IL-1

IL-6

TNF-alpha

Gram positive

[image]

[image]

Where are beta lactamases found on the bacteria?

How are they significant?

Int he periplasm

they are responsible for drug resistance to penicillins

Some Killers Have Nice Sexy Capsule Bodies

Step. pneumonia

Klebsiella pneumonia

Haemophilus influenza B

Neisseria Meningitidis

Salmonella

Cryptococcus neoformans

Group B Strep

Quelling for a Shelling

Quelling reaction where antibodies bind to the capsule (shell)

• H. influenzae type B vaccine
• meningococcal vaccines
• S. pneumoniae vaccine (pneumovax)

Neisseria

gram- cocci

[image]

Which bacteria lacks a peptidoglycan cell wall and has cholesterol in its cell membrane?

What agar is it cultured on?

Mycoplasma

non-gram staining

Eaton's Agar

responsible for "walking/atypical pneumonia"

[image]

A 26-year-old female goes to her primary care physician complaining of severe vaginal itching with a malodorous yellow-green discharge. Her past medical history is unremarkable, and she does not take any medications. She is sexually active with one male partner and uses condoms inconsistently. Urinalysis is positive for white blood cells. Wet mount results are shown below.

[image]

Which of the following is the most appropriate next step in management for her partner

The lung of a 45-year-old Caucasian male who died from Mycobacterium tuberculosis infection reveals the following at autopsy. Of the steps leading to the formation of this structure, which occurs first?

[image]

Pt is taking Ethambutol

Toxic side-effects include retrobulbar neuritis that results in color-blindness, decreased visual acuity, and central scotoma. Ethambutol is a bacteriostatic agent that works by obstructing the formation of the tubercular cell wall through its inhibition of arabinogalactan synthesis.

[image]

The patient's infection would most likely be resistant to rifampin, which works by inhibiting bacterial DNA-dependent RNA polymerase

[image]

Primary tuberculosis is characterized by a fibrocavitary disease of the middle or lower lobes of the lung with/without involvement of hilar/mediastinal nodes. Together, these findings are termed a Ghon complex when visible on chest radiograph.

[image]

Borriela

Plasmodium

Trypanosomes

Chlamydia

• glycogen
• mucopolysaccharides
• used to diagnose Whipple's disease (Tropheryma whippelii)

"PAS the sugar before I whip you"

Acid fast organisms

• Mycobacterium
• Nocardia (partially acid fast)
• Cryptosporidum oocysts

• Cryptococcus neoformans
  • stain is not taken up by polysaccharide capsule, creating a transparent halo
  • mucicarmine can also be used to stain capsule red
  [image][image]

Fimbria or Pili

Periplasm

reason for a lot of penicillin resistance

spores

[image]

Gram -

"These Rascals May Microscopically Lack Color"

Tryponema

Rickettsia

Mycoplasma

Mycobacterium

Legionella

Chlamydia

• A systemic coagulation disorder with
  • pathologic hypercoagulation with formation of microthrombi
  • become hypocoagulable as coagulation factors are consumed
• May occur secondary to
  • sepsis
    • most commonly E. coli, N. meningitidis
      • endotoxins released damage vessels walls and stimulate coagulation
      • N. meningitidis may lead to Waterhouse-Friderichsen syndrome 
  • neoplasms
    • acute promyelocytic leukemia
      • caused by release of Auer rods/primary granules
    • adenocarcinomas
      • caused by release of procoagulant mucin
  • trauma/crush injuries
    •  caused by release thromboplastin which activates extrinsic cascade
  • rattlesnake bite
    • venom is procoagulant
  • obstetric complications
    • abruptio placentae

α-toxin→ hemolysis

β-toxin→ sphingomyelinase

γ-toxin Proteins A, B, and C→ A+B=hemolysin,

B+C= leukocidin

Hemolysin→hemolysis

Leukocidin→destroys leukocytes

Enterotoxins A-E →food poisoning→vomiting & diarrhae

TSST-1→release of cytokines→Toxic Shock Syndrome

Epidermolytic/Exfoliative→epithelial lysis→scalded skin syndrome

[image]

(Group A Strep)

Streptolysin O→ hemolysis (oxygen labile-*ASO titers* )

Streptolysin S→ hemolysis (oxygen stabile)

Erythrogenic/pyrogenic→ skin rash and fever (Scarlet fever)

[image]

What is the causative agent causing the pseudomembrane?

