Random Missed Uworld - Week 1 Flashcards
What artery mainly supplies the pelvic organs?
Internal illiac artery
AKA: hypogastric artery
Other arteries branch off:
uterine arteries –> uterus
[note: ovarian a. branches from abdominal aorta]
What artery would supply the perinuem?
internal pudenal branch of the internal illiac artery
Acute promyeocytic leukemia (APL):
What is the chromosomal abnormality?
What does this lead to?
What is a viable treatment?
APL type M3 of AML, results from a t(15;17) –> PMR/RAR fusion gene, which is unable to signal for proper cellular differentiation, unlike normal retinoic acid receptor.
This could present as DIC
TX: all-trans-retinoic-acid (ATRA), which is a vitamin A derivative
Polymyositis
Clinical presentation
Biopsy findings
Lab findings
Related ddx
Clinical Presentation: progressive symmetric proximal muscle weakness
Biopsy Findings: endomysial inflammation with CD8+ T cells
Lab findings: anti-ANA, anti-Jo-1 (anti-histidyl-tRNA-synthetase), anti-Mi-2
Related ddx: dermatomyositis (like poly but with skin presentations as well - malar rash/similar to SLE)
SCID
severe combined immunodeficiency disorder
Etiology
Inheritance
Clinical Features
Tx:
DDX:
Characterized by defective T-cell development and B cell dysfunction
A genetic defect leads to failure of proper T cell development –> absence of T-cells leads to B cell dysfuction.
Inheritance could either be X-linked recessive or autosomal recessive
Recurrent infections - viral, fungal, bacterial and opportunistic! [sinusitis, otitis media, j. joveii infection…]
Failure to thrive
chronic diarrhea
tx: stem cell transpant ONLY (must be done ASAP)
DDX: congenital HIV [failure to thrive + recurrent infections - need to differentiate]
What is the candidal antigen skin test used for?
What are they key cells involved?
To determine the presence of cellular or T-cell mediated immunity through the detection of delayed-type hypersensitivity reaction (type IV)
key cells: macrophages, cytotoxic CD8+ T cells, and CD4+ helper T cells
SCID pt – anergy – no reaction
What are some tumors that can present psammoma bodies histologically? (5)
Meningioma
papillary thyroid carcinoma
mesothelioma
papillary serous CA of the ovary
papillary serous CA of the endometrium
Explain how the clearance of lithium could lead to its side effects seen?
What are some drug interactions?
Mgmt:
Acutely, lithium side effects include: GI upset (V/D) and later neurological findings (excitability, delirium) as it penetrates the CNS
Chronic toxicity, could be due to the way lithium is cleared. Lithium is mostly renally excreted thus anything that decreases glomerular filtration could lead to an increase in reabsorption at the proximal tubule (volume depletion/hyponatremia, CHF, cirrhosis)
These AEs: ataxia, fasiculations, confusion and agitaiton
Drug interactions with: thiazide diuretics, NSAIDS (not aspirin), ACE inhibitors
Mgmt: hemodyalisis for severe cases
Deficiency of what enzyme could lead to propionic acedemia, which presents with poor feeding, vomiting, hypotonia, lethargy, dehydration and anion gap acidosis?
Metabolism of what amino acids (4), would worsen this condition?
Deficiency of propionyl CoA carboxylase prevents the conversion of propionyl CoA to methylmalonyl CoA, which hten leads to propionic acedemia as it accumulates
Metabolism of valine, isoleucine, threonin, methionine results in the initial production of propionyl CoA
VOMIT = valine, odd chain FA, methionine, isoleucine, threonine.
What is isolated systemic hypertension and what are some causes…
Increased systolic BP with normal (<90) diastolic BP
This is mostly seen in the aging population due to increased arterial stiffness –> dec compliance of aorta and major peripheral arteries
Other causes: severe aortic regurg, anemia, hyperthyroidism
Meckel diverticulum is known as the dz of 2’s why? (5)
what is the cause?
