Must Knows and Reminders Flashcards
AB exotoxin bacteria
ABCDES
Pseudomonas Aeruginosa Bordetella pertussis Cholera, Clostridia Diphtheria E. coli Shigella
P. aeruginosa
[Exotoxin, MOA]
Exotoxin A.
>Inhibits EF-2 (elongation factor) – inhibits protein synthesis – host cell death, necrosis
B. pertussis
[Exotoxin, MOA]
Pertussis toxin.
>Inhibits Gi – overactivates adenylyl cyclase – inc. cAMP – phagocyte dysfxn
V. cholera
[Exotoxin, MOA]
Cholera toxin.
>Overactivates adenylate cyclase – inc. cAMP – activates CFTR – inc. Cl- secretion, H20 secretion – “Rice water” diarrhea
C. botulinum
[Exotoxin, MOA]
Botulinum toxin.
>Protease that cleaves SNAREs – prevents ACh release into NMJ – flaccid paralysis
C. tetani
[Exotoxin, MOA]
Tetanospasmin.
>Protease that cleaves SNAREs – prevents GABA/glycine release into spinal cord – spastic paralysis
C. diphtheriae
[Exotoxin, MOA]
Diphtheria toxin.
>Inhibits EF-2 (elongation factor) – inhibits protein synthesis – pseudomembranous pharyngitis
Enterotoxic E. coli (ETEC)
[Exotoxin, MOA]
Labile toxin.
>Overactivates adenylyl cyclase – inc. cAMP – activates CFTR – inc. Cl- secretion, H2O secretion – watery diarrhea.
>Similar to cholera
Enterohemorrhagic E. coli (EHEC)
[Exotoxin, MOA]
Shigella-like toxin (SLT; verotoxin).
>Inhibits 60s ribosomal subunit – inhibits protein synthesis, inc. cytokine release – bloody diarrhea (HUS).
>Similar to Shigella, but doesn’t invade host cell
Shigella
[Exotoxin, MOA]
Shigella toxin.
>Inhibits 60s ribosomal subunit – inhibits protein synthesis, inc. cytokine release – damages gut epithelium – bloody diarrhea (HUS)
ABC carboxylase (3)
ATP, Biotin, CO2.
>Pyruvate carboxylase (gluconeogenesis).
>Acetyl-CoA carboxylase (FA synthesis).
>Propionyl-CoA carboxylase.
TLCFN dehydrogenase (3)
Thiamine, Lipoic acid, CoA, FAD+, NAD+.
>Pyruvate dehydrogenase.
>a-ketoglutarate dehydrogenase.
>Branched chain ketoacid dehydrogenase.
Intracellular organisms
Rickettsia, Chlamydia
Listeria, Legionella, Mycobacteria, Salmonella, Neisseria
Catalase (+)
Cats Need PLACESS
Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E. coli, Staphylococcus, Serratia
Encapsulated organisms (polysaccharide capsule)
S. pneumonia, H. influenzae type B, N. meningitidis, E. coli, Salmonella, Klebsiella pneumoniae, GBS
Aerobic bacteria
Mycobacteria
Pseudomonas
Nocardia
(have superoxide dismutase)
Anaerobic bacteria
Actinomyces
Bacteroides
Clostridium
Fusobacterium
Chocolate agar.
Selective for what organism?
H. influenzae type B
Has Factor V (NAD+) and X (hematin)
Sabouraud agar.
Selective for what organism?
Fungi
Thayer-Martin agar.
Selective for what organism?
Neisseria
Vancomycin, Trimethoprim, Colistin, Nystatin
Charcoal yeast extract (w/ Cysteine + iron).
For what organism?
Legionella
needs Cysteine
Loffler agar.
For what organism?
C. diphtheriae
Regan-Lowe agar.
For what organism?
B. pertussis
Charcoal, blood, antibiotics
Lowenstein-Jensen agar.
For what organism?
Mycobacteria
Eaton agar.
For what organism?
Mycoplasma
Tellurite agar.
For what organism?
C. diphtheriae
Bordet-Gengou agar.
For what organism?
B. pertussis
Potato
MacConkey agar.
For what organisms?
Lactose fermenters (pink) E. coli, Klebsiella
Poor gram staining bugs
Treponemia Mycobactera Mycoplasma Legionella Rickettsia Chlamydia
Biofilm producers
S. epidermidis – prosthetic devices, IV catheters
Viridans strep – dental carries, endocarditis
P. aeruginosa – Pneumonia, CF, contacts
H. influenzae – otitis media, other mucosal infxns
DNA viruses
HHAPPPPy
Hepadna Herpes Adeno Pox Parvo Papilloma Polyoma
DNA virus properties
> dsDNA (except Parvo – ssDNA).