[image]

Cornyebacterium Diptheria

Elongation Factor-2 is the exotoxin that causes pseudomembranous pharyngitis

do not scrape! can cause toxin to get into circulation and can be lethal to the heart and neurons

[image]

What does the guy with the accordion represent?

[image]

This image is Pseudomonas

the guy represent the exotoxin A that inhibits EF-2

(like diptheria)

Clostridium botulinum

botulinum toxin

[image]

alpha toxin

Clostridium perfiringens

[image]

Tetanospasmin

[image]

Enterotoxin: exotoxin that causes water and electrolyte imbalances and diarrhea

Vibrio Cholera

E.Coli

Salmonella

Shigella

Staph. Aureus

Viridans Strep

Enterococci

Coagulase negative Staph (S.epidermidus)

A woman is breast feeding and develops redness and swelling of her right breast over a period of 24 hours.

Exam reveals a warm fluctuant mass. What is the diagnosis?

Pyogenic:

Pharyngitis

Endocarditis

Skin infections

Necrotizing fascitis

Bacteremia

Toxin-mediated:

Scarlet Fever

Toxic Shock Syndrome

Autoimmune mediated:

Acute Glomerulonephritis

Rheumatic Fever

HORMONES:

Stimulatory:

Histamine and Gastrin

Inhibitory:

Prostaglandins

Somatostatins

Secretin

GIP

________________________

DRUGS

PPIs

H2 blockers

Antimuscarinics (atropine)

Penicillin or Erythromycin + anti-toxin

-immunize the patient

Clostridium species (C.perferingins, tetani, botulinum)

Bacillus species (B. anthracis, cereus)

Coxiella Burnetti (Rickettsial species)

Can't Breath Air

Clostridium

Bacteroides

Actinomyces

lack the enzymes to neutralize oxygen

Metronidazole and Clindamycin

[image]

Nocardia

Bacillus Anthracis

Mycobacterium Tuberculosis

Pseudomonas

Group B strep

Listeria Monocytogenes

E.Coli

BACTERIOCIDAL:

cell wall inhibitor that binds PBP

blockd transpeptidase cross linking of cell wall

activates autolytic enzymes

gram + bacteria

strep

spirochetes (syphillis) Penicillin G

Toxicity: HSR

[image]

same as penicillins but a wider spectrum

they are not resistant to enzymes like penicillinase, beta lactamase

Gram+ bacteria

Gram- rods

UTIs, Neonatal Infections

HEELPSS

H.Influenza

E.Coli

Enterococci

Listeria

Proteus Mirabilis

Salmonella

Shigella

Amoxicillin: Oral

Ampicillin: IV

Toxicity:

HSR like penicillin

Rash with/after mononucleosis infection

Pseudomembranous colitis

Methicillin

Nafcillin

Dicloxacillin

same mechanism as penicillan but have resistance

uses: Staph Aureus infections except MRSA

Toxicity: HSR

INnterstitial nephritis

Ticarcillin

Carbenicillin

Pipercillin

not resistant to penicillinase

used for pseudomonal infections

Sulbactam

Clavulanic Acid

used combined with a penicillin

What are the first generation Cephalosporins?

Clinical use?

bacteriocidal antibiotics

Cephazolin

Cephalexin

Gram positive cocci and PEK

Proteus

E.Coli

Klebsiella

Uses:

-UTIs

-URIs

-prophylaxis against skin infections and S.viridans endocarditis from dental procedures

What are the 2nd generation Cephalosporins?

Cefoxitin

Cefaclor

Cefuroxime

gram positive cocci and HENS PEcK and Anaerobes

Haemophilus influenzae

Enterobacter aerogenes

Neisseria

Serratia

Proteus

E.Coli

Klebsiella

Uses

What are the 3rd generation cephalosporins?

clinical uses?

Remeber -Triaxone is a tri generation. Triax, Tax, Taz, dinir

Ceftriaxone (Meningitis, CAP, Gonorrhea)

Cefotaxime

Ceftazidime (Pseudomonas)

Cefdinir

as a whole:

 more serious Gram negative infections

more resistant to beta lactamases

Cefepime

very broad

strong gram positive, gram negative and pseudmonas

LAME

Listeria

Atypicals (Mycoplasma and Chlamydia)

MRSA

Enterococci

• HSR

• Aminoglycosides (Gentamicin)+Cephalosporins= Nephrotoxicity

[image]

• Ethanol + some Cephalosporins= Disulfuram like reaction

inhibition of acetaldehyde dehydrogenase

• severe allergy to penicillin may also have reaction to Cephalosporins

Metronidazole

[image]

some obscure cephalosporins..