Meckel’s diverticulum is a TRUE diverticulum (includes all layers not just mucosa), due to the presistence of the vitelline duct before week 9 –> vitelline cyst/omphalomesenteric duct
It is the most common congenital GI tract anomaly
Can cause: melena, RLQ pain, intussusception, volvulus, obstruction near terminal ileum
Rule of 2’s:
2 in long
2 feet from ileocecal valve
2% of population
commonly presents in the first 2 years of life
May have 2 types of epithelial (gastric / pancreatic)
-called ectopy NOT metaplasia-
What nerve innervates the skin of the pubic region?
iliohypogastric (branches off the L1 never root)
- this nerve also innervates the anteriorlateral abdominal wall muscles and the gluteal region*
(recall: the iliohypogastric artery supplies most of the pelvic organs)
Microorganisms invovled in:
Cat bites (2)
Dog bites (3)
Human bites (3)
Cat bites:
Pasturella multocida (mouse-like odor)
Bartonella Henselae (immunocomp host)
Dog bites:
Pasturella multocida
Strep
Staph A.
Human:
Anarobes
Strep
Eikenella Corrodens
What is ID50 (infectious dose) stand for?
The minimum number of organisms required to cause disease in 50% of the individuals
What is the most common form of male and female baldness?
How is it transmitted?
What is the clinical presentation?
Androgenetic aloplecia is the most common form of battern baldness in both males and females [reason why one of the treatments is 5-alpha reductase as it blocks the conversion to DHT]
It will present with increasing baldness, especially starting in the temporal and vertex, but the pattern and severity will depend on both circulating HORMONES and GENETICS
This condition is POLYGENIC inheritance with VARIABLE EXPRESSIVITY
Other dz that are polygenic:
androgenic aloplecia
schizophrenia
DM II
Epilepsy
HTN
glaucoma
Ischemic heart disease
How is cystic fibrosis diagnosed in a newborn?
What symptomatic electrolyte imbalance can this lead to?
What is a recommended supplementation?
It is screened for, but positive results should be confirmed with a sweat test - it will be ISOTONIC to ECF
Normally, as the sweat travels through the duct, Cl- will be absorbed, followed by Na+ and H20 –> hypotonic sweat; CF patients are not able to do this, thus their sweat would be high in sodium and chloride
–> hyponatremia (excessive loss)
RF: high temperatures, exercise
Salt supplemenation is recommended
What effect do alpha-adrenergic agonist have on systemic blood pressure and heart rate?
On visera?
alpha-adrenergic agonist increase systemic BP by stimulating adrenergic 1 receptors of the vascular walls, which –> vasoconstriction
This, effectively, will stimulate baroreceptors located in the carotid sinus and aortic arch –> reflexive vagal stimulation that will inhibit SA node, slow conudction of AV and overall DEC myocardial contractility / HR
INC cardiac afterload, INC pul cap pressure, INC LVEDP
ON visceral organs: vasoconstriction of renal and splanchnic arteries –> DEC perfusion to kidney and other visceral organs
What anti-hypertensive medication is recommended for heart failure patients due to their additional, independent protective factor in the prevention of deleterious cardiac remodeling? (2 categories)
ACE inhibitors
Angiotension II Receptor Blockers
[others: diuretics for symptomatic relief, but no long-term benefits; beta-blockers for compensated HF - contraindicated for cardiogenic shock and should be used with caution in decompensated HF]
What is phenytoin used for?
What is a common side effect?
What are common AEs?
anti-convulsive, used for grand-mal seizures, status epilepticus and partial seizures
Common side effect: gingival hyperplasia (also seen in calcium channel blockers), others include coarsing facial features and hirtuism
AEs: inteferes with folic acid, and can cause megaloblastic anemia;
contraindicated in preg, CNS manifestations such as ataxia and nystagmus,
Lateral epicondyle serves as the primary attachment for what muscle?
What is the function of this muscle?
What injury is frequently seen here?
Extensor Carpi Radialis Brevis and Extensor Digitorum
involved in wrist extension
overuse –> microtrauma –> angiofibroblastic tendonitis@ its insertion point –> lateral epicondyilitis = tennis elbow
What are the three major types of vaginitis:
For each - major examination findings, lab dx, tx
1. Bacterial Vaginosis (Gardnerella vag)
off-white, fishy order with no inflammation; clue cells, positive whiff test with KOH, >pH; tx with metronidazole or clindamycin
2. Trichomoniasis (trichomonas vaginalis)
thin yellow-green, malodorous frothy discharge w/inflammation; motile trichomonadas, >pH; tx with metronidazole and treat partner
3. Candida vaginitis (candidia albicans)
thick, cottage-cheese discharge, vag inflmmation; pseduhyphae with nl pH (3.8-4.5); tx with fluconazole
The method of “matching” is used in what type of studies most frequently to control what type of bias?
