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Symptoms for rheumatic fever include
subcutaneous plaques, polyarthritis, erythema marginatum, chorea, and carditis
Name the characteristics of S. pyogenes
gram (+) cocci, beta hemolytic, bacitracin sensitive, group A
Titers of this can detect recent S. pyogenes infection
ASO
Most important virulence factor, determine the type of Group A, beta hemolytic strep,
M protein
3 important inflammation related enzymes possessed by S. pyogenes
hyaluronidase, streptokinase, and DNase
degrades hyaluronic acid, the ground substance of subcutaneous tissue, facilitates rapid spread of infection

hyaluronidase
converts plasminogen to plasma
streptokinase
degrades DNA in exudates or necrotic tissue
DNase
determine the group of beta hemolytic strep, located in the cell wall and its specificity determined by amino sugar
C carbohydrate
Toxins and hemolysins possessed by S. pyogenes
Erythrogenic toxin, streptolysin O and S, pyogenic exotoxin A, exotoxin B
causes rash of scarlet fever, acts as a superantigen, only produced by certain strains of S. pyogenes
Erythrogenic toxin
hemolysin that is inactivated by oxygenation, causes beta hemolysis when colonies grown on blood agar
Streptolysin O
hemolysin S, not inactivated by O2, NOT antigenic
Streptolysin S
Responsible for cases of TSS from S. pyogenes, same mode as Staph aureus
Pyogenic exotoxin A
protease that rapidly destroys tissue, produced by the "flesh-eating stains of S. pyogenes
Exotoxin B
Diseases caused by S. pyogenes
Cellulitis, pharyngitis, scarlet fever, TSS, rheumatic fever, glomerulonephritis, necrotizing fasciitis
Drugs used to treat S. pyogenes
Penicillin G and erythromycin
Rash that begins on trunk and spreads outward
Sandpaper rash of scarlet fever
Signs of poststreptococcal glomerulonephritis
Hematuria, hypertension, edema of face and ankles in 2-3 weeks

pustular lesions and honey comb-like crusts after strep skin infections
impetigo
Subepithelial IC deposits with granular IF; ICs activate alternative complement pathway; hematuria 1-3 weeks after infection

Findings of poststreptococcal glomerulonephritis
most common cause of nephrotic syndrome of children, more common in girls than boys
minimal change disease
Negative IF findings, fusion of podocytes and no deposits on EM
Minimal change disease
unlike focal segmental glomerulosclerosis, patients with this typically respond well the steroids
minimal change disease
most common cause of nephrotic syndrome in adults
Membranous glomerulonephritis
Minimal change disease typically occurs after
immunization
Peak incidence of minimal change disease is ages
2-6
Although most cases of idiopathic (85%), other causes of membranous glomerulonephritis are
DISC
Drugs- (penicillamine)
Infections (hepatitis B,C, syph)
Systemic (SLE, DM)
Cancer



Light microscopy of membranous glomerulonephritis shows
diffuse thickening of the capillary walls
Silver stains in membraneous glomerulonephritis shows
basement membrane projections (spikes)
Immunofluorescence in membranous glomerulonephritis shows and electron microscopy displays
Granular and linear pattern of IgG and C3
Subepithelial deposits along the basement membranes with effacement of podocyte foot processes
The variable course of membranous glomerulonephritis includes
spontaneous remission, persistent proteinuria or end-stage renal disease
Immunofluorescence in APSGN includes
granular deposits of IgM, IgG and C3 throughout the glomerulus
"lumpy-bumpy"
Characteristics of nephritic syndrome
Hematuria (RBC casts), hypertension, azotemia, oliguria, proteinuria (
Characteristics of nephrotic syndrome
"Leaky" basement membranes, deposits change charge allowing albumin to leak out
Severe proteinuria (>3.5g)
Hypoalbuminemia (

Renal calculi occur in __% of the population
6
Most renal calculi are composed of
Calcium oxalate
Type of kidney stones seen in gout, leukemia, and patients with acidic urine
Uric acid stones
Magnesium ammonium phosphate stones are associated with infection by
urea-splitting bacteria, these stones often form large staghorn calculi
True or false: Calcium stones are radiolucent and cannot be seen on x-ray
False, they are radiopaque
Spike and dome appearance
Membranous glomerulonephritis
Lipid accumulation in renal tubule cells
lipoid nephrosis/ minimal change disease
Cystine stones are almost always associated with
cystinuria or genetically determined aminoaciduria
Two urease positive organisms that can cause staghorn calculi are
Proteus vulgaris and Staphylococcus
Symptoms of UTIs are
Urinary frequency, dysuria, pyuria, hematuria, bacteriuria
Common causative organisms or UTIs or pyelonephritis are
E. coli, Proteus, Klebsiella, and Enterobacterium
Predisposing factors of developing acute pyelonephritis include
Urinary obstruction, vesicoureteral reflux, pregnancy, urethral instrumentation, DM, BPH
By age 60 __% of men have BPH __% of men have it by 70
70% and 80%; incidence increases with age
Chapman's point for the prostate
Along the IT band, PSIS and L5 spinous process
The gross appearance of BPH includes
enlarged prostate with well-demarcated nodules in the transition and central (periurethral) zones
Microscopic appearance of BPH
glandular and stromal hyperplasia
Clinical signs of BPH
decreased caliber and force of stream, trouble starting and stropping stream, postvoid dribbling, urinary retention and incontinence
Treatment options for BPH include
Transurethral resection of prostate (TURP), the 5-alpha reductase inhibitor, finasteride (Proscar) and the selective alpha-1 receptor blockers terazosin and prazosin
Levels of PSA seen in BPH
Complications of BPH
UTIs, urinary bladder trabeculation and diverticula formation, hydronephrosis and renal failure (rare)
5% of calcium oxalate stones are associated with hyperoxaluria or acquired overabsorption in pts with enteric diseases which is also seen in
vegetarians because of their diet that is high in oxalates
Potential inhibitors of kidney stones formation include
diphosphonate, citrate, glycosaminoglycans osteopontin and a glycoprotein called nephrocalcin
These stones are most hazardous because they may pass into ureters producing colic and ureteral obstruction
small stones
These are classified as microcytic anemia which have an MCV
TAILS
Thalassemia
Anemia of chronic disease