Linear (except Papilloma, Polyoma, hepadna – circular).
Icosahedral (except Pox).
Replicates in nucleus (except Pox).
Naked viruses
> DNA: Parvo, Adeno, Papilloma, Polyoma
>RNA: Calici, Picorna, Reovirus, Hepevirus
(+) RNA viruses
Calici, Corona
Retro, Toga
Flavi, Hepe, Picorna
(-) RNA viruses
Always Bring Polymerase Or Fail Replication
Arena, Bunya
Paramyxo, Orthomyxo
Filo, Rhabdo
Segmented RNA viruses
ROBA parts
Reovirus
Orthomyxo
Bunya
Arena
Reoviruses
Rotavirus (fatal diarrhea in kids)
Coltivirus
Picornaviruses
>Poliovirus (Sabin, Salk) >Echovirus - aseptic meningitis >Rhinovirus - common cold >Coxsackievirus - hand-foot-mouth dse, aseptic meningitis. >HAV
Hepevirus
HEV
Calicivirus
Norovirus - viral gastroenteritis
Flaviviruses
HCV Yellow fever Dengue West nile virus St. Louis encephalitis
Togavirus
Rubella
Easter/Western equine encephalitis
Retroviruses
HIV - AIDs (lentivirus)
HTLV - T cell leukemia (oncovirus)
Have reverse transcriptase
Coronavirus
Coronavirus - common cold
SARS
Orthomyxoviruses
Influenza virus
Paramyxoviruses
> Parainfluenza - croup
RSV - bronchiolitis in babies
Measles, Mumps
Rhabdovirus
Rabies
Filoviruses
Ebola/Marburg hemorrhagic fever
Arenaviruses
> LCMV - lymphocytic choriomeningitis virus
>Lassa fever encephalitis
Bunyavirus
> California encephalitis
Sandfly/Rift Valley fevers
Crimean-Congo hemorrhagic fever
Hantavirus - hemorrhagic fever, pneumonia
Delta virus
Defective virus – needs HBV to replicate
IL-1
Secreted by macrophages.
Acute inflammation.
Fever.
Recruits WBCs.
IL-6
Secreted by macrophages.
Acute phase reactant prodn.
IL-8
Secreted by macrophages.
Neutrophil chemotactic.
IL-12
Secreted by macrophages.
Th1 differentiation.
Activated NK cells.
TNF-alpha
Secreted by macrophages.
Mediates septic shock.
WBC recruitment, vascular leak.
IL-2
Secreted by T cells.
T cell growth.
IL-3
Secreted by T cells.
Growth and differentiation of BM stem cells.
IFN-gamma
Secreted by Th1 cells.
Stimulates macrophages to kill.
Activated NK cells to kill.
IL-4
Secreted by Th2 cells.
Th2 differentiation.
B cell growth – IgE, IgG.
IL-5
Secreted by Th2 cells.
B cell diff – IgA.
Eosinophils.
IL-10
Secreted by Th2 cells.
Attenuates immune response, inflammation.
Inhibits macrophages and dendritic cells.
TCR.
What cells? Binds to?
T cells.
Binds Ag-MHC complex
CD28.
What cell? Binds to?
T cells.
Binds to B7 on APCs
CD40L.
What cell? Binds to?
Helper T cells.
Binds to CD40 of B cells
CD21.
What cell? Binds to?
B cells.
Receptor for EBV
CD40.
What cell? Binds to?
B cells.
Binds to CD40L of Helper T cells
MHC II.
What cell? Binds to?
APCs (B cells, macrophages).
Binds to TCR of CD4+ T cells
B7.
What cell? Binds to?
APCs.
Binds to CD28 on T cells
Fc and C3b receptors.
What cell? Function?
Macrophages.
To enhance phagocytosis
CD4.
What cell?
Helper T cells
CD8.
What cell?
Cytotoxic T cells
CD16.
What cell? Binds to?
NK cells.
Binds to Fc of IgG, for antibody-dependent cell-mediated cytotoxicity.
CD56.
What cell?
Unique marker for NK cells
BCR-ABL.
Tumor?
CML, ALL
BCL-2.
Tumor?
Follicullar lymphoma, undifferentiated lymphoma
BRAF.
Tumor?