In case-control studies, matching is used to try to pair similar patients in the case group with the population of the control group. This tries to address the issue of confounding factors.
The matching factors should try to address potential confounding factors such as age, race, socioeconomic, smoking status, environmental…
an example) colorectal CA patients are the cases, and their neighbors are selected for the control, trying to match age, race, socioeconomic factors, environment; controls are choosen to match the variables of the case patients.
What allows for elastin’s elastic properties, especially during inspiration?
What dz impairs this property of elastin?
extensive cross-linking between elastin monomers, which is facilitated by lysyl oxidase
alpha-1-antitrypsin –> excessive alveolar elastin dedegration due to a protease inhibitor deficiency, thus can lead to early-onset of lower-lobe predominent emphysema
- leads to PANACINAR emphysema
What makes ribosomal RNA?
Where does synthesis occur (describe this location).
What is one clinical significant of being able to visualize a nucleolus?
Ribosomal RNA is made by RNA POL I
Synthesis, assembly and maturation of ribosomal subunit occurs in the NUCLEOLUS
Usually, increasingly differentiated cells have a smaller nucleolus since less ribosomes are needed for protein production BUT in MALIGNANT CELLS, high metabolic activity usually have a large number of active rRNA genes and a PROMINENT NUCELOUS (basophili/dark!)
Obstructive lung disease is characterized by …(lung volumes)
What are causes of obstructive lung disease (2):
complications..
Obstruction of air flow –> air trapping in the lungs/airways close prematurely at high lung volumes =
INC RV
DEC FVC
PFTs: DEC FEV1, DEC FVC – DEC FEV1/FVC ratio, V/Q mismatch
Examples:
- anatomical obstruction, such as chronic bronchitis, where hyperplasia of mucus-secreting glands in bronchi, anatomically decrease the amt of air that is able to leave the lungs
- blue bloater*
- DEC in lung wall elasticity, such as in emphysema, due to destruction of interalveolar wall –> compression during expiration, and unable to breath air out
- barrel-shaped chest, pink puffer*
Sarcoidoisis:
What are hallmark clinical presentation
What can be seen in imaging
what can be seen in labratory
Hallmark for sarcoidosis: young, African-american female, presenting with SOB, cough, chest pain, UVEITIS, skin lesions, lofgren syndrome (acute presentation: bilateral hilar adenopathy, erythema nodosum, polyathralgia/polyarthritis)
Imaging: bilateral hilar adenopathy, pulmonary reticular infiltrates
Labs: INC ACE, INC Ca2+
non-caseating granulomas (high presence of T-lymphocytes CD4+)
What is Kartagener Syndrome?
What are the consolation of clinical pres?
What is its caused by?
it is a form of PRIMARY CILLIARY DYSKINESIA [dynein arm defect affecting cilia function]
Clinical pres: Sinus Invertus, chronic sinusitus, bronchiectasis [due to impaired mucociliary clearance], infertility
Occurs due to mutations that impairs the structure or function of cilia
Inheritance is auto recessive via wide variety of mutations
What effect would hypOventilation have on PCO2?
less breathing = holding PCO2 in = INCREASED levels of PC02
more breathing = more expelling = DEC CO2 levels (ie- panic attack)
If it is acute process (such as heroin overdose), then there will be uncompensated respiratory acidosis:
HI PCO2, low pH (nl: 7.35-7.45), nl to mildly elevated bicarb (renal compensation requires at least 24 hours of persistent respiratory acidosis)
What microtubules are associted with the establishment and recurrence of hereps infection?
Dynein, responsible for retrograde travel (+ –> -) helps ESTABLISH infection (goes towards cell body)
Kinesin, responsible for antegrade travel (- –> +) helps infection REOCCUR, taking the virus back to the skin surface
What can the sensitivity and specificity of a test help you determine?