These are considered microcytic anemias which have an MCV
TAILS
Thalassemia
Anemia of chronic disease
Iron deficiency
Lead poisoning
Sideroblastic anemia




Causes of normocytic anemia with a low reticulocyte count
Ineffective erythropoiesis:
Marrow failure
Aplastic anemia
Myelofibrosis
Leukemia/Metastasis
Renal failure
ACD





Causes of normocytic anemia with a high reticulocyte count
Sickle cell anemia
G6PD deficiency
Hereditary spherocytosis
Autoimmune hemolytic anemia
Paroxysmal Nocturnal Hemoglobinuria



Iron panel for iron deficiency anemia
Serum iron: decreased
TIBC: Increased
% saturation: decreased
Serum ferritin


Iron panel for anemia of chronic disease
Serum iron: decreased
TIBC: decreased
% saturation: decreased
Serum ferritin: increased (iron trapped in macrophages)


Storage form of iron
ferritin
Form of iron precipitated in tissues in the form of degraded ferritin mixed with lysosomal debris
hemosiderin
dietary deficiency of iron is seen in
elderly, children, poor
Molecule that transports iron
transferrin
Clinical features of iron deficiency
free erythrocyte protoporphyrin, epithelial atrophy if Plummer-Vinson syndrome is present, koilonychia (concave nails) and pica
Patients with beta-thalassemia begin to show symptoms at
6 months- when hemoglobin F levels decline
Erythroid hyperplasia in beta-thalassemia causes
"crewcut" skull x-ray and increased size of maxilla (chipmunk face)
Blood smear in patients with beta-thalassemia can show
microcytic anemia with target cells and increased reticulocytes
Most common cause of death in beta-thalassemia major
Congestive heart failure
Seen when one of the beta-globin chain genes has been damaged
beta-thalassemia minor; asymptomatic
Damage to Beta globin genes is mainly to due these mutations
point
This can result from the lifelong blood transfusions necessary for beta-thalassemia major
Secondary hemochromatosis
Hemoglobin electrophoresis in beta-thalassemia major shows
increased hemoglobin F (90%) and hemoglobin A2 and decreased hemoglobin A
Genetic disorder affecting the hexose monophosphate shunt pathway
G6PD deficiency
Hereditary spherocytosis is autosomal dominant or recessive?
Dominant
Patients with this are at increased risk of red cell aplasia due to parvovirus B19
Hereditary spherocytosis
Hereditary spherocytosis is typically due to a defect in
ankyrin or spectrin of the erythrocyte membrane which causes a decrease in the erythrocyte surface membrane
Tx for hereditary spherocytosis
splenectomy
Lab testing of patients with hereditary spherocytosis shows
Increased osmotic fragility
Normal MCH
Increased MCHC

These cells are not flexible and therefore are removed by the spleen by macrophages
Spherocytes
Signs of hereditary spherocytosis
splenomegaly
increased bilirubin
increased risk for jaundice and pigment gallstones secondary to chronic hemolysis

Formed by oxidation of hemoglobin, can be visualized with supravital stains
Heinz bodies; eaten by splenic macrophages to form bite cell erythrocytes
The rate limiting enzyme in the hexose-monophosphate shunt
glucose 6 phosphate dehydrogenase
This antioxidant is reduced in G6PD deficiency
Glutathione; normally protects by breaking down Hydrogen peroxide
G6PD is inherited through what pattern
X-linked
In african americans (A- type) with G6PD deficiency, the hemolysis is secondary to
acute oxidative stress such as
oxidative drugs (primaquine, sulfonamides, and anti-Tb drugs)
and viral or bacterial infections

In individual with the mediterranean type of G6PD deficiency disease is associated with
favism due ingestion of fava beans; has more severe hemolysis because all erythrocytes have decreased G6PD activity in that there is both decreased synthesis and decreased stability
Inflammatory mediator associated with increased hepatic production of hepcidin
IL-6
Effects of hepcidin on iron and rbc production
inhibits ferriportin function in macrophages
reduces the transfer of iron from the storage pool to developing erythroid precursors in the bone marrow
hepcidin has what effect on erythropoietin levels
directly or indirectly suppresses
hepcidin is structurally related to this family of peptides that have intrinsic antibacterial activity
defensins
Potential explanation for iron sequestration in the setting of inflammation
enhance the body's ability to fend off certain types of infection, particularly those that require iron for pathogenicity
Potential causative agents of aplastic anemia
alkylating agents, chloramphenicol, chemical agents (benzene, insecticides), infection (EBV, CMV, parvovirus, hepatitis) or whole body radiation
if present, the dx of aplastic anemia should be seriously questioned
splenomegaly
Signs and symptoms of aplastic anemia
Anemia- progressive weakness, pallor and dyspnea
Thrombocytopenia- petechiae and ecchymoses
Neutropenia- frequent and persistant minor infection or sudden onset of chills, fever and prostration

dry tap
aplastic anemia; bone marrow often contains only fat cells, fibrous stroma and scattered lymphocytes and plasma cells
bronze diabetes
hemochromatosis
Epidemiology of hemochromatosis
Affects males 5x more than females
common in people of Northern European descent
disease of increased levels of iron, leading to tissue injury
hemochromatosis
HFE is located on chromosome
6
recessive disorder of the HFE gene
primary (hereditary) hemochromatosis
Most common mutation of the HFE gene
C282Y mutation, increases small-intestin absorption of Fe2+
Tx of hemochromatosis
phlebotomy
Dx of hemochromatosis
markedly elevated serum iron and ferritin or
increased tissue iron levels (Prussian blue stain) on liver biopsy
micronodular cirrhosis
hepatocellular carcinoma (200 times the normal risk ratio)
secondary DM
hyperpigmented skin (bronzing)
CHF
cardiac arrhythmias
hypogonadism





