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OriginalAlphabetical Diabetic neuropathy symptoms Numbness and tingling of extremities Dysesthesia (abnormal sensation to a body part) Diarrhea Erectile dysfunction Urinary incontinence (loss of bladder control) Facial, mouth and eyelid drooping Vision changes Dizziness Muscle weakness Difficulty swallowing Speech impairment Fasciculation (muscle contractions) Anorgasmia *Burning or electric pain* Glipizide Second generation sulfonylurea Close K+ channel in β-cell membrane, so cell depolarizes → + triggering of insulin release via ↑ Ca2+ influx. Stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type 1 DM Toxicity: Hypoglycemia NF-κB Activation occurs when it's inhibitor, I- κB, is phosphorylated by specific protein kinase (IKK) & degraded

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OriginalAlphabeticalDiabetic neuropathy symptomsNumbness and tingling of extremitiesDysesthesia (abnormal sensation to a body part)DiarrheaErectile dysfunctionUrinary incontinence (loss of bladder control)Facial, mouth and eyelid droopingVision changesDizzinessMuscle weaknessDifficulty swallowingSpeech impairmentFasciculation (muscle contractions)Anorgasmia*Burning or electric pain*GlipizideSecond generation sulfonylurea

Close K+ channel in -cell membrane, so cell depolarizes + triggering of insulin release via Ca2+ influx.

Stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type 1 DM

Toxicity: HypoglycemiaNF-BActivation occurs when it's inhibitor, I-B, is phosphorylated by specific protein kinase (IKK) & degraded-Leads to synthesis of prostaglandins and leukotrienesIBReleases NF-B after undergoing phosphorylationInsulin secretion1. Glucose binds Glut2 receptor on -cells2. Glucose oxidizes to ATP closes K channels in cell membrane depolarization of -cells3. Depolerizatino opens Ca channels intracellular [Ca] [name of this card]GlucokinaseLiver and cells of pancreasLow affinity (High Km), high capacity (High Vm)Induced by insulin

It's a *glu*ton has high Vmax b/c it can't be satisfied

At low glucose concentration, hexokinase sequesters glucose in the tissues.Ah high glucose concentration, excess glucose is stored in the liverGlucose-6-phosphataseIn ERGlucose-6-P Glucose

Liver (Not present in muscle)Probably stimulated by glucacon

Deficient in Von Gierke's disease-Severe fasting hypoglycemia- glycogen in liver- blood lactate-hepatomegalyGlycogen phosphorylaseRate determining enzyme for glycogenolysis

Skeletal component deficient in McArdle's disease- glycogen in muscle, but can't break it down-Painful muscle cramps, myoglobinuria w/ strenuous exercisePhosphoenolpyruvate carboxykinaseIrreversible enzyme in GluconeogenesisPhosphorylase kinaseAn early component of GluconeogenesisBranchial apparatusCAP Covers outside from insideClefts = ectodermArches = mesodermPouches = endoderm1st Brachial archCartilage:Meckel's (Mandible, Malleus, Mandibular)

Muscles:Muscles of mastication (Masseter, medial pterygoids, Mylohyoid)

Neves:CN V2, V3-ChewTreacher Collins Syndrome1st arch neural crest fails to migrate-Mandibular hypoplasia-Facial abnormalities2nd Brachial archCartilage:Reichert's (Stapes, Styloid, Stylohyoid)

Muscles:Stapedius, Stylohyoid

Nerves:CN VII-Smaile3rd Brachial archCartilage:Greater horn of hyoid

Muscles:Stylopharyngeus-Stylopharyngeus innervated by glossopharyngeal nerve

Nerves:CN IX-Swallow stylishlyCongentio pharyngo-cutaneous fistulaPersistence of cleft and pouch fistula between tonsillar area, cleft in lateral neck4th-6th Brachial archesCartilage:Thyroid, cricoid,

Muscles:4 = pharynheal constrictors6 = intrinsic muscles of larynx

Nerves:4 = CN X (superior laryngeal branch)-Simply swallow

6 = CN X (recurrent laryngeal branch)-SpeakArches 3 & 4Posterior 1/3 of tongueBrachial Arches (Pneumonic)When at the golden arches,1. Chew2. Smile3. swallow stylishly or 4. simply swallow6. speak

There is no 5!micrognathiaJaw is undersizedglossoptosisDownward displacement or retraction of the tongueS. pyogenes (Group A)The bacteria behind post-streptococcal glomerulonephritis

PHaryngitis can results in PHever & glomerulonePHritisStratificationStrata are constructed based on values of prognostic variables and a randomization scheme is performed separately within each stratum