Melanoma
Non-hodgkin lymphoma
C-myc.
Tumor?
Burkitt lymphoma
HER2/neu (c-erbB2).
Tumors?
Breast, ovarian, gastric CA
L-myc.
Tumor?
Lung tumor
N-myc.
Tumor?
Neuroblastoma
RAS.
Tumors?
Colon, lung, pancreatic cancer
RET.
Tumors?
MEN 2a, 2b
Medullary thyroid cancer
APC.
Tumor?
Colorectal cancer (FAP)
BRCA1/BRCA2.
Tumor?
Breast, ovarian cancer
NF1, NF2.
Tumors?
Neurofibromatosis type 1 (neurofibromin)
Neurofibromatosis type 2 (Merlin/schwannomin)
p16.
Tumor?
Melanoma
p53.
Tumors?
Most human cancers, Li-Fraumeni
PTEN.
Tumors?
Breast, prostate, endometrial cancers
Rb.
Tumor?
Retinoblastoma, osteocarcinoma
VHL.
Tumor?
Von Hippel-Lindau dse
Renal cell carinoma
TSC1, 2.
Tumor?
Tuberous sclerosis (hamartin; tuberin)
DCC.
Tumor?
Colon cancer
DPC4/SMAD4.
Tumor?
Pancreatic cancer
Cancer screening.
How many cell divisions for early ssx? Purpose of screening? Examples?
At least 30 divisions of a single mutated cell will result in early ssx. Each division has inc. mutations, so poor prognosis if cancer detected late.
>Purpose: 1) detect dysplasia before CA, 2) detect CA before clinical sx arise.
>Examples: pap smear, mammogram, colonoscopy
Psammoma bodies.
Found in what diseases?
>Laminated, concentric spherules w/ dystrophic calcification. >Papillary CA of thyroid. >Serous papillary cystadenoCA of ovary. >Meningioma. >Malignant mesothelioma.
Cholinesterase inhibitor poisoning. (organophosphates: Echothiophate, Malathion, Parathion; Nerve gas Sarin)
DUMBBEELSS
> Irreversibly inhibit AChE.
Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle/CNS, Lacrimation, Sweating, Salivation.
Tx: Atropine + Pralidoxime (regenerates AChE if given early).
Atropine
[Action, SE, Tx]
Muscarinic antagonist; Blocks DUMBBEELSS
>Mydriasis, cycloplegia; Dec. airway secretions; Dec. gastric acid secretion, Dec. peristalsis; Dec. urinary urgency
>SE: inc. body temp (dec. sweating), dry mouth, flushed skin, cycloplegia, disorientation
>Tx: Physostigmine (Neostigmine, Edrophonium)
CYP450 Inducers
Chronic alcohol and Gritty Carbs NevR Stop Phen-Phen
Chronic alcohol use St. John's wort Phenytoin Phenobarbital Rifampin Griseofulvin Carbamazepine Nevirapine
CYP450 Inhibitors
Alcohol abuse and Grapefruit juice RACK QuIMs
Acute alcohol abuse Ritonavir (-avirs) Amiodarone Cimetidine Ketoconazole Sulfonamides INH Grapefruit juice Quinidine Macrolide's (except azithromycin)
CYP450 substrates
Anti-epileptics
Warfarin
Theophylline
OCPs
Sulfa drugs
[Drug names, ssx of sulfa allergies]
Probenecid, Furosemide, Acetazolamide, Celecoxib, Thiazides, Sulfonamides, Sulfasalazine, Sulfonylureas
Sulfa allergies: fever, UTI, SJS, hemolytic anemia, thrombocytopenia, agranulocytosis, urticaria
CAMP factor.
Which bacteria? Function?
> Produced by S. agalactiae (GBS). Enlarges the area of hemolysis formed by S. aureus.
Arrowhead clearing at junction of the 2 organisms)
Culture tests for C. perfringens
> “Stormy fermentation” on milk media.
Double zone of hemolysis.
Nagler reaction on egg yolk agar (opalescence around colonies)
Whipple Triad (of insulinoma)
> Low Blood glucose
Ssx of Hypoglycemia
Ssx disappear w/ normalization of glucose levels
Cushing reflex is the body’s way of maintaining cerebral perfusion in the setting of inc. ICP (brain injury). What are the roles of the chemoreceptors and baroreceptors in this reflex?