clinical features of hemochromatosis
Skin pigmentation in hemochromatosis is due to
hemosiderin and melanin deposition
autoimmune causes of aplastic anemia can be due to
cytotoxic T cells
most common intracorpuscular inherited hemolytic anemia observed in whites
hereditary spherocytosis
most common human enzyme deficiency
G6PD
Basophilic stippling
thalassemias, anemia of chronic disease, iron deficiency, lead poisoning
Fanconi's anemia
inherited defect in DNA repair, cause of aplastic anemia
positive osmotic fragility test in hypotonic solution
hereditary spherocytosis
slapped face
parvovirus B19
5 most common pediatric diseases with rash:
Measles, rubella, scarlet fever, roseola and erythema infectiosum
Characteristic of parvovirus erythrovirus
DNA virus, icosahedral nucleocapsid, nonenveloped, SS linear
smallest clinically important virus
parvovirus B19
Fetal infection of parvovirus can cause
severe anemia and hydrops fetalis
reason parvovirus infects only rbc precursors not mature red cells
only replicates when the cell is in S phase
B19 virus infects primarily two types of cells
red blood cell precursors (erythroblasts) in the bone marrow, which accounts for the aplastic anemia, and
endothelial cells in the blood vessels, which accounts, in part, for the rash associated with erythema infectiosum.
Parvovirus infection in adults, especially women can cause this
arthritis of the small joints of the hands and feet bilaterally which can resemble RA
Findings associated with erythema infectiosum
bright red rash that is most prominent on the cheeks, low-grade fever, runny nose (coryza), and sore throat.
A "lacy," less intense, erythematous rash appears on the body.
Symptoms resolve in about 1 week.



contribute to the pathogenesis of the rash and to the arthritis that is seen in some adults infected with B19 virus
Immune complexes composed of virus and IgM or IgG
end in -prazole
Proton pump inhibitors
Ome-, esome-, lanso-, rabe-
end in tidine
H2 blockers
Cime-, Famo-, Niza-, Rani
MOA of PPIs
Covalently bind to and thus irreversibly inhibit the proton pump, K+/H+ ATPase
Active form on PPIs
thiophilic sulfonamide
Prodrug activated metabolically in an acid dependent manner in parietal cells
PPIs
Clinical indications of PPIs
Peptic ulcers

GERD
Zollinger-Ellison syndrome


Major side effects of PPIs
Decreased B12 absorption due to decreased gastric acid
GI upsets
Headache, arthralgias and myopathy
Metabolized by P450 in the liver


Antibiotics used in the treatment of H. pylori
Amoxicillin
Bismuth
Clarithromycin
Metronidazole
Tetracycline
Usually 2-3 antibiotics are used with a PPI
ex Amox + Clarith + Omeprazole





MOA of H2 blockers
Suppression of Gs mediated cAMP-PKA chain reaction in parietal cells
Proton pump is inactivated leading to decreased gastric acid secretion
Clinical uses of H2 blockers
Peptic ulcers, GERD (alt. to PPIs)
Gastritis caused by stress
dyspepsia

H2 blocker that inhibits P450
cimetidine
Side effects specific to cimetidine
gynecomastia or galactorrhea
Side effects of H2 blockers
Bradycardia, intestinal upset leading to diarrhea, headache, fatigue and myalgias
all of the H2 blockers inhibit first pass metabolism of ethanol except
famotidine
For maximum effect, PPIs should be taken
30 minutes before breakfast or the largest meal of the day
Inhibits the metabolism of warfarin, phenytoin, diazepam, and cyclosporine
Omeprazole
patients must be counseled to discontinue PPI therapy if they have diarrhea for several days because these drugs can cause increased
C diff colitis
modified form of endotoxin
LOS- lipooligosaccharide
contained on N. gonorrhea
Gram (-) diplococci that oxidizes glucose not maltose
N. gonorrhea
inactivates C3b component of complement, present in strains that disseminate
porin protein A
Allows N. gonorrhea to attach to mucosa and are antiphagocytic
Pili
yellowish-green exudate
N. gonorrhea
incubation time of N gonorrhea
2-6 days
Media used to grow N. gonorrhea
Thayer-Martin
chocolate agar w/antibiotics: vancomycin, nystatin, colistin, trimethoprim
Typically symptomatic in men and asymptomatic in women
Gonorrhea
Tx for gonorrhea
Ceftriaxone, erythromycin eye drops for neonates or silver nitrate
Clinical presentations of gonorrhea
Urethritis, epididymis, purulent vaginal discharge and intermenstrual bleeding (cervicitis), salpingitis, anorectal infections
pharyngitis, opthalmia neonatorum
infection of the liver capsule
Fitz-Hugh-Curtis syndrome
Most common STD in the US
Chlamydia
white-clear discharge
chlamydia
elementary bodies
metabolically inactive form of chlamydia
reticulate bodies are the active form
Reiter's syndrome
associated with chlamydia infection, in males esp HLA-B27 patients
can't see, cant pee, cant climb a tree
Treatment for chlamydia
Azithromycin/ tetracycline
Stains used to visualize intracytoplasmic inclusions of chlamydia
iodine and Giemsa
can also culture with cycloheximide
Incubation period of chlamydia
2-3 wks
ulcers, lymphadenopathy, rectal strictures
lymphogranuloma venereum
chlamydia serovars L1-L3
clinical features of chlamydia trachomatis (D-K)
urethritis, cervicitis, conjunctivitis, Reiter's syndrome, PID
antibody dependent complement pathway
classical; C1 binds to Fc portion of IgM or IgG
Mannose binding protein binds sugars on the surface of pathogens and associated proteases cleave C4 and C2
Lectin complement pathway- antibody independent
always active at a low level, amplified when active C3 binds to a surface that lacks regulatory proteins
Alternative complement pathway
disrupts binding of factor B to C3b
decay accelerating factor
Characteristics of H. pylori
Gram - bacilli, curved, urease +, growth on Campy agar
What percent of duodenal and gastric ulcers are due to H. pylori
100% and 70%
gastritis limited to the antrum due to H pylori can lead to
decreased somatostatin secretion by antral D cells, causing acid hypersecretion
risk of duodenal ulcers
gastritis that extends throughout the stomach in helicobacter pylori infections
acid hyposecretion causing chronic infection and inflammation
risk of gastric ulcers, gastric carcinoma
Dx of helicobacter pylori
14C labeled urea breath test: labeled urea ingested and labeled CO2 exhaled if bacteria urease present
biopsy
IgG titer in serum