Put another way:Achieved by performing a separate randomisation procedure within each of two or more subsets of participantsTrapezium boneForms the radial border of the carpel tunnelDistal to the Scaphoid

Some might say it is in close proximity to-Abductor pollicis longus-Extensor pollicis brevis

That being side, is not the right answer for the question that you seek!Scaphoid boneMost commonly fractured carpel bone

Prone to avascular necrosis due to retrograde blood supply

Receives its blood primarily from the distal end

Failure of the fracture to heal ("non-union") can result in loss of blood supply to the proximal pole- Can result in avascular necrosis of the proximal segment.SNoW DRoPSouthern = DNANorthern = RNAWestern = ProteinSouthwestern blotIdentifies DNA-binding proteinsAffinity column chromatographyMethod of separating biochemical mixtures-Based on a highly specific interaction such as that between antigen and antibody, enzyme and substrate, or receptor and ligand.

Can be used to.1. Purify and concentrate a substance from a mixture into a buffering solution2. Reduce the amount of a substance in a mixture3. Discern what biological compounds bind to a particular substance4. Purify and concentrate an enzyme solution.Density Gradient CentrifugeUsed to separate certain organelles from whole cells for further analysis of specific parts of cells1. A tissue sample is first homogenised to break the cell membranes and mix up the cell contents.2. The homogenate is then subjected to repeated centrifugations, each time removing the pellet and increasing the centrifugal force.3. Finally, purification may be done through equilibrium sedimentation, and the desired layer is extracted for further analysis.ImmunohistochemistryProcess of detecting antigens (e.g., proteins) in cells of a tissue section by exploiting the principle of antibodies binding specifically to antigens in biological tissuesIncidenceLooks at new incidentsPrevalenceLooks at all current casesImatinibA small molecular inhibitor of bcr-abl tyrosine kinase

Treatment of CML

Trade name GleevecHydroxyureaInhibits ribonucleotide reductase DNA Synthesis (S-phase specific)

Used with:Melanoma, CML, Sickle cell disease ( HbF)

Toxicity:Bone marrow suppressionGI upsetCytarabinePyrimidine analog inhibition of DNA polymerase

Used with:Leukemia, lymphomas

Toxicity:LeukopeniaThrombocytopeniaMegaloblastic anemiaIL-5From Th cellPromotes differentiation of B-cellEnhances class switching of IgA.Stimulates the growth of and differentiation of eosinophilsInterferonsProteins that place uninfected cells in an antiviral state

Induce production of ribonuclease that inhibits viral protein synthesis by degrading viral mRNA (but not host mRNA)

& : inhibit viral protein synthesis: MHC I & II expression and antigen presentation in all cellsActivate NK cells to kill virus-infected cellsLeukemiaUnregulated growth of leukocytes in *bone marrow* or in # of circulating leukocytes in blood

Marrow failure anemia (RBC), infections (WBC), hemorrhage (platelets)

Infiltrates in liver, spleen, and lymph nodes possibleLymphomaDiscrete tumor masses arising from lymph nodes.Chronic myelogenous leukemia (CML)30 - 60 year olds

Myeloid stem cell proliferation- neutrophils, metamyelocytes, basophils


Low leukocyte alkaline phosphatase (as opposed to leukemoid reaction)Leukemoid reactionAcute inflammatory response to infection

WBC count with neutrophils and neutrophil precursors such as band cells leukocyte alkaline phosphataseDeoxyhemoglobinBetter buffer for H than oxyhemoglobin-Advantageous that hemoglobin has been deoxygenated by the time it reaches the venous end of the capillariesCarbaminohemoglobinCO bound to hemoglobin-Account for very small amount of CO in bloodLoading doseCp x Vd(mass/volume) x (volume)

Remember:If volume of distribution is given in L/kg-Need to multiply by body weight to find actual volume distributionMaintenance doseCp x CL/F

Cp = target plasma concentration

Remember:If volume of distribution is given in L/kg-Need to multiply by body weight to find actual volume distributionOxytocinStimulates labourUterine contractionMilk let downControls uterine hemorrhageH1 (Histamine)Found on smooth muscle, endothelium, and central nervous system tissue

Causes:BronchoconstrictionBronchial smooth muscle contractionVasodilationSeparation of endothelial cells (responsible for hives)Pain and itching due to insect stings;

the primary receptors involved in allergic rhinitis symptoms and motion sickness;sleep and appetite suppression.H2 (Histamine)Located on parietal cells and vascular smooth muscle cells

Causes:Primarily involved in vasodilationAlso stimulate gastric acid secretionSalmonella entericaMost cases of salmonellosis are caused by food infected with w/ this bacteria, which often infects cattle and poultry

