta-thal)
describe skeletal abnormalities w/ extramedullar hematopoesis
expanding mass of progenitor cells in bone thins bony cortex and impairs bone growth. can see pathologic fractures in children. characterestic “chipmunk facies” – maxillary overgrowth and frontal bossing
amatoxins in poisonous mushrooms (i.e. amanita phalloides – death cap) cause..
GI absorption –> liver –> active transport by OATP (organic anion transporting polypeptide) and NTCP (sodium taurochloate co-transporter) concentrates in liver cells. bind to DNA-dependent-RNA pol II. HALT MRNA synthesis. 6-24 hrs post ingestion: abdominal pain, vomiting, severe cholera-like diarrhea w/ blood and mucous. acute hepatic and renal failure. urine test: for alpha-amantin
ricin (from castor oil plant Ricinus communis)
toxin that inhibits protein synthesis by cleaving rRNA of eukaryotic 60S subunit.
RNA pol I
ribosomal RNA
RNA pol II
mRNA
RNA pol III
tRNA
glucagonoma
rare pancreatic tumor. present w/ (1) necrolytic migratory erythema. elevated erythematous rash typically affecting groin area. other features: (2) hyperglycemia, stomatitis (inflammed mouth sore), cheilosis, abdominal pain, (3) anemia
(1) DM (2) necrolytic erythema (3) anemia
glucagonoma
pancreatic VIPoma
vasoactive intestinal peptide. intractable diarrhea, metabolic acidosis, hypokalemia. usu have hypotension secondary to both dehydration and vasodilatory effects of VIP.
somatostatinoma (rare pancreatic tumor of delta cells)
abdominal pain, gallbladder stones, constipation, steatorrhea. (due to inhibition of insulin, glucagon, gastrin, CCK, secretin, and gastrointestinal motility)
patients w. elevated PTHrP have
humoral hypercalcemia of malignancy
colonic manifestations of CMV
multiple ulcers and mucosal erosions. biopsy: cytomegalic cells w/ inclusion bodies
colonic manifestations of cryptosporidium
nonulcerative inflammation. biopsy: basophillic clusters seen on surface of intestinal mucosal cells
colonic manifestations of entamoeba histolytica
numerous discrete, flask-shaped ulcerative lesions. biospy: trophozites containing RBCs
colonic manifestations of kaposi sarcoma HHV-8
reddish/violet, flat maculopapular lesions or hemorrhagic nodules. biopsy: spindle-shaped tumor cells w/ small vessel proliferation.
colonic manifestations of ulcerative colitis
contiguous area of erythematous, friable, granular mucosa w/ possible pseudopolyps. biopsy: inflammatory infiltrate involving the mucosa & submucosa w/ CRYPT ABSCESSES.
kaposi sarcoma (HHV-8) organs affected
skin involvement is characterestic, but extracutaneous spread to lungs and GI tract is common.
adenocarcinoma histology
dysplastic mucosal cells w/ variable degree of gland formation. depending on tumor differentiation.
rare but serious adverse effect of ACE inhibitor therapy?
angioedema. swelling of tongue, lips, or eyelipds. laryngeal edema and difficulty breathing. due to bradykinin accumulation (potent vasodilator –> increases vascular permeability,
most common benign liver tumor
CAVERNOUS HEMANGIOMA. typically presents in 30-50 y/o adults. thought to be congenital malformations that enlarge by ectasia – distension/dilation (not hyperplasia or hypertrophy)
cavernous hemangioma presentation in liver
singly or multiples. well-circumscribed masses of spongy consistency (measure <5cm in width). cavernous blood-filled vascular spaces of variable size lined by single epithelial layer. usu asymptomatic, but can have abdominal pain / right upper quadrant fullness. prognosis = excellent. surgical resection
vast majority of hemangiomas are (benign or malignant)
BENIGN.
regression of hepatic adenomas w/..
discontinuation of oral contraceptives.
hepatocellular carcinoma can be associated w/..
hemochromatosis
is biopsy of cavernous hemangioma of liver indicated?
NO. known to cause fatal hemorrhage & low diagnostic yield.
how does hemoglobin S look on electrophoreses?
moves slowly (v. normal hgb) due to loss of negatively charged glutamate.
which can be done earlier, amniocentesis or chorionic villus sampling.
chorionic villus sampling of placenta
increased HR and CO w/ preservation of ARTERIAL partial pressures of O2 and CO2 are most consistent w/..
integrated cardiorespiratory response to exercise. venous blood has more CO2 and less O2
(1) neuronal cell body rounding, (2) peripheral displacement of nuclei, (3) dispersion of Nissl substance to periphery of cells. why does this happen
axonal reaction. cell body edema. central chromatolysis (granular nissl everywhere). visible 24-48 hrs after injury. maximal changes 12-days after injury. changes reflect: increased synthesis of proteins by the cells in order to regenerate severed axon.!
severed axon affects
both proximal (& cellbody) and distal axon (wallerian degeneration:
describe process of wallerian degeneration
1st swelling and irregularity in distal segment. within 1 wk, axon destroyed & fragments are digested by Schwann cells & macrophages.
axonal reaction is..
changes seen in neuronal body after axon is severed.
compression atrophy of neurons characterized by..
decrease in SIZE and # of neurons
degenerative disease loss of neurons characterized by? how does this differ from aging?
progressive neuronal loss w/ associated reactive glial changes. AGING: loss of neurons with NO REACTIVE GLIAL CHANGES.