microaerophilic spirochete, sensitive to high temperature
treponema pallidum
Treatment of syphilis
penicillin G
This can result from treatment of syphilis due to lysis of the treponeme which releases endotoxin-like factors
Jarisch-Herxheimer reaction
Symptoms of Jarisch-Herxheimer reaction
fever, chills, and myalgias
Patients with these can have a false positive VDRL test due to anti-cardiolipin antibodies
SLE and infectious mono; clarify with FTA-ABS test
Diseases associated with a palm and sole rash
syphilis, coxsackievirus, and Rocky Mt. Spotted fever
appears 6 weeks after exposure to syphilis
painless chancre of primary syph
due to organism multiplying at inoculation site
heals spontaneously over 6 weeks

wart-like painless lesions in moist area
condyloma lata
Findings of secondary syphilis
condyloma lata, meningitis, hepatitis, arthritis, maculopapular rash on palms and soles
visible 6 wks after syphilitic chancre heals
Secondary syphilis; disseminated spirochetes proliferate forming lesions throughout the body
cycle of secondary syphilis can repeat multiple times
detects anti-treponemal antibodies
FTA-ABS; specific diagnostic test
detects reagin antibodies against cardiolipin
VDRL -nonspecific
Transplacental transmission of syphilis
congenital syphilis: stillbirth, fetal abnormalities
CN VIII deafness, mulberry molars, saber skins, saddle nose, Hutchinsons incisors
congenital syphilis
accommodates of near objects but does not react to light
Argyll-Robertson pupil
Findings of tertiary syphilis
gummas
CV: aortitis, ascending aortic aneurysm
CNS: tabes dorsalis, general paralysis, meningitis, Argyll-Robertson pupil

Enveloped, DS circular DNA virus
Hepadnaviridae Orthohepadnavirus
antigen found in mammalian mitochondrial membranes and treponemes
Cardiolipin; cheap source is cow heart
benzathine penicillin
used for primary and secondary syphilis and close contacts
penicillin G is used for congenital and late syphilis
Dane particle
infectous HBV
Clinical presentation of hepatitis B
Acute: occasionally sever
Chronic infection: 5-10% of adults, 90% of infants
Primary hepatocellular carcinoma, cirrhosis

Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice
symptoms of hepatitis
incubation time of hepatitis B
2-24 weeks
end in thromycin
macrolides; ery, azi, clari
MOA of macrolides
Inhibit translocation of peptidyl-tRNA from acceptor to donor site (-static)
Binds to 50S subunut
Side effects of macrolides
Motility enhanced GI disturbances
Auditory toxicity (reversible)
Cholestatic jaundice
Cardiac arrhythmias (increase QT interval)


Clinical uses of macrolides
Gram (+) cocci -not MRSA
Atypical organisms (Chlamydia, Mycoplasma and ureaplasma)
Legionella
Campylobacter and helicobacter
mycobacterium avium-intracellulare (MAC)
Pertussis




Macrolides have what effect on cytochrome P450
Inhibition
Primary mechanism of resistance to fluoroquinolones
change in sensitivity to inhibition of target enzymes; increased activity of transport systems that promote drug efflux
Mechanism of resistance to macrolides
Active transport out of cells
Formation of methyltransferases that alter drug binding sites on the 50S ribosomal subunit
Mechanism of resistance to penicillins
Production of beta-lactamases which cleave the beta-lactam ring
change in penicillin binding proteins
change in porins

Quinolones are bactericidal or bacteriostatic
bactericidal
Fluoroquinolones end in
-Floxacin; cipro
MOA of fluoroquinolones
inhibit topoisomerase II (DNA gyrase) and topoisomerase IV (responsible for separation of replicated DNA during cell division)
Clinical uses of quinolones
UTIs, STDs, GI infections, pseudomonal and legionella, mycobacteria, meningococcal meningitis, staph and strep
Group 2 quinolones are most potent against
gram (-) bacteria; cipro, en, levo
Group 3 quinolones are most potent against
Gram (+) bacteria; moxi, spari, gati
Iron and calcium limit their absorption
Reduce dose in renal dysfunction
Fluoroquinolones
Side effects of fluoroquinolones
Tendonitis, tendon rupture
photosensitivity, rashes
CNS effects- insomnia, dizziness, headache
Contraindicated in pregnancy and children
Liver toxicity
Cardiac QTc interval prolongation
Elevated/decreased glucose levels in diabetics





Inhibition of DNA gyrase by quinolones is more significant than that of topoisomerase IV in
Gram - bacteria
the opposite is true for gram + bacteria
MOA of penicillin
Bind to PBPs, block the crosslink of peptidoglycan by inhibiting transpeptidase
Also activates bacterial autolytic enzymes
Bactericidal

Side effects of penicillins
Allergy- in the form of skin rash, Stevens-Johnson syndrome, angioedema, or anaphylaxis
Enteric disturbances
Nephritis-interstitial (methicillin)
Neurotoxicity- seizures in pts with renal failure


Clinical uses for penicillin
PEN SACS
Pneumococci
Enterococci
N. meningitidis
Strep and Staph
Anthrax
Actinomyces
Clostridium
Spirochetes







Very narrow spectrum, beta-lactamase resistant
Naficillin, methicillin, oxacillin
Used for staph (not MRSA)
Extended spectrum, antipseudomonal, beta-lactamase sensitive penicillins
Ticarcillin piperacillin, azlocillin
Increased activity against gram - rods including pseudomonas aeruginosa
Broad spectrum, aminopenicillins, beta-lactamase sensitive
Ampicillin, amoxicillin
Predisposing risk factors for developing peptic ulcers, besides H. pylori
NSAIDs- which causes direct chemical irritation and suppresses PG syntheses
Steroid use- suppress PG synthesis and impair healing
smoking- impairs mucosal blood flow and healing