Sensitivity = how likely a person WITH a disease will test positive [less chance of false negative, correctly identifies those with a disease]
Specificity = how likely a person WITHOUT a disease will test negative [less chance of false positives, correctly identifies ppl without dz]
Remember: SNOUT and SPIN
SeNsitiivty helps you rule OUT a dz
SPecificity helps you rule IN a dz
What is the filtration fraction equation of the kidney?
FF = GFR / RPF
Renal plasma flow could be determined from the renal blood flow via, RPF = (renal blood flow)* (1-hematocrit)
Expression cloning is similar to southerwestern blot; how does expression cloning function, and what types of molecules can it detect?
Both are used to detect DNA-binding proteins
examples include: transcription factors, steroids, thyroid proteins, vitamin D receptor, retinoic acid R, DNA transcription and replication proteins, etc…
expression cloning is a type of DNA cloning, where the signal for translation and transcription are included in the clone portion; allows for the use of bacteria in the process as a mRNA is able to be made into a cDNA which then can be inserted in a plasmid, made and then identified using a DNA probe.
Which cytokine is needed for isotype change?
IgM –> IgE or IgG requires IL- 4
switch to IgA requires IL-5
remember: HOT T-BONE stEeAK
IL 1- fever (hot, )
IL 2- (stimulates T cells - helper, cytotoxic, regulatory)
IL 3- stimualtes bone marrow growth and differentiation
IL 4 - induces differentiation of TH0-TH2, promotes growth of B cells and enhances class switch to IgG and IgE
IL 5 - promotes differentiation of B cells. Enhances class swith to IgA stimulates growth and differentiation of eosinophils
IL 6 - stimulates aKute phase protein production, and fever
What are 4 drugs with low therapeutic index that we need to be careful with:
digoxin
lithium
theophylline
warfarin
“THE WAR Does Last”
What are some signs of sickle cell disease
recurrent episodes of anemia, jaudice and painful swelling of the hands and feet
Autosomal Recessive inheritance
What causes gout and what are some of the dz etiology?
Gout is caused by tissue deposition of monosodium urate crystals
Elevated uric acid levels are a known risk factor for gout
-one thing that could cause hyperuricimia, in via increased purine metabolism
PRPP synthease is the enzyme resposible for the activated ribose needed to make de novo synthesis of purine and pyramidine nucleotides
What are the structures are retroperitoneal?
Which ones are secondary retroperitoneal?
SAD PUCKER:
S: suprarenal/adrenal glands
A: aorta and IVC
D: duodenum (2nd and 3rd part only)
P: Pancreas (minus tail)
U: Ureters
C: Colon (desending and ascending)
K: Kidneys
E: Esophagus (thoracic portion)
R: Rectum (partially)
Secondary means that they are originally suspended in the mesentary then move to the retroperitoneal space
What is the equation of odds ratio?
In a standard table, it is equal to
= AD/BC
(attach image)
Only odds ratio should be used in case-control studies
What occurs during an allergic reaction?
Anaphylactic and atopic reactions are type I hypersensitivity reactions.
Free antigen cross links with IgE on PRE-SENSITIZED mast cells and basophils –> cross links triggers immediate release of vasoactive amines that act POSTcapillary VENULES (histamine, etc)
Reaction is RAPID due to PREFORMED antibody IgEs
Delayed response follows due to production of arachidonic acid metabolites (leukotrinenes)
What are the major types of immune rejection associated with transplant?
What major cell lines are involved?
1. Hyperacute:
within minutes
PRE-EXISTING RECPIENT IgG antibodies react to donor antigen (type II hypersen, activate compliment)
2. Acute:
- weeks - months*
cellular: CD8+ T cells activated against donor MHCs
humoral: type II hypersensitivity (ab develop against donor)
3. Chronic
months to years
CD4 + T cells respond to recipeint APC presenting donor peptides, including allogenic MHC
Both cellular and humoral components
–> proliferation of vascular smooth muscle and parenchymal fibrosis; dominated by arteriosclerosis
4. Graft versus host disease
varies
GRAFTED immunocomponent T cells proliferate in the immunocompromised host and reject host cells with foreign proteins
How can the renal excretion of a substance be determined?