> Inc ICP compresses cerebral arteries – cerebral ischemia, inc. PCO2 – chemoreceptors send signals to vasomotor center to inc. peripheral vasoconstriction – inc. CO, inc. MAP (HTN) – more blood to brain, better cerebral perfusion
Reflex Bradycardia due to stimulation of peripheral baroreceptors from increased stretch – signals sent to VMC to dec. HR
What is the cause of decreased, irregular respiration (respiratory depression) in Cushing reflex?
> Reduced perfusion of brainstem from swelling or possible brain herniation (due to inc. ICP) – occurs if condition is not caught early enough. (Central chemoreceptors in medulla oblongata detect pCO2 in brain CSF).
Cushing triad: HTN, bradycardia, respiratory depression
Diagnostic tests for MI
> Gold standard for first 6 hrs: ECG.
Troponin I: rises after 4 hrs, elevated for 7-10 days, specific.
CK-MB: rises after 6-12 hrs, normal after 48 hrs; diagnose reinfarction, nonspecific (skeletal muscle).
Duke’s criteria for Bacterial endocarditis
B.E.F.E.V.R (2 major / 1 major, 3 minor/ 5 minor)
>Major: (+) Blood culture, (+) Endocardial involvement on Echo.
>Minor: Fever > 38C, Vascular phenomenon (Janeway lesions, emboli, infarct), Evidence of micro/immuno findings (Osler nodes, Roth spots), Risk factors.
Jones criteria for Rheumatic Fever
J.O.N.E.S (2 major / 1 major, 2 minor) Joints (migratory polyarthritis) ❤️ (pancarditis) Nodules (Subcutaneous) Erythema marginatum Sydenham chorea >Minor: Fever, arthralgia, inc. acute phase reactants
Aortic stenosis murmur
> Systolic murmur, Crescendo-decrescendo w/ peak mid-systole.
Inc. LV pressure»_space; aortic pressure
“Pluses parvus et trades”: pulses weak w/ delayed peak.
Syncope, Angina, Dyspnea (SAD).
Due to age-related calcification or early-onset calcification of bicuspid aortic valve
Mitral/Tricuspid regurgitation murmur
> Holosystolic, high-pitched “blowing” murmur.
Mitral - apex radiating to axilla, IHD (post-MI), doesn’t usually intensify w/ inspiration.
Tricuspid - tricuspid area radiating to right sternal border, intensifies w/ inspiration
Assctd w/ RF and infective endocarditis.
Mitral valve prolapse murmur
> Late systole; crescendo w/ midsystolic click.
Most frequent valve lesion.
Loudest just before S2, apex.
Predisposes to infective endocarditis.
Caused by myxomatous degeneration, RF, chord rupture.
VSD murmur
Holosystolic, harsh-sounding.
Loudest at tricuspid area.
Aortic regurgitation murmur
> Early diastolic murmur, high-pitched “blowing” murmur.
Hyper dynamic pulse when severe and chronic (head bobbing, bounding pulses).
Due to aortic root dilation, bicuspid aortic valve, endocarditis, RF.
Can progress to left HF
Mitral stenosis murmur
> Diastolic murmur; opening snap ff. by rumbling.
Inc. LA pressure»_space; LV pressure.
Due to RF; Can lead to LA dilatation.
PDA murmur
> Continuous, machine-like.
Loudest at S2, left infraclavicular area.
Due to congenital rubella, prematurity.
High anion gap metabolic acidosis (MUDPILES)
Methanol (formic acid) Uremia DKA Propylene glycol Iron tablets, Isoniazid Lactic acid Ethylene glycol (antifreeze) Salicylates
Normal anion gap metabolic acidosis (HARD-ASS)
Hyperalimentation Addison disease (dec. aldosterone) Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion
Acute PSGN (LM, IF, EM)
> LM: enlarged, hypercellular glomeruli.
IF: “starry sky” granular appearance (Ig, IgM, C3).
EM: sub epithelial IC humps
RPGN (LM, IF)
> LM, IF: crescentic moon shape filled w/ fibrin and plasma proteins
DPGN (LM, EM, IF)
> LM: “wire looping” of capillaries.
EM: subendothelial IgG-based IC deposits.
IF: granular.
IgA nephropathy (LM, EM, IF)
> LM: mesangial proliferation.
EM: mesangial IC deposits.
IF: IgA-based IC deposits in mesangium
Alport syndrome (LM, EM)
LM, EM: thinning and splitting of GBM
MPGN type I (EM, IF, PAS, H and E)
> EM: subendothelial deposits.
IF: granular.
PAS, H and E stains: “tram-track” due to GBM splitting caused by mesangial ingrowth.
MPGN type II (EM findings)
EM: intramembranous deposits, “dense deposits”
FSGS (LM, IF, EM)
> LM: segmental sclerosis, hyalinosis
IF: nonspecific for focal deposits of IgM, C3, C1.
EM: effaced foot processes
MCD (LM, IF, EM)
> LM: normal glomeruli (maybe lipid in PCT cells).
IF: nonspecific deposits.
EM: effaced foot processes
Membranous nephropathy (LM, IF, EM)
> LM: diffuse capillary and GBM thickening.
IF: granular.
EM: “spike and dome” w/ sub epithelial deposits
Amyloidosis nephrotic syndrome (LM findings)
LM: Apple-green birefringence under polarized light w/ congo red stain
Diabetic glomerulonephropathy (LM findings)
LM: GBM thickening, mesangial expansion, Kimmelstiel-Wilson lesions (eosinophilic nodular glomerulosclerosis)
External carotid branches (SALFOPMS, from bottom up)
Superior thyroid artery Ascending pharyngeal artery Lingual artery Facial artery Occipital artery Posterior auricular artery Maxillary artery (terminating branch) Superficial temporal artery (terminating branch)
Process of Ammoniagenesis in PCT cells
> Site for RECLAIMING HCO3 that’s been filtered.
Intracellular CA combines CO2 and H20 into H2CO3 –> dissolves into H+ and HCO3 –> HCO3- reabsorbed while H+ secreted into urine (Na/H antiporter) –> H+ combines w/ urine HCO3 to become H2CO3 –> CA dissolves H2CO3 into CO2 and Water, w/c diffuse back into cell to continue cycle.
HCO3- regenerated and reabsorbed in Collecting ducts
CO2 from renal interstitium diffuses into cell and combines w/ H2O via CA to become H2CO3 –> dissolves into H+ and HCO3- –> HCO3 reabsorbed while H+ secreted (H-ATPase) –> H+ combines w/ acid buffers to be secreted (NH3, PO4).
Renal collecting duct is the primary sign for K+ excretion (Na/K-ATPase) and excretion of excess H+ (H/K-ATPase). How are these channels affected by Aldosterone?
> In principal cells, aldosterone enhances action of ENaC (Na reabsorbed), epithelial K channels (K loss), and N/K pump –> K+ excretion.
In alpha-intercalated cells, aldosterone enhances H/K pump to secrete H+ in exchange for K+. H+ is excreted w/ HPO3 and NH3 as H2PO4 and NH4+.
Pathogenesis of RTA type 1 (distal)
> Inability to regenerate HCO3- due to dysfunctional H/K-ATPase (H out, K in) in collecting tubules – Severe Hypokalemia.
Urine pH > 5.5 (alkaline, dec. titratable acid in urine).
Dec. HCO3, H+ combines w/ Cl- in blood –> Normal anion gab metabolic acidosis.
Causes: amphora, lithium, Sickle cell trait/dse
Pathogenesis of RTA type 2 (proximal)
> Inability of PCT to reclaim HCO3.
Urine is initially at pH > 5.5 (alkaline), but when serum HCO3 finally equals the lowered renal threshold for HCO3 reclamation, the PCT can go back to reclaiming HCO3 and urine pH
Pathogenesis of RTA type 4 (Hyperkalemic)
MC RTA in adults.
>No aldosterone – Na loss, K retention – Hyperkalemia, w/c inhibits ammoniagenesis in PCT – transcellular switch b/w H+ and K+, so K+ enters cell while H+ exits – intracellular alkalosis inhibits ammonia synthesis from glutamine, no generation of HCO3.
>Normal anion gap Metabolic Acidosis.
>Causes: dec. Aldosterone prod (ACEi, ARBs), aldosterone resistance (K-sparing diuretics, nephropathy due to obstruction)
Structures found at vertebral levels T4, T8, T10, T12
> T4: sternal angle of Louis, begin and end of aortic arch, end of superior mediastinum, trachea bifurcates.
T8: IVC.
T10: esophagus, CN X.
T12: aorta, thoracic duct, azygous vein.
What is the mechanism of gastric H+ secretion by gastric parietal cells?
After a meal, CO2 is extracted from the blood and converted, w/ H20, by CA into H+ and HCO3. Activation of parietal cell by Histamine, Gastrin, and ACh stimulates the H/K-pump to secrete the H+ in exchange for K+. The HCO3 is absorbed into bloodstream (“alkaline tide” of venous blood) in exchange for Cl-. Cl- maintains (-) potential of stomach lumen, and Cl- is also secreted w/ H+ to form HCl.