Although more than 70% of individuals with PUD are infected with H pylori, fever than __% of H pylori infected individuals develop peptic ulcer
20
Duodenal ulcers are more common in patients with
blood group O
MEN I
ZE syndrome
cirrhosis
COPD
chronic renal failure




classic presentation of duodenal peptic ulcer
burning epigastric pain that 1-3 hours after eating relieved by food- WT GAIN
Classic presentation of gastric peptic ulcers
burning epigastric pain, which worsens with eating
WT LOSS
Small (
gastric peptic ulcers
Hemorrhage, iron deficiency anemia, penetration into adjacent organs, perforation, and pyloric obstruction
Complications of peptic ulcers
Ranks 4th in both annual physician visits and costs among all GI diseases
PUD
arises most frequently in the upper and middle third of the esophagus
Squamous cell carcinoma
Most common after age 50, increased incidence in men, people with blood group A
Carcinoma of the stomach
Incidence of gastric carcinoma is higher in those geographic areas
Japan, Finland, Iceland
Dietary risk factors for developing gastric carcinoma
Nitrosamines, smoked meats and fish, pickled vegetables, benzpyrene, decreased intake of fruits and vegetables and excessive salt intake
Left supraclavicular lymph node
Virchow node- metastasis of gastric carcinoma
Krukenberg tumors
bilateral involvement of the ovaries by metastatic carcinoma of the stomach
tumor cells have abundant mucin- signet ring cells
linitis plastica
thickened leather bottle appearance of stomach in gastric carcinoma
Clinical findings of gastric carcinoma
Wt loss and anorexia
epigastric abdominal pain mimicking a peptic ulcer
early saiety and occult bleeding with iron deficiency anemia

infiltration of the stomach by poorly differentiated tumor cells, frequently numerous signet ring cells and linitis plastica
Diffuse type of gastric carcinoma
polypoid (fungating) carcinoma which forms a solid mass projecting into the lumen of the stomach
high degree of association with H pylori
Intestinal type gastric carcinoma
Most common type of esophageal cancer in the world but not in the US
Squamous cell carcinoma
Risk factors for squamous cell carcinoma
heavy smoking, alcohol use, achalasia, Plummer-Vinson syndrome, tylosis and prior lye ingestion
Treatment for gastric carcinoma
gastrectomy; 5 year survival of 20%
Affects males more than females
Blacks more than whites
typical age is older than 50