A remarkable large number of fimbrial and non-fimbrial adhesins are present in Salmonella-Mediate biofilm formation and contact to host cells

Secreted proteins are also involved in host cell invasion and intracellular proliferation-Two hallmarks of Salmonella pathogenesis

Usually does not need ABs (Only if complicated in people at risk such as infants, small children, the elderly)-Will lead to prolonged fecal excretion of bacteriaCarnitine deficiencyInability to transport LCFA (Long chain fatty acids) into mitochondriaResults in toxic accumulation in the cytoplasm

Causes weakness, hypotonia, hypoketotic hypoglycemiaPhytanic acidBranched chain fatty acid that humans can obtain through the consumption of dairy products, ruminant animal fats, and certain fish

Undergoes -oxidation in the peroxisome, where it is converted into pristanic acid by the removal of one carbonPeroxisomeMembrane-enclosed organelle involved in catabolism of very long fatty acids (VLFA) & amino acidsPipecolic acidAccumulates in Pipecolic acidemia- Very rare autosomal recessive metabolic disorder that is caused by a peroxisomal defectHypokinesisDiminished or abnormally slow movementRight Coronary ArterySupplies blood to right ventricle & 25-30% of left ventricle

In 85% of patients, gives off posterior descending artery

Supplies SA nodal artery in 60% of patients

Give off branch to right marginal artery

If lungs are clear to auscultation, no LVF. Think RVF!HypoxemiaDecrease in arterial PoA-a gradientUsed to compare causes of hypoxemiaPAo - Pao

Normal < 10-O normally equilibrates between alveolar gas and arterial blood (PAo ~ Pao) (High altitude, hypoventilation)

If > 10-O does not equilibrate between alveolar gas and arterial blood (diffusion defect, V/Q defect, right to left shunt)HypoxiaDecreased O delivery to tissues

O delivery = Cadiac output x O content of blood

Dependes on:Hemoglobin concentrationO-binding capacity of hemoglobin% saturation of hemoglobin by O (Depends on Po)

Can be caused by: cardiac output O-binding capacity of hemoglobin arterial Po cardiac output blood flow hypoxiaHypoxemiaPao causes %saturation of hemoglobin hypoxiaAnemia Hb concentration causes O content of blood hypoxiaCarbon monoxide poisoning O content of blood hypoxiaCyanide poisoning O utilization by tissues hypoxiaMesoblastic nephromaType of kidney tumor that is usually found before birth by ultrasound or within the first 3 months of life.

It contains fibroblastic cells (connective tissue cells), and may spread to the other kidney or to nearby tissueNephroblastoma (Wilms tumor)Most common renal malignancy of early childhood (Age 2-4)

Contains embryonic glomerular structure

Presents with huge flank mass / hematuria

Deletion of WT1 on chromosome 11

Can be hypervascular....Tanner stagesI. Childhood (9 and under)II. Pubic hair appears; breast bud formsIII. Pubic hair darkens and becomes curly; penis size/length ; breast enlargesIV. Penis width , darker scrotal skin, developed glans; raised areolaeV. Adult; areolae are no longer raised (14 and over)Anabolic steroidsLeads to sex-hormone binding globulin free testosterone-Gynecomastia resultsUbiquitinTags proteins for destruction by proteasomepVHLAn E3 ligase that ubiquitinates HIF1 and causes its degradation by the proteasome.

In low oxygen conditions or in cases of VHL disease where the VHL gene is mutated-pVHL does not bind to HIF1.-This allows the subunit to dimerise with HIF1 and activate the transcription of a number of genes (vascular endothelial growth factor, platelet-derived growth factor B, erythropoietin and genes involved in glucose upatake and metabolism)Type I errorStating there is an effect when none existType II errorStating there is not an effect when there is oneFluoxetineSSRI

Use:Depression, generalized anxiety disorder, panic disorder, OCD, bulimia, social phobias, PTSDLorazepamFacilitates GABAa action by frequency of Cl channel opening

Use:AnxietySpasticityStatus epilepticusDetoxificationOlanzapineAtypical antipsychotic

Use:Schizophrenia - both +ve and -veBipolar, OCD, anxiety disorder, depression, mania

Fewer extrapyramidal side effects than traditional antipsychoticsValproic acidA wide spectrum seizure medication-1st line for tonic-clonic

Not for status epilepticusMedial Longitudinal faciculusPair of tracts that allow for cross talk between CN VI & CN VIII nuclei

Coordinate both eyes to move in the same horizontal direction

Highly myelinated (Communicate quickly so eye's move at the same time)

Lesion:Lack of communication such that when CN VI nucleus activates ipsilateral rectus, contralateral CN III nucleus does not stimulate medial rectus to fire (impaired abduction)Abducting eye get's nystagmus (CN VI overfires to stimulate CN III)Convergence normalAlbinismCongenital deficiency in:TyrosinaseDefective tyrosine transporter ( tyrosine melanin)

Can result from lack of migration of neural crest cells

Lack of melanin results in risk of skin cancerSlipped-strand mispairingDenaturation and displacement of the DNA strands, resulting in mispairing of the complementary bases.