Cefotetan

Cefamandole

Cefoperazone

Procarbazine

1st gen sulfonylureas (Tolbutamide)

1st or 2nd

Cephazolin

Cephalexin

Cefoxitin

Cefaclor

Cefuroxime

2nd generation

Cefoxitime

Cefaclor

Cefuroxime

3rd generation

Cetriaxone

Cefotazidime

Cefotaxime

Cefdinir

3rd or 4th

Tax, Taz Triaxone

Cefipime

2nd generation

Cefoxitin

Cefaclor

Cefuroxime

different mechanism of action but the spectrum of coverage is similar

Aztreonam covers gram negative rods only and aerobes

good to use in pts allergic to penicillin, bad kidneys and gram- infection

• pts with penicillin allergy

• pts with renal insufficiency (can't tolerate aminoglycosides)

• in combination with an antibiotic with gram + coverage (vancomycin+aztreonam)

synergistic with aminoglycosides

Pt has disseminate N. Gonococcal infection which can be treated with a 3rd generation cephalosporin like ceftriaxone.

Cefrtiaxone blocks cell wall synthesis

Gentamycin

"My 30 yo Genta-men"

Vancomycin

[image]

Cilistatin

Cilistatin inhibits renal dehydropeptidase l which inactivated imipiniem in the renal tubules

empiric treatment of life threatening infections

ICU pts

very broad range: gram +, gram-, anaerobes

*BUT DOES NOT COVER MRSA or mycoplasma*

usually combined with vancomycin to cover MRSA

Impipenin/Cilistatin and Meropenem

seizures (meropenem reduced risk)

nausea

vomiting

[image]

GI upset

[image]

Skin rash

[image]

Allergy

[image]

Gram +

MRSA

Enterococcus (except VRE obviously)

C.diff (oral form)

Staph epidermidus (coag- staph)

Toxicity: NOT

Nephrotoxicty

Ototoxicty

Thrombophlebitis

Red man syndrome

itchy, redness, flushing

what to do: pretreat with antihistamine and slow infusion of Vancomycin

[image]

Augmentin

(Amoxicillin + Calvulinic Acid)

Penicillin V

Aminopenicillin

Cephalexin

Oral vancomycin

*metronidazole is first line, but is not a cell wall inhibitor*

Cefepime

Aztreonam

Carboxypenicillins

amino acid change from

D-ala D-ala→ D-ala D-lac

[image]

What genetic syndrome fits the following treatment

Rx: no nutrasweet, increased dietary tyrosine

What genetic syndrome fits the following treatment

Rx: Decreased methionine, increased cysteine + B6

Homocystinuria

[image]

What genetic syndrome fits the following treatment?

Rx. Acetazolamide to alkaline urine

What genetic syndrome fits the treatment?

Rx: decreased fructose and sucrose intake

Fructose Intolerance

(aldolase B deficiency)

[image]

Which genetic syndrome fits the treatment?

Rx: increased intake of ketogenic nutrients (fats)

Pyruvate dehydrogenase deficiency

[image]

Which genetic syndrome fits the treatment?

Rx:exclude galactose and lactose from the diet

extrapulmonary tuberculosis that impacts the spine, Pott's disease has an effect that is sometimes described as being a sort of arthritis for the vertebrae that make up the spinal column. More properly known as tuberculosis spondylitis

[image]

What is the distinction between a Ghon Complex and a Ghon Focus?

Ghon focus: calcified lung scar

Ghon complex: hilar lymphadenopathy and a calcified lung scar

seen in primary TB

Which Mycobacterium species fits the following:

• Causes leprosy
• Causes pulmonary TB-like symptoms in COPD pts
• Causes cervical lymphadenitis in children
• Causes disseminated disease in AIDS patients
• Causes hand infection in aquarium workers

• Causes leprosy=Mycobacterium leprae

• Causes pulmonary TB-like symptoms in COPD pts= Mycobacterium kansasii

• Causes cervical lymphadenitis in children= Mycobacterium scrofulaceum

• Causes disseminated disease in AIDS patients