Squamous cell carcinoma of esophagus
Progressive dysplagia, wt loss and anorexia, bleeding, hoarseness or cough
Clinical presentation of SCC of esophagus
often asymptomatic until late in the course
celiac sprue is associated with HLA..
B8, DR3 and DQ
skip lesions
Crohns
Most common site for Crohn's
Terminal ileum
Lead pipe deformity on barium study
UC; due to loss of haustra
Most common site for UC
Rectum, progresses backwards
Crohn's or UC: limited to mucosa and submucosa
UC
Crohn's or UC: String sign on barium study
Crohns
"creeping fat"
Crohn's
Crohn's or UC: complications include toxic megacolon and CA
UC
Crohn's or UC: Complications include strictures, obstruction, abscesses, fistulas, sinus tracts
Crohns
Common extraintestinal manifestations of both Crohn's and UC
arthritis, spondylitis, primary sclerosing cholangitis, erythema nodosum, pyoderma gangrenosum, uveitis
Microscopic appearance shows loss of villi, increased intraepithelial lymphocytes and increased plasma cells in the lamino propria
Celiac sprue
rare immune disorder that is often associated with celiac sprue
dermatitis herpetiformis
subepidermal blister formation with itchy, grouped vesicles and occasional bullae on the extensor surfaces
Dermatitis herpetiformis
granular IgA deposits at the tips of dermal papillae
Dermatitis herpetiformis
Routine microscopy of dermatitis herpetiformis shows
microabscesses at the tips of dermal papillae that can lead to eventual subepidermal separation causing blister formation
raised, erythematous, painful nodules of subcutaneous adipose tissue, typically on anterior shins
Erythema nodosum
Associated with granulomatous diseases and strep infection
Crohn's or UC: Bimodal distribution with peaks at ages 10-30 and 50-70
Crohn's
Crohn's or UC: peaks at 20-30
UC
Presentation of inflammatory bowel disease
bloody diarrhea, stools with mucus, crampy lower abdominal pain or fever
Can present with malabsorption or mimic appendicitis
Crohn's disease
Usually presents in childhoos with malabsorption, abdominal distention, bloating, flatulence, diarrhea, steatorrhea and wt loss
Celiac sprue
Tx of celiac sprue
restriction of gluten
Approximately 10-15% of cases lead to small intestine malignancy, most often enteropathy type T cell lymphoma
Celiac sprue
Crohn's or UC: crypt abscess in which there are infiltrates of neutrophils in the crypts of Lieberkuhn
UC
Crohn's or UC: Red granular appearance of mucosa
UC
Crohn's or UC: pseudopolyps, mucosal remnants of previous severe ulceration
UC
associated with ret gene
MEN 2A and 2B
Inheritance pattern of MEN syndromes
Autosomal dominant
Sipple's syndrome
MEN 2A
Wermer's syndrome
MEN 1
Characteristics of MEN 1
Parathyroid tumors, pituitary (prolactin or GH), Pancreatic (Zollinger Ellison syndrome, insulinoma, VIPomas, glucagonomas)
Commonly presents with kidney stones and stomach ulcers
Multiple, intractable peptic ulcers in duodenum, jejunum and stomach
Gastrin levels >1000
Zollinger-Ellison syndrome
Sister Mary Joseph's nodule
subcutaneous periumbilical metastasis of stomach carcinoma
acanthosis nigricans
features of gastric adenocarcinoma
Spread pattern of GI tract tumor
lymph nodes, liver, lungs
Used for screening of celiac sprue
tissue transglutaminase antibodies
Autoimmune-mediated intolerance of gliadin (wheat) leading to steatorrhea
Celiac sprue
Celiac sprue is commonly found in people of
Northern European descent
Treatment of crohn's
Corticosteroids, infliximab
Possible etiology of Crohn's
Disordered response to intestinal bacteria
Primary sclerosing cholangitis
think UC more than Crohn's
treatment of UC
ASA preparations (sulfasalazine), infliximab, colectomy
3rd most common cancer and 3rd most deadly
colorectal cancer
CEA tumor marker
colorectal cancer
autosomal dominant mutation of APC gene on chromosome 5q
Familial adenomatous polyposis (FAP)
Risk factors for colorectal cancer
IBD, Strep bovis bacteremia, tobacco use, large villous adenomas, juvenile polypsos syndrome, Peutz-Jeghers syndrome, High fat diet
Most common cause of primary hyperparathyroidism
Adenomas (80%); can be associated with MEN I
15% of hyperparathyroid cases due to this
parathyroid hyperplasia- diffuse enlargement of all four glands
Clinical features of hyperparathyroidism
Most asymptomatic; may cause kidney stones, osteoporosis, osteitis fibrosa cystica, metastatic calcifications or neurologic changes
Condition that can result from chronic renal failure, vitamin D deficiency or malabsorption
secondary hyperparathyroidism
Causes of hypoparathyroidism
Surgical removal of glands during thyroidectomy, DiGeorge syndrome, radiation to neck or idiopathic
Twitching of ipsilateral facial muscles after tapping muscles
Chvostek sign- suggestive of neuromuscular excitability by hypocalcemia
inflating a bp cuff above systolic blood pressure for several minutes so that if hypocalcemia is present, muscular contractions, including flexion of the wrist and metacarpophalangeal joints, hyperextension of the fingers and flexion of the thumb on the p
Trousseau sign
Osteitis fibrosa cystica
von Recklinghausen's syndrome
cystic bone spaces filled with brown fibrous tissue
Autosomal-dominant kidney unresponsiveness to PTH, hypocalcemia, shortened 4th/5th digits, short stature, mental retardation
Pseudohyperparathyroidism
(Albright's hereditary osteodystrophy)
Lab findings in primary hyperparathyroidism
hypercalcemia, hypercalciuria, hypophosphatemia, increased PTH and alk phos, increased cAMP in urine
Lab findings in secondary hyperparathyroidism
hypocalcemia, hyperphosphatemia, increased alk phos and PTH
Perioral numbness and tingling
sign of hypoparathyroidism
fluke found in undercooked fish, causes inflammation of the biliary tract which can lead to pigmented gallstones
Clonorchis sinensis
Charcot's triad of cholangitis
Jaundice, fever, RUQ pain
inspiratory arrest on deep palpation
positive Murphy's sign
Native Americans tribes with increased incidence of cholesterol gallstones
Pima and Navajo
Risk factors for cholelithiasis
4 F's: female, fat, fertile, forty
Pigmented bilirubinate stones are composed of
Calcium salts and unconjugated bilirubin
Risk factors for developing pigmented bilirubinate stones
chronic hemolytic anemia, cirrhosis, bacterial infection, old age and parasites
radiopaque
Cholesterol stones are associated with
obesity, Crohn's, cystic fibrosis, advanced age, clofibrate, estrogens, multiparity, rapid weight loss and Native American origin
Complications of cholelithiasis
cholecystitis, biliary tract obstruction, pancreatitis, choledocholithiasis, cholangitis, gallstone ileus
Macrovesicular fatty change that may be reversible with alcohol cessation
Hepatic steatosis
Gross appearance is enlarged, yellow, greasy
acute illness that usually follows a heavy drinking binge
alcoholic hepatitis
Microscopic changes that occur is alcoholic hepatitis
hepatocyte swelling (ballooning) and necrosis
Mallory bodies- eosinophilic inclusions of cytokeratin intermediate filaments
Micronodular, irregular shrunken liver with hobnail appearance
Sclerosis around central vein
Has manifestations of chronic liver disease

Alcoholic cirrhosis- final and irreversible form of alcoholic liver disease
AST > ALT
alcoholic hepatitis
most common cause of renal artery stenosis
atheromatous plaque
Sources of estrogen
ovary- 17beta-estradiol
placenta- estriol
blood- aromatization
peripheral- estrone


Estrogen or progesterone: causes cervical mucus to be thin and watery
Estrogen; makes it easy for sperm to traverse
Theca cells have receptors for
LH; produce androstenedione from cholesterol which it sends to granulosa cells
Source of progesterone
Corpus luteum, placenta, adrenal cortex, testes
Estrogen or progesterone: Development of genitalia and breast, female fat distribution
Estrogen
Granulosa cells have receptors for what
FSH throughout cycle
LH added late in follicular phase
produce estrogen from androstenedione

Estrogen or progesterone: stimulation of prolactin secretion but blocks its action at breast
Estrogen
Estrogen or progesterone: Growth of follicle, endometrial proliferation, increased myometrial excitability
estrogen
Estrogen or progesterone: maintenance of pregnancy
progesterone
Estrogen or progesterone: stimulation of endometrial glandular secretions and spiral artery development
progesterone
Estrogen or progesterone: decreased myometrial excitability
progesterone
Estrogen or progesterone: production of thick cervical mucus, which inhibits sperm entry into uterus
progesterone
Estrogen or progesterone: increases body temperature 0.5-1.0F
progesterone
Estrogen or progesterone: inhibitiion of gonadotropins (LH, FSH)
progesterone
Estrogen or progesterone: Uterine smooth muscle relaxation
progesterone
Phase of menstrual cycle that is constant 14 days
luteal phase
follicular can vary in length
Frequent but irregular menstruation
metorrhagia
heavy menstruation
menometrorrhagia
> 35 day cycle
oligomenorrhea
polymenorrhea
blood from ruptured follicle causes peritoneal irritation that can mimic appendicitis
Mittelschmerz
removes restraint of meiosis I prophase which oocyte has been in since fetal life; 1st polar body extruded
LH surge
Parts of the Graafian follicle that are ovulated
oocyte and corona radiata
Component that secondary follicle has but primary doesn't
theca layer
Components that differentiate tertiary follicle from a secondary follicle
antrum, theca externa and interna, multiple layers of granulosa cells
DNA content of primary oocyte
4N
DNA content of secondary oocyte
2N
Meiosis II is arrested in
Metaphase until fertilization
DNA content of ovum
1N, Haploid
Fertilization more commonly occurs where
upper end of the fallopian tube (the ampulla)
Occurs within 1 day of ovulation
fertilization
Implantation occurs within how many days of fertilization
6
Source of hCG
Syncytiotrophoblast of placenta
Maintains the corpus luteum (thus progesterone) for the 1st trimester by acting like LH
hCG
Components of HELLP syndrome
Hemolysis
Elevated LFTs
Low Platelets