Can result in either insertions or deletions.Insertions are thought to be self-accelerating: as repeats grow longer, the probability of subsequent mispairing events increasesTestosteronePre-peripubertal:Causes growth spurt / accelerated bone maturation

Pubertal:Completion of bone maturation / termination of growthHyperparathyroidismStone, Bones, and Groans

HypercalcemiaHypercalciuria (Stones)Hypophosphatemia

PTH, Alk Phos, cAMP in urinePTHCa+ resorption from Kidney (Inhibits PO4 resorption)Stimulates Vit D. synth-Increased Ca+ absorbed from intestine

Ca+ release from bone

serum calciumHistone deacetylaseRemoves acetyl groups from AA-Allows histones to wrap DNA more tightly

Actions are opposite to that of histone acetyltransferase

These would affect transcription of DNA!!!!Internal urethral orificeOpening of the urinary bladder into the urethraUreteric orificePlaced at the postero-lateral angles of the trigonum vesicae, and are usually slit-like in formSupraspinatusAbduction of the arm at the shoulder joint-Main agonist muscle for this movement during the first 10-15 degrees of its arc

Can test:Shoulder at 90%Empty can (Wrists pronated)Wound healing1. Inflammatory (immediate)-Platelets, neutrophils, macrophages

2. Proliferative (2-3 days after wound)-Fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages-Granulation tissue depostion, angiogenesis, wound contraction (mediated by myofibroblasts)

3. Remodeling (1 week after wound)-Fibroblasts-Type III collagen replaced by type I collagenMyofibroblastCell that is in between a fibroblast and a smooth muscle cell in differentiation

Can contract by using smooth muscle type actin-myosin complex, rich in a form of actin called alpha-smooth muscle actin-These cells are then capable of speeding wound repair by contracting the edges of the woundScurvySwollen gumsBruisingHemarthrosisAnemiaPoor wound healingVitamin CRequired fro the hydroxylation of specific purine and lysine residues-If deficient, will cause scurvy--Inadequate hydroxylation of collagen peptidesIrradiated packed RBCsDestroys DNA in WBCs-Prevents graft vs host disease occurring from transfusion

Important if transfusion is from:1. Close family relation2. Someone who is immunocompromised (Di George Syndrome, Wiskott Aldrich, and SCID)Packed RBCs with adenine-saline addedAllows the blood to flow readily without the addition of salineWashed packed RBCsRBCs washed in sterile saline to remove:WBCsLytic mediatorsNon-self antigens

Most useful in IgA deficient persons who have circulating anti-IgA Abs-Use febrile, urticarial and anaphylactic reactionsWhole bloodBlood that is unmodified except for the presence of an anticoagulant

Usually not used because the extra plasma can contribute to transfusion associated circulatory overload (TACO), a potentially dangerous complicationTransfusion associated GVHResults from transfusion of immunocompetent T cells capable of engrafting and initiating an immune response against recipient antigens

The most susceptible patient groups are those who are severely immunocompromised

Gamma irradiation abolishes the proliferative activity of the lymphocytes in the donor blood.

Fresh frozen plasma and cryoprecipitate do not contain viable lymphocytes and thus do not need to be irradiated1st Brachial PouchMiddle ear cavityEustachian tubeMastoid air cells2nd Brachial PouchEpithelial lining of palatine tonsil3rd Brachial PouchDorsal wings-Inferior parathyroids

Ventral wings-Thymus

3 structuresThymus, right & left parathyroids4th Brachial PouchDorsal wings-Superior parathyroidBrachial pouch pneumonicEar, tonsils, bottom to top

1(ear)2(tonsils)3 dorsal (bottom for inferior parathyroid)3 ventral (to = thymus)4 (top = superior parathyroids)DiGeorge syndromeAberrant development of 3rd & 4th pouches:T-cell deficiency (thymic aplasia)Hypocalcemia (failure of parathyroid development)Homonymous hemianopsiaVisual field loss that respects the vertical midline, and usually affects both eyes

Vascular and neoplastic (malignant or benign tumours) lesions from the optic tract, to visual cortex can cause-If lesion is in optic tract, will be pupillary reflex problem!