Excretion = total filtration - total tubular reabsorption
total filtration = GFR * [plasma]
inulin clearance could be used to estimate GFR
- Creatinine could also be used BUT it will be slightly over estimated since, creatinine is moderately secreted by the renal tubules*
- FF = GFRXRPF –> GFR = RPF/FF*
What is the flow of CSF in the brain?
CSF is made in 4 choroid plexus found in each ventricle
Choroid plexus is made of epedymal covered out growths of pia, they are fenestarted and act as teh CSF/Brain barrier
Lateral ventricles, via the foramen of Monroe –> third ventricle, then via the cerebral aqueduct of Sylvus –> 4th ventricle –> subarachnoid space via 3 openings (2 lateral foramen of luschka or foramen of Magendie)
CSF is then returned to the venous circulation via arachnoid villi (granulations)
In Pellegra, Niacin is deficient –> Dementia, diarrhea, dermatitis.
How can niacin be produced endogenously?
Niacin is either obtained through dietary intake or endogenously made by TRYPTOPHAN
Deficient state:
In developing countries: in communities where corn is the staple food (niacin is bound and not absorable)
In devloped countries: nutritional deficiency states such as alcoholics, chronic illness; also in those with carcinoid syndrome, prolong isonizaid therapy, Hartnup dz
When are erythropoeiten agents recommended to use?
What is a potential side effect of their use?
They are recommended for use with anemia related to chronic kidney disease; reduce the need for blood transfusions and the complications that could lead to prolong anemia [cardiac dysfunction, weakness, mental status changes…]
However, they could an increase in the viscosity of the blood which can lead to thromboembolic events* (vascular graft thrombosis, stroke..); also could lead to *increase of blood pressure, due to possible activation of erythropoeitin receptors on the walls of vascular endothelium and smooth muscle
What are the 3 ddx for urinary incontience:
main sx and main cause?
1. INC stress - loss of urethra support and inc intraabdominal pressure > sphincter pressure –> leakage with laughter, cough, sneezing, etc
2. Urge - detrussor overactivity –> sudden, overwhelming and frequent need to empty bladder (could be due to MS! lose CNS inhibition of micturition
3. Overflow - impaired detrussor contractility or obstruction at bladder outlet –> involuntary dribbling of urine and incomplete emptying
People with down’s are at an increased risk for what 2 cancers?
Acute myelogenous lekemia/acute megakaryoblastic leukemia (before 5 y/o -m for mini)
Acute lymphoblastic leukemia (usually after 5y/o)
What are some risk factors for osteoporotic bone fractures? (10)
advancing age
female
white, hispanic, asian (AA women have increased bone density and thus decrease risk!) - LOW bone density
personal/family hx of fractures
decreased physical activity
low BMI
poor calcium and vitamin D intake
excessive alcohol and tobacco use
premature menopause
glucocorticoid, anticonvulsant, anticoag, thyroid replacement meds
What is first line treatment for generalized anxiety disorder?
cognitive behavioral therapy
SSRI, SNRI
benzos are second line, not recommended for chronic anxiety disorder, could be used temporarily while SNRI/SSRI kick in, but are contraindicated in pt with a history of substance abuse
What are common signs and symptoms of primary biliary cirrhosis?
PBC is an autoimmune destruction of intrahepatic bile ducts and interlobules,
typically, it is middle aged women, presenting with fatigue, prutitis, jaundice, (pancreatic type of sx) + XANTHOMAS
increased inflammation, granulommas and increased lymphocyte infiltration
+ANA, and many times associated with other autoimmune conditions
T. solium
dz and presentation
Pork tapeworm
neurocyticercosis
endemic in south and central america
presents with seizures and cystic brain lesions in immunocompenent patients,
transmitted via ingestion of eggs in stool from infected individuals in infected undercooked pork
what type of symptoms could be expected with occlusions to the middle cerebral artery?
in MCA occlusions, we could expect CONTRALATERAL hemiparesis* and *hemisensory loss involving the face and upper limb
If the occlusion were to occur in the dominant hemisphere (usually left), we can possible also see expressive and receptive aphasia due to infraction of broca’s and wernike’s areas. Speech areas are usually located in the dominant side of the brain
Which is the polymerase that has 5’ –> 3’ exonuclease activity?
what is the significance of this?
DNA polymerase I is the only one that has this ability - thus it can descise RNA primers and replace them with DNA during DNA replication
What are red neurons and when can we expect to see them after an ischemic event?
12- 24 hours after irreversible ischemic damage
neurons containing:
esinophilic cytoplasm
pyknotic nucleus/shrunken and basophilic
loss of Nissl substance
What does the normal jugular venous pulse encompass?
3 positive waves: a, c and v
2 negative waves: x and y
a = right atrial contraction (absent in a. fib)
c = bulging tricuspid into right atrium during right ventricular contraction/systole
x = R atrial relaxation
v = continued inflow of venous blood
y= passive emptying of r. atrium after tricuspid valve opening / abrupt decrease in pressure
What CT findings would be suggestive of Constrictive pericarditis?
The patient would show what symptoms?
Causes?
Contrast with hypertrophic cardiomyopathy heart on CT:
Thickening and calcification of the pericardium
slow and progressive dyspnea, chronic edema and ascites
On the jugular venous pressure tracing, you would get a rapid Y descent that becomes deepr and steeper with inspiration
Causes: radiation to the chest, cardiac surgery and tuberculosis [key: pt immigrating from an area TB endemic!]
Contrast with hypertrophic cardiomyopathy heart on CT: dyspnea and changes to the jugular pressure wave, prominent a wave - CT will not show thickening or calcification of the pericardium (could show thickening of the interventricular space)
In ischemic heart disease - you might see calcifications of the coronary arteries and aorta
What are the biochemical change that occur in early ischemic injury?
Major early biochemical change is cessation of a_erobic glycolysis_ and initiation of anaerobic glycolysis…this occurs within minutes, so almost immediately/60seconds, the affected portion of the myocardium stops contracting
–> stunned myocardiocytes
you will get depletion of ATP, and INC ADP, AMP and adenosine, INC of lactate..adenosine can leak out of the cell and act as a vasodilator to help meet demand
ischemia less than 30 minutes causes REVERSIBLE changes, the myocardium will return to normal hours - days
Ischemia > 30 minutes –> IRREVERSIBLE injry
What is the action of opiates, and what are some side effects?
Morphine (one type of opiate), binds mu receptors, as an agonist
modulates the synpatic transmission, by opening K+ channels and closing Ca2+ channels –> decrease synaptic transmission
–> inhibits release of Ach, NE, 5HT, glutamate and substance P
by acting on mu R in the gut - it could cause constipation; could also cause smooth muscle contraction at the Sphincter of Oddi –> spasms and increase in common bile duct pressures, rarely leading to biliary colic
What requirement is needed to refer a patient to hospice?
survival prognosis of < 6 months WITH advanced metastatic cancers or terminal illness
requires documentation proving irreversible decline in clinical and functional status
focuses on comfort and quality of life, with multidisciplinary team, within various different settings (home, nursing, specialized)
What is the significance of the absence of a biceps reflex?
Reflex should activate biceps brachi tendon that passes through the cubital fossa –> activates the muscle receptors that communicate via the musculocutaneous nerve with lower motor neurons in the anterior horn of C5-C6
C5-C6 also control the brachioradialis reflex
Stronger reflex?? Upper motor neuron lesion
Absent/weak reflex?? lower motor neuron @ spinal cord
What nerve groups mediate the triceps reflex?
C7 and C8
What do the follwing nerve groups innervate?
C4
C5
C5,C6
C7,
C8
T1
C4 - shoulder/scapula elevation
C5- shoulder abduction
C5,C6 - elbow flexion, wrist extension
C7 - elbow extension, finger extension
C8 - wrist flexion, finger flexion
T1 - finger abduction
Acute mesenteric ischemia could lead to inadequate oxygen delivery to intestinal tissues
DEC oxygen –> affects metabolic fate of pyruvate during glycolysis; low oxygen means it can’t go into TCA, why does this occur?
Usually, with oxygen, pyruvate preferentially converts to acteyl coA by pyruvate dehydrogenase
then acetyl coA could enter the mitocondria and udnergo TCA
Under HYPOXIC conditions, there is intracellular accumulation of *_NADH*_ –> inhibits pyruvate dehydrogenase; and thus increased pyruvate –> LACTATE by lactate dehydrogenase
This allows the regeneration of NAD+, from NADH, which allows for anaerobic glycolysis to continue.
With significant tissue ishcemia, lactate begins to accumulate in the circulation –> lactic acidosis
SX: hyperventilation (try to eliminate CO2), via induced compensatory respiratory alkalosis
How can one contract enterohemorrhagic E.Coli 0157:H7?
Sx and complications?
Mxn of pathogenesis?
Distinguishing features
undercooked groud beef
Could cause bloody diarrhea, and lead to hemolytic-uremic sydrome (HUS)
Elaborates a Shiga-Like toxin (phage encoded) capable of inhibiting protein synthesis in colonic mucosal cells and renal endothelial cells
production enhanced by iron deficiency
INACTIVATE 60S ribosomal subunit –> inhibition of protein synthesis and eventual cell death
UNABLE to ferment SORBITOL
DOES NOT PRODUCE GLUCORONIDASE
Unlike enteroinvasive Ecoli, EHEC doesNOT invade intestinal mucosa
Unlike enterotoxigenic E coli (ETEC), ehec does NOT produce health labile toxin or heat-stable toxin
Name the toxin and MXN of path:
Bacillus anthracis
Anthrax EXOtoxin
–> Edema Factor (EF) and lethal factor (LF)
Edema factor INC cyclic AMP concentration by acting as an adenylate cycalse, causing edema and phagocyte dysfunction
Lethal factor - ZINC depenent protease that inhibits mitogen activates protein kinase signaling, causing apoptosis and mutli-sys physiologic disruption
Name the toxin and MXN of path:
Bordetella pertussis
Pertusssis toxin and Adenylate cyclase toxin
Pertussis toxin: disinhibits adenyl cycalse through G1 ADP=ribosylation, increasing cyclic AMP levels
causes edema and phagocyte dysfunction
Adenylate cycalse toxin: functions as an adenylate cycalse, increasing cyclic AMP levels, causes edema and phagocyte dysfunction
Name the toxin and MXN of path:
Clostridium botulinum
Botulinum toxin
Blocks PREsynpatic release of acetylcholine at the neuromucular junction, resulitng in flaccid paralysis
Name the toxin and MXN of path:
Clostridium difficile
Toxin A and Toxin B
Toxin A- recruits and activates neutrophils, leading to release of cytokines that causes mucosal inflammation, fluid loss and diarrhea
Toxin B- induces actin depolymerization, leading to mucosal cell death, bowel wall necrosis and pseudomembrane formation
Name the toxin and MXN of path:
Shingella dysenteriae
Shiga toxin
Halts protein synthesis by disabling the 60s ribosomal subunit –> intestinal epithelial cell death and diarrhea (bloody)
Name the toxin and MXN of path:
Streptococcus pyogenes
Pyrogenic exotoxin, Streptolysin O and S, DNAse
Pyrogenic exotoxin- acts as a superantigen, inducing fever and shock. associated with scarlet fever, stretococcal toxic shock syndrome
Streptolysin O and S- damages erythrocyte membranes, causing beta-hemolysis
What are the functions of the different types of interferon produced during infection?
(alpha, beta, gamma)
Type I interferons (alpha and beta) - synthesized by most human cells in response to viral infections, bind type I interferon receptors found on infected and neighobring cells and act via autocrine and paracrine signaling.
–> transcription of antiviral enzymes capable of halting protein synthesis (RNase L, endonucelase that degrades all RNA in the cell) and protein kinse R (incativates eIF-2, inhibiting translation intiation).
_Enzymes become active ONLY in the presence of DS-RNA (_forms in the infected cell as a result of viral replication = selectively inhibit virally infected cells
Increase expression of MHC class I on all cells and stimualte NK and cytotoxic T cells
Type II Inteferon gamma- mainly produced by T cells and NK cells; promoate Th1 differentiation, increases expression of class II MHC molecules on antigen presenting cells, and improves the intracellular killing ability of macrophages
[virally infected cells secrete interferon a and B NOT gamma]
Trisomy 18:
Name the syndrome
Common sx
prognosis
Trisomy 18 = Edwards Syndrome
complete or partical extra copy of chromosome 18, inhertited as a meiotic nondisjunction
error in oocyte divison occurs prior to ovulation and fertilization and increases with material age >35
sx: micrognathia, low-set ears, prominent occiput, rocker bottom feet, clenched hands with overlapping fingers, (at 18 you’re able to rock out!) cardia anomalies (ASD, VSD), genitourinary defects (horeshoe kidney), gastrointestinal defects (omphacelocele, meckel’s diverticulum, malrotation), mental retardation
prenatal US findings = fetal growth restrictions
Majority affected die in utero, half of life births die before age of 2 weeks, suriving pt have severe intellectual disabilties
What are signs of gastric cancer?
Metastasis to ovaries is called what? what could be seen histologically?
unintential weight loos, early satiety - signs for malignantcy
+ epigastric pain and gastric thickening on CT
+ abdominal pressure and adnexal mass
suggestive of gastric and ovarian invovlement
Krukenberg tumor
= primary gastricCA that has metastasized to the ovary
histo: nets of signet ring cells, appearance due to a large amounts of mucin displacing the nucleus
What are circumstances in which minors do not require consent?
Who are emancipated minors?
Emergency care
STI, contraception
substance abuse (most states)
prenatal care (most states)
Emancipated minors - do NOT need parental consent for medical treatment of any kind
homeless, are a parent, married, military, financially independent, high school graduate
VIPoma =?
What sx could this lead to/name the syndrome
VIPoma is a pancreatic islet cell tumor, with excess vasoactive intestinal peptide (VIP) secretion
–> WATERY diarrhea, hypokalemia, achlorhydria syndrome [=WDHA syndrome, pancreatic chloera]
VIP –> stimulates pancreatic bicar and chloride secretion, binding to intestinal epithelial cells –> adenylate cyclase activation* and *increased cyclic AMP production, causing sodium, chloride and water secretion into the bowel (secretory watery diarrhea often >3L/day)
somatostain decreases production of many GI hormones; thus inhibits VIP production.
CCK?
–> INC of pancreatic enzymes and bicarbonate, gallbladder contraction and inhibition of gastric emptying
DOES NOT cause WHDA syndrome
produced by I cells of the proximal small bowel mucosa in response to fatty acids and amino acids
Myasthenia gravis:
what are the first symptoms
What are the common underlying etiologies
muscle weakness, with extraocular muscles most commonly affected; pt often experience ptosis and diplopia – muscle weakness worsens with activity and pt often note that their sx are worse at the end of the day
Most have found to have a thymoma or thymic hyperplasia
[thymus is derived from the THIRD PHARYGEAL POUCH as are the inferior parathyroid gland]
What is the structure of a case-control study?
What is typically measured?
People with diseaes of interest (cases) and people without the disease (control) asked about previous exposure to the varibale being studied.
The main measure of association is the exposure odds ratio = what is the odd for someone to have the disease with expsoure vs without exposure
What are gram negative rods that are non-lactose fermenters?
Shigella (no H2S production )
Salmonella and proteus (H2s production)
Pesudomonas aerugionos (ox positive)
“Shig, Sal, and Ari protest lactose”
E coli and Enterobactr cloaecae are both common causes of UTI in women,
what is one distinguishing feature?
Both are gram negative rods that are fast fermenters of lactose (pink colonies)
One distinguishing feature is that E. Coli indole positive = ability to covert tryptophan to indole
All pancreatic enzymes (except amylase and lipase) are synthesized and secreted in an incative form to protect the pancreas from autodigestion (zymogens)
what are some protective mechanisms in place to limit the amount of trypsinogen that becomes prematurely activates
If this is disrupted, what could this lead to?
Trypsinogen –> trypsin (via duodenal enterokinase) –> activate all the other proenzymes and other trypsinogens thus a small amount of activated trypsin can result in an activation cascade
Serine peptidase inhibitor Kazal type 1 (Spink1)
trypsin itself can be its own inhibitor by cleaving other trypsin molecules and rendering them inactive = critical to prevent large amounts of trypsin from forming within pancreatic tissue
–> pancreatitis!
hereditary pancreatitis is a rare disorder that results from mutations invovling the trypsinogen or SPINK1 genes –> pancreatic autodigestion