HTN, proteinuria and edema in pregnancy
preeclampsia
Occurs in 7% of pregnant women from 20 weeks gestation to 6 weeks postpartum
preeclampsia
Increased incidence of preeclampsia in pts with
preexisting HTN, DM, chronic renal disease, and autoimmune disorders
Risk factors for preeclampsia
prior hx, obesity, age older than 35 or younger than 18, African american race, nulliparity, multifetal pregnancy, hydratidiform mole, fetal hydrops
Begins 1st day of menses
Follicular phase
If estrogen levels are still rising, this has not occurred
ovulation
Begins 24-36 hours before ovulation when granulosa cells become receptive (gain receptors for) LH
luteal phase
Etiology of preeclampsia
placental ischemia due to impaired vasodilation of spiral arteries resulting in increased vascular tone
Signs and symptoms of severe preeclampsia
headache, blurred vision, abdominal pain , altered mentation, hyperreflexia, edema of face and extremities, thrombocytopenia, hyperuricemia
Treatment of preeclampsia
Delivery of fetus as soon as viable
Bed rest, salt restriction, monitoring and treatment of HTN
IV mag sulfate and diazepam to prevent and treat seizures

Most common site for ectopic pregnancy
Fallopian tubes (~90%), ovary, abdominal cavity, intrauterine portion of the fallopian tube
Tubal damage such as in pelvic inflammatory disease
prior ectopic pregnancy
prior tubal surgery
nonwhite race
age 35-44
current IUD
Endometriosis





Risk factors for having an ectopic pregnancy
Signs and symptoms of ectopic pregnancy
Severe abdominal pain
Evidence of intra-abdominal bleeding including hypotension and collapse
Adnexal mass
Vaginal bleeding
Signs of peritoneal irritation
Absence of gestational sac on ultrasound with beta-hCG level >2500mIU/mL




Treatment of choice in ectopic pregnancy
Methotrexate
Contraindicated if;
hCG > 15,000mIU/mL, adnexal mass >3cm, patients hemodynamic state is unstable

Etiology of placenta previa
implantation by the zygote low in the uterine cavity
defective decidual vascularization, resulting from inflammation or atrophy has been implicated
Signs and symptoms of placenta previa
Painless vaginal bleeding- generally not present until late 2nd or early 3rd trimester
Should not be performed until diagnosis of placenta previa has been excluded
Pelvic exam, ultrasound is most accurate at diagnosing
Major classifications of placenta previa
Complete placenta previa
Partial- placenta partially covers internal cervical os
Minor classifications of placenta previa
marginal- placental edge reaches but does not cross internal os
low-lying placenta- lower edge reaches within 2cm of os but does not cover it
premature separation of the placenta from the uterine sidewall
placental abruption
Causes of placental abruption
HTN, trauma to the abdomen, decompression of an overdistended uterus, cocaine use
Vaginal bleeding
Abdominal, back or uterine pain
Fetal bradycardia or late decelerations
uterine irritability, tachysystole, tetany, elevated baseline intrauterine pressure
maternal hypotension or signs of volume loss



Signs and symptoms of placental abruption
DIC may be associated
Clinical uses of leuprolide (GnRH agonist)
Infertility- pulsatile
Prostate CA, uterine fibroids- continuous
Drugs that decrease the effectiveness of OCs
Anticonvulsants
Barbs, phenytoin, carbamazepine, toprimate
Antiinfectives
Rifampin, Griseofulvin


Common side effects of Oral contraceptives
Break-through bleeding (initially and later due to endometrial atrophy)
Breast Tenderness
Headache (may also treat headache)
Nausea (related to estrogen dose)
Mood Changes, change in libido
Edema




Oral contraceptives can help prevent
Bone loss
Fibrocystic/benign breast disease
Pelvic inflammatory disease
Ectopic pregnancy