Only monosaccharides are absorbed by enterocytes. What is the transporter for Glucose and Galactose? For Fructose? What transports all monosaccharides in the blood?
> Glucose, Galactose: SGLT1 (Na dependent).
Fructose: GLUT5.
Blood transporter: GLUT2.
What is the D-xylose absorption test? Where is it useful?
D-xylose is a monosaccharide that doesn’t need pancreatic enzymes for digestion before absorption, but requires only intact mucosa. Differentiates GI musoca damage from other causes of malabsorption.
In pancreatic insufficiency, the test has normal absorption w/ normal urinary excretion. If there is an intestinal mucosal defect or bacterial overgrowth, there is dec. excretion due to a problem w/ absorption.
Opioid intoxication ssx
Respi/CNS depression Pupillary constriction (pinpoint pupils) Seizures (overdose)
Opioid withdrawal ssx
Sweating
Dilated pupils
Piloerection
Flu-like ssx (diarrhea, nausea, rhinorrhea, fever)
Amphetamine intoxication ssx
Euphoria, grandiosity Pipillary dilation Prolonged wakefulness and attention HTN, tachycardia Severe: cardiac arrest, seizure
Amphetamine withdrawal ssx
Anhedonia
Hypersomnolence
Existential crisis
Cocaine intoxication ssx
Impaired judgment Pupillary dilation Hallucinations (tactile) Combative, uncooperative Sudden cardiac death (potent vasoconstrictor)
Cociaine withdrawal ssx
Hypersomnolence
Psychological craving
Depression/suicidality
Barbiturate intoxication ssx
Low safety margin
Marked respi depression
Barbiturate withdrawal ssx
Life-threatening cardiovascular collapse
Delirium
BZD intoxication ssx
Greater safety margin vs Barbs
Minor respi depression
Ataxia
BZD withdrawal ssx
Rebound anxiety
Depression
Sleep disturbance
PCP intoxication ssx
Belligerence Impulsivity Homocidality (violent behavior) Psychosis Delirium Nystagmus
LSD intoxication ssx
Perceptual distortion (visual, auditory)
Depersonalization
Possible flashbacks
Marijuana (cannabinoid) intoxication ssx
Euphoria, Paranoid delusions
Perception of slowed time
Conjunctival injection
Hallucinations
Marijuana withdrawal ssx
[peak, detectability]
Depression, Insomnia, Nausea, Anorexia.
Peaks in 48 hours, lasts 5-7 days.
Detectable in urine up to 1 month (stored in lipophilic tissues, slowly released).
What is the antibiotic of choice for treating Lung abscesses?
Clindamycin can cover a combination of anaerobic oral flora (Bacteroides, Fusobacterium, Peptostreptococcus) and aerobic bacteria.
C.R.A.B. of Multiple myeloma
> C: Hypercalcemia (GI ssx).
R: Renal involvement (thirst).
A: Anemia (fatigue, pallor), thrombocytopenia.
B: Bone lytic lesions, Back pain (fractures).
Chromosomal translocations: Burkitt lymphoma, CML, Mantle cell lymphoma, Follicular lymphoma, AML-M3
> Burkitt lymphoma: t(8;14), c-myc activation.
CML: t(9;22) Philadelphia chromosome, BCR-ABL hybrid.
Mantle cell lymphoma: t(11;14), cyclin D1 activation.
Follicular lymphoma: t(14;18), Bcl-2 activation.
AML-M3: t(15;17)
Dermatomes: C2, C3, C4, T4, T7, T10, L1, L4
>C2: posterior skull >C3: neck (turtleneck) >C4: low collar >T4: nipple line >T7: xiphoid >T10: umbilicus >L1: inguinal ligament >L4: kneecap
Clinical reflexes: biceps, triceps, patella, achilles, anal wink, cremaster
>Achilles: S1, S2 >Patella: L3, L4 >Biceps: C5, C6 >Triceps: C7, C8 >Anal wink: S3, S4 >Cremaster: L1, L2
Describe the regulation of iron absorption.
> Dec. iron stores: upregulate DMT, ferroportin; dec. liver hepcidin secretion – DMT absorbs Fe from gut lumen, ferroportin releases Fe into blood – transferrin transports Fe to liver and marrow.
Inc. iron stores: DMT downregulated, liver releases hepcidin w/c degrades ferroportin.