The more posterior the cerebral lesion, the more symmetric (congruous) symptoms will be

1. Person who has a lesion of the right optic tract will no longer see objects on his left side2. Person who has a stroke to the right occipital lobe will have the same visual field defect, usually more congruent between the two eyes, and there may be macular sparingHemispatial neglectResults most commonly from brain injury to the right cerebral hemisphere, causing visual neglect of the left-hand side of space

A stroke affecting the right parietal lobe of the brain can lead to neglect for the left side of the visual field, causing a patient with neglect to behave as if the left side of sensory space is nonexistent (although they can still turn left)-Extreme case, a patient with neglect might fail to eat the food on the left half of their plate, even though they complain of being hungry-Someone with neglect is asked to draw a clock, their drawing might show only numbers 12 to 6, or all 12 numbers on one half of the clock face, the other side being distorted or left blankTemporal lobe lesionUpper quadrantic anopiaParietal lobe lesionLower quadrantic anopiaOptic chiasm lesionBitemporal anopiaAplasiaLack of growthExcess lymphoblastsAge < 15Found in acute lymphoblastic leukemia (ALL)

TdT+ (Marker of pre-t & pre-b cells)CALLA+

t(12;21) = good prognosis

Increased incidence in people with Down SyndromeMegaloblastosis (Megaloblastic anemia)Results from inhibition of DNA synthesis in red blood cell production-Most often due to hypovitaminosis, specifically a deficiency of vitamin B12 and/or folic acid

Characterized by:Many large immature and dysfunctional red blood cells (megaloblasts) in the bone marrowHypersegmented neutrophils (those exhibiting five or more nuclear lobes ("segments"), with up to four lobes being normal)Parvovirus inclusionsFifth disease-Develop the illness after an incubation period of four to fourteen days.-Fever and malaise while the virus is most abundant in the bloodstream-Patients are usually no longer infectious once the characteristic rash of this disease has appeared

Parvovirus B19 is a cause of chronic anemia in individuals who have AIDS

Aplastic anemia-Patients have an arrest of erythropoiesis (production of red blood cells) during infection-Patients who have sickle cell anemia or hereditary spherocytosis are heavily dependent on erythropoeisis due to the reduced lifespan of the red cells

Infection in pregnant women is associated with hydrops fetalis due to severe fetal anemiaRinged sideroblastsBody has iron available but cannot incorporate it into hemoglobin, which red blood cells need to transport oxygen efficiently

Abnormal nucleated erythroblasts (precursors to mature red blood cells) with granules of iron accumulated in perinuclear mitochondria-Seen in aspirates of bone marrow

Most common cause of is excessive alcohol use

Primary pathophysiology = failure to completely form heme molecules (whose biosynthesis takes place partly in the mitochondrion)Rouleaux formationStacks of red blood cells (RBCs) which form because of the unique discoid shape of the cells in vertebrates

Conditions which cause:InfectionsMultiple myelomaInflammatory and connective tissue disordersCancersOccurs in diabetes mellitus (one of the causative factors for microvascular occlusion in diabetic retinopathy)SLE Criteria4 out of 11 of the following

1. Malar rash2. Discoid rash3. Serositis: Pleurisy or Pericarditis4. Oral ulcers5. Arthritis6. Photosensitivity7. Blood disorder: Hemolytic anemia, leukopenia, lymphopenia, thombocytopenia, ~hypocomplementemia8. Renal disorder9. ANA +ve10. Immunologic disorder11. Neurologic disorderCase ControlTwo existing groups differing in outcome are identified and compared on the basis of some supposed causal attributeCase seriesMedical research descriptive study that:1. Tracks patients with a known exposure given similar treatment2. Examines their medical records for exposure and outcome

Can be retrospective or prospectiveUsually involves a smaller number of patients than more powerful case-control studies or randomized controlled trials

May be consecutive or non-consecutive-Depends on whether all cases presenting to the reporting authors over a period were included, or only a selection

May be confounded by selection bias-Limits statements on the causality of correlations observed

-Physicians who look at patients with a certain illness and a suspected linked exposure will have a selection bias in that they have drawn their patients from a narrow selection (Their hospital)ARDSInflammation of the lung parenchyma leads to impaired gas exchange with systemic release of inflammatory mediators, causing:InflammationHypoxemiaFrequently multiple organ failure.

Condition has a 90% death rate in untreated patients. With treatment, usually mechanical ventilation in an intensive care unit, the death rate is 50%.

A less severe form is called acute lung injury (ALI)

3 main clinical causes1. Sepsis (most important)2. Severe multiple trauma3. Aspiration of saliva / gastric contents

Any cardiogenic cause of pulmonary edema should be excluded-Done by placing a pulmonary artery catheter for measuring the pulmonary artery wedge pressure

4 main criteria for ARDS:1. Acute onset2. Chest X-Ray: Bilateral diffuse infiltrates of the lungs3. No cardiovascular lesion4. No evidence of left atrial hypertension: PaO2/FiO2 ratio equal to or less than 200 mmHg.Alveolar ventilationThe volume of gas per unit time that reaches the alveoliLeft sided heart failure signsTachypnea (increased rate of breathing)Increased work of breathing (non-specific signs of respiratory distress)Rales or crackles, heard initially in the lung bases, and when severe, throughout the lung fields-Suggest the development of pulmonary edema (fluid in the alveoli)-Cyanosis which suggests severe hypoxemia, is a late sign of extremely severe pulmonary edema.PaO2/FiO2 ratioThe ratio of partial pressure arterial oxygen and fraction of inspired oxygen

Comparison between the oxygen level in the blood and the oxygen concentration that is breathed

Helps to determine the degree of any problems with how the lungs transfer oxygen to the blood

If equal to or less than 200 mmHg is one criteria for diagnosing ARDSErythropoietinIts primary effect on red blood cell progenitors and precursors (which are found in the bone marrow in humans) is promoting their survival through protecting these cells from apoptosisBacillus subtilisGram-positive, catalase-positive bacteriumRod-shapedHas the ability to form a tough, protective endospore, allowing the organism to tolerate extreme environmental conditions

Only known to cause disease in severely immunocompromised patientsBacteroides fagilisGram-negative bacillus bacterium speciesInvolved in 90% of anaerobic peritoneal infections

Predominates in bacteremia associated with intraabdominal infections, peritonitis and abscesses following rupture of viscus, and subcutaneous abscesses or burns near the anusClostridium perfringensGram-positive, rod-shaped, anaerobic, spore-forming bacterium

Infections show evidence of tissue necrosis, bacteremia, emphysematous cholecystitis, and gas gangrene

Toxin involved in gas gangrene is known as -toxin-Inserts into the plasma membrane of cells, producing gaps in the membrane that disrupt normal cellular functionStaphylococcus aureusFacultative anaerobic Gram-positive coccal bacteriumAppears as grape-like clusters when viewed through a microscope, and has large, round, golden-yellow colonies, often with hemolysis, when grown on blood agar platesCatalase-positive-Able to convert hydrogen peroxide (H2O2) to water and oxygenVirulence factors:Enzymes-Coagulase clots plasma and coats the bacterial cell which probably prevent phagocytosis-Hyaluronidase breakdown hyaluronic acid and help in spreadingToxins-Superantigens (TSST-1) induce toxic shock syndrome (TSS), usually from prolonged tampon use. Cause non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release (IFN)-Enterotoxin that is the causative of gastroenteritis that is self-limiting, characterized by vomiting and diarrhea one to six hours after ingestion of the toxin with recovery in eight to 24 hours. Symptoms include nausea, vomiting, diarrhea, and major abdominal pain.-Exfoliative toxins implicated in (SSSS), which occurs most commonly in infants and young children. Protease activity of the exfoliative toxins causes peeling of the skin observed with SSSS.Other-Protein A, an IgG-binding protein, binds to the Fc region of an antibodyListeria monocytogenesGram-positive bacteriumMotile via flagella at 30C and belowCan move within eukaryotic cells by explosive polymerization of actin filaments (known as comet tails or actin rockets).

Facultative anaerobic bacterium (Capable of surviving in the presence of oxygen)Can grow and reproduce inside the host's cellsOne of the most virulent food-borne pathogens, with 20 to 30 percent of clinical infections resulting in death

Due to its frequent pathogenicity, causing meningitis in newborns (acquired transvaginally), pregnant mothers are often advised not to eat soft cheeses-It is the third-most-common cause of meningitis in newbornsPartial hydatidiform moleOccurs when an egg is fertilized by two sperm or by one sperm which reduplicates itself yielding the genotypes of 69,XXYComplete hydatidiform moleCaused by a single (90%) or two (10%) sperm combining with an egg which has lost its DNA

The genotype is typically 46,XX (diploid)Placenta accretaAbnormally deep attachment of the placenta to the myometrium without penetrating it.

Placenta grows completely through the endometrium

Great risk of haemorrhage during placental removal-Commonly requires surgery to stem the bleeding and fully remove the placenta-In severe forms can often lead to a hysterectomy or be fatalWernicke's aphasiaFluent aphasia with impaired comprehension.Wernicke's area-superior temporal gyrus of temporal lobe.

Wordy, but makes no senseBroca's aphasiaNonfluent aphasia with intact comprehension.DiaphoresisExcessive sweating-ALA dehydrataseLead poisoning

Accumulates:Protoporphyrin, -ALA

Microcytic anemia, GI and kidney disease.Children-exposure to lead paint -+ mental deterioration

Adults-environmental exposure (battery/ ammunition/radiator factory) -+ headache, memory loss, demyelination-ALA synthaseSideroblastic anemiaFerrochelataseLead poisoning

Accumulates:Protoporphyrin, -ALA

Microcytic anemia, GI and kidney disease.Children-exposure to lead paint -+ mental deterioration

Adults-environmental exposure (battery/ ammunition/radiator factory) -+ headache, memory loss, demyelinationPorphobilinogen deaminaseAcute intermittent porphyria

Accumulates:Porphobilinogen, -ALA, uroporphyrin

5 P's1. Painful abdomen2. Port wine-colored urine3. Polyneuropathy4. Psychological disturbances5. Precipitated by drugsUroporphyrinogen decarboxylasePorphyria cutanea tarda

Accumulates:Uroporphyrin (tea colored urine)

Blistering cutaneous photosensitivity. Most common porphyria.Holosystolic murmurTricuspid insufficiency-Best heard over the fourth left sternal border, radiates to right sternal border-Intensity can be accentuated following inspiration--Due to increased regurgitant flow in right ventricular volume-most often secondary to pulmonary hypertension

Mitral regurgitation-Best heard at the apex with diaphragm, radiates toward axilla-No intensification upon inspiration-Difference in pressure extends throughout systole and can even continue after the aortic valve has closed

Ventricular septal defect-Best heard over the left third and fourth intercostal spaces and along the sternal border-S2 Normal (Distinguish from pulmonary stenosis, which has a wide splitting S2)-No intensification upon inspirationHyperammoniaCan be acquired (e.g., liver disease) or hereditary (e.g., urea cycle enzyme deficiencies)

excess NH4+ depletes a-ketoglutarate inhibition of TCA cycle

Rx: limit protein in dietRTA1 ("distal", Renal tubular acidosis)Defect in collecting tubule's ability to excrete H+urine pH >5.5hypokalemia

risk for calcium phosphate kidney stones as a result of urine pH and bone resorptionRTA2 ("proximal", Renal tubular acidosis)Defect in proximal tubule HC03- reabsorptionFanconi's syndromeurine pH < 5.5hypokalemia

risk for hypophosphatemic ricketsRTA4 ("hyperkalemic", Renal tubular acidosis)Hypoaldosteronism or lack of collecting tubule response to aldosteroneResulting hyperkalemia impairs ammoniagenesis in the proximal tubule

buffering capacity and urine pHAmmoniagenesisOccurs within proximal tubular cells

Glutamine made in the liver, is received from peritubular capillaries and is metabolized into

1. Alpha-keto glutarate (Metabolized further into two HCO3- ions, which then leave the cell and enter systemic circulation by crossing the basolateral membrane)

2. NH4+ (Secreted into renal tubules)CN III Palsyeye is "down and out" with ptosis and pupil dilationPosterior Communicating ArteryCommon site ofsaccular (berry) aneurysm.

CN III Palsy: Eye is "down and out" with ptosis and pupil dilation

Lesions are typically aneurysms, not strokesAvoidant Personality DisorderDisplay a pervasive pattern of social inhibition, feelings of inadequacy, extreme sensitivity to negative evaluation, and avoidance of social interaction

Consider themselves to be socially inept or personally unappealing and avoid social interaction for fear of being ridiculed, humiliated, rejected, or dislikedDysthymic disorderMood disorder consisting of the same cognitive and physical problems as in depression, with less severe but longer-lasting symptoms, which may persist for at least 2 years

A serious state of chronic depression, which persists for at least 2 years; it is less acute and severe than major depressive disorder

Sufferers may experience symptoms for many years before it is diagnosed, if diagnosis occurs at allMajor depressive disorderCharacterized by episodes of all-encompassing low mood accompanied by low self-esteem and loss of interest or pleasure in normally enjoyable activities

Presence of a severely depressed mood that persists for at least two weeksNarcissistic personality disorderBeing excessively preoccupied with issues of personal adequacy, power, prestige and vanityObsessive compulsive disorderCharacterized by intrusive thoughts that produce uneasiness, apprehension, fear, or worrySchizotypal personality disorderCharacterized by a need for social isolation, anxiety in social situations, odd behavior and thinking, and often unconventional beliefs

May feel extreme discomfort with maintaining close relationships with people, and therefore they often do not

May display peculiar manners of talking and dressing and often have difficulty in forming relationships.

May react oddly in conversations, not respond or talk to themselves

Frequently misinterpret situations as being strange or having unusual meaning for them; paranormal and superstitious beliefs are not uncommon

Peptic ulcersChronic inflammation due to Helicobacter pylori that colonizes the antral mucosa


Some studies have found correlations between smoking and ulcer formation

Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, have not been found to affect ulcers to any significant exten

Substance Abuse TeratogensAlcohol:Leading cause of birth defects and mental retardation; fetal alcohol syndrome

Cocaine:Abnormal fetal development and fetal addiction; placental abruption

Smoking:Preterm labor, placental problems, IUGR, ADI-IDPrenatal cocaine effectsAssociated with premature birth, birth defects, attention deficit disorderAbsence seizureBrief (usually less than 20 seconds), generalized epileptic seizures of sudden onset and termination

Clinically, the impairment of consciousness (absence)Electroencephalography (EEG) shows generalized spike-and-slow wave discharges ~3Hz

Absence seizureBrief (usually less than 20 seconds), generalized epileptic seizures of sudden onset and termination

Clinically, the impairment of consciousness (absence)Electroencephalography (EEG) shows generalized spike-and-slow wave discharges ~3HzComplex partial seizureOften preceded by a seizure aura.-A simple partial seizure.

Aura may manifest itself as a feeling of dj vu, jamais vu, fear, euphoria or depersonalization.

Seizure aura might also occur as a visual disturbance, such as tunnel vision or a change in the size of objects (macropsia or micropsia).

Once consciousness is impaired, the person may display automatisms such as lip smacking, chewing or swallowing.

There may also be loss of memory (amnesia) surrounding the seizure event.

Person may still be able to perform routine tasks such as walking, although such movements are not purposeful or planned.

Witnesses may not recognize that anything is wrong.Generalized tonic clonicGeneralized seizure that affects the entire brain

Divided into two phases, the tonic phase and the clonic phase. Preceded by aura

Tonic = skeletal muscles tenseClonic = Rapid contraction and relaxation of musclesSimple partial seizuresConsciousness is not impaired

Often precursors to larger seizures, where the abnormal electrical activity spreads to a larger area of (or all of) the brain, usually resulting in a complex partial seizure or a tonic-clonic seizure-In this case they are often known as an auraLeukocidinType of cytotoxin created by some types of bacteria

Is a type of pore forming toxin

Get their names by killing ("-cide") leukocytes

Associated with increased virulence of certain strains (isolates) of Staphylococcus aureus

Cause of necrotic lesions involving the skin or mucosa, including necrotic hemorrhagic pneumoniaStaph -toxinThe major cytotoxic agent released by bacterium Staphylococcus aureus and the first identified member of the pore forming beta-barrel toxin familyMuscarinic ACh receptorReceptors that form G protein-receptor complexes in the cell membranes of certain neurons and other cells

Play several roles, including acting as the main end-receptor stimulated by acetylcholine released from postganglionic fibers in the parasympathetic nervous systemNicotinic ACh receptorReceptors that form ligand-gated ion channels in the plasma membranes of certain neurons and on the postsynaptic side of the neuromuscular junction

As ionotropic receptors, these are directly linked to ion channels and do not use second messengers (as metabotropic receptors do).Dysostosis multiplexHereditary disease (autosomal recessive) consisting of an error is mucopolysaccharide metabolism

Characterized by severe abnormalities in development of skeletal cartilage and bone and mental retardationLysosomal storage diseaseCaused by lysosomal dysfunction usually as a consequence of deficiency of a single enzyme required for the metabolism of lipids, glycoproteins (sugar containing proteins) or so-called mucopolysaccharides

When a particular lysosomal enzyme exists in too small an amount or is missing altogether, substances accumulate in the cell.

In other words, when the lysosome doesn't function normally, excess products destined for breakdown and recycling are stored in the cell.inclusion cell disease (I-cell disease)Inherited lysosomal storage disorder

Failure of addition of mannose-6-phosphate to lysosome proteins-Enzymes are secreted outside the cell instead of being targeted to the lysosome

Presentation:Coarse facial featuresClouded corneasRestricted joint movementHigh plasma levels of lysosomal enzymesInferior mesenteric lymph nodesSigmoid colin Colic

Ends up in these lymph nodesInternal iliac lymph nodesRectum (lower portion) of anal canal (Above pectenate line)

Ends up in these lymph nodesSuperficial inguinal lymph nodesAnal canal (below pectenate line)ScrotumThighs

Ends up in these lymph nodesInternal iliac lymph nodesReceive lymphatics from:All the pelvic visceraDeeper parts of the perineum-membranous and cavernous portions of the urethraButtock and back of the thighCervix!

Not: Ovary, testis, or superior half of the rectum

Gonads drain to the paraaortic lymph nodesSuperior half of the rectum drains to the pararectal lymph nodes