Cancers reduced by use of oral contraceptives
Ovarian, endometrial, colorectal
absolute contraindications of oral contraceptives
Pregnancy, hx of CVA, DVT, PE, heart disease, smoking >20 cigarettes/day, migraines, current breast CA, viral hepatitis, liver disease
primary oocyte with surrounding single layer of pregranulosa cells
primordial follicle
primary oocyte surrounded by a single layer of cuboidal granulosa cells
primary follicle
primary oocyte surrounded by several layers of cuboidal granulosa cells and theca cells
secondary follicle
granulosa cells closest to the oocyte secrete the mucopolysaccharides that form the
zona pellucida- immediately surrounded the oocyte
Most important molecular event in process of capacitation
removal or modification of protective protein coat from the sperm cell membrane
receptors on the plasma membrane of the sperm cell bind to___ which induces the sperm cell to undergo
ZP3; acrosomal reaction
Contains hydrolyzing enzymes necessary for the sperm to penetrate the zona pellucida
acrosome
two methods by which sperm enters zona pellucida
Chemical- hydrolytic enzymes in acrosome
Mechanical- oscillation of sperm head
A rise in ____ inside the oocyte triggers the ________ in which there is exocytosis of granules beneath the plasma membrane which harden the zona pellucida
Ca2+, cortical reaction
induces completions of the oocyte's 2nd meiotic division
rise in intracellular Ca2+
specialized endometrium of pregnancy
decidua
Oxytocin is synthesized mostly in the
paraventricular nucleus
stimuli for oxytocin secretion include
dilatation of the cervix and vagina
suckling at the breast
Which stimulates and what inhibits oxytocin release
Estradiol, relaxin
causes contraction of the myoepithelium that surrounds alveolar channels in the mammary gland
oxytocin
stimulates the frequency and force of contraction
oxytocin
OC effects on clotting time possibly due to
increase in factors VII, VIII, IX and X and a decrease in antithrombin III
Beta0 mutations
absent beta-globin synthesis
beta+ mutations
reduced but detectable beta-globin synthesis
Most common cause of beta+ thalassemia
splicing mutations
Most common cause of Beta0 thalassemia
Chain terminator mutations- create stop codon or frameshift
Individuals with two beta-thalassemia alleles (B+/B+, B+/B0, B0/B0) have a severe transfusion depended anemia called
thalassemia major
heterozygotes with one beta thalassemia gone and one normal gene (B+/B, B0/B) have a mild asymptomatic microcytic anemia called
beta thalassemia minor
Loss of which tumor suppressor genes are involved in developing SCC of esophagus
p53 and p16/INK4alpha
Most common cause of small bowel obstruction
adhesions after abdominal surgery
second most common cause of SBO
incarceration of a groin hernia
Pain associated with small bowel obstruction may be
crampy and intermittent
periumbilical or diffuse
Clinical features of small bowel obstruction
Abdominal pain
Vomitus in proximal obstruction
Constipation
Abdominal tenderness, distention
tympanic to percussion
high pitched bowel sounds




Should make one suspect bowel gangrene, intra-abdominal abscess or peritonitis
leukocytosis or >20,000/mm3 or left shift
Leukemia of pts newborn to 14 years old
ALL
Patient 15 to 39 years old
pts 40-60
AML
leukemia of patients over 60 years old
CLL
Most common overall leukemia
CLL
leukemia in pts 40-60 yrs old
CML
t9:22 translocation of ABL proto-oncogene
Chronic myelogenous leukemia (CML)
proto-oncogene fuses with the break cluster region (BCR) in chromosome 22
Splinter shaped to rod shaped structures in the cytosol of myeloblasts
Auer rods- NOT present in CML
Leukemia that is most common in middle aged men
Type of B cell leukemia
Hairy cell leukemia
Lab findings in hairy cell leukemia
pancytopenia
leukemic cells have hair-like projections
positive tartrate-resistant acid phosphatase stain (TRAP)

Only leukemia without lympadenopathy
Hairy cell
Numerous smudge cell (fragile leukemic cells)
Chronic lymphocytic leukemia
HLA alleles seen in almost all people with celiac disease
HLA-DQ2 and DQ8
There is an association of celiac disease and other immune diseases including
type 1 diabetes, thyroiditis, Sjogren syndrome as well as ataxia, autism, depression, some forms of epilepsy, IgA nephropathy, Down and Turner syndrome
Most common celiac disease associated cancers
enteropathy associated T cell lymphoma and small intestine adenocarcinoma
inhibits the secretion of penicillins by competing for active tubular secretion via the organic acid transporter and, thus, can increase blood levels
probenecid
drug is effective against many of the same organisms as penicillin G; therefore, it is used in patients who are allergic to the penicillins.

erythromycin
methylation of an adenine in the 23S bacterial ribosomal RNA causes
a decreased affinity for the 50S ribosomal for macrolides
Interference with the metabolism of drugs such as theophylline and carbamazepine has been reported in
clarithromycin- possibly other macrolides
distributes well to all body fluids except CSF
erythromycin
the antibiotic eliminates a species of intestinal flora that ordinarily inactivates digoxin, thus leading to greater reabsorption of the drug from the enterohepatic circulation
Macrolides
A synthetic progestin employed in combination oral contraceptive preparations is
norgestimate
connective tissue cells in the outermost layer of the follicle that make collagen
theca externa cells
Compared with healthy pregnancies, in cases of pre-eclampsia and miscarriage the ratio of Foxp3(+) Treg to IL-17-expressing CD4(+) T cells is:
A. not significantly different
B. increased
C. decreased




decreased
While vertical transmission can occur at any stage of syphilis, the highest transmission rate occurs in which stage?



secondary stage
The thick colostrum secreted initially after a birth has high concentrations of:
immunoglobulins and lactoferrin
the superior parathyroid glands develop from
endoderm of pharyngeal pouch 4
RL is a 40-year-old male who suffers from Crohn's disease, which is currently in remission. Which of the following dietary recommendations is most appropriate for him at this time?
low fat
persistent lymphocytic infiltrate in liver biopsies > 6 months
definition of chronic viral hepatitis
A common site of obstruction of a ureteral calculus is:
at the intramural passage through the bladder wall
Baby's head stretches cervix
Cervical stretch excites fundic contraction
Fundic contraction pushes baby down and stretches
cervix some more
Cycle repeats over and over again



Theory for the onset of intensely strong contractions during labor
True or false: abdominal contractions
add greatly to the force that causes expulsion of
the baby.

True; Once uterine contractions become strong during labor, pain signals originate both from the uterus itself and from the birth canal. These signals elicit neurogenic reflexes in the spinal cord to the abdominal muscles, causing intense contractions of these muscles.
Besides prolactin, estrogen and progesterone, what hormones are needed for the secretion of milk
insulin, growth hormone, cortisol and parathyroid hormone
Effects of parathyroid hormone
Increased Ca2+ reabsorption in the early distal tubule
Decreased phosphate reabsorption in the proximal tubule
Decrease reclamation of bicarbonate in the proximal tubule
Increases bone resorption
Stimulated by hypocalcemia and hyperphosphatemia



Technetium-99m-sestamibi radionuclide scan

Dx for primary hyperparathyroidism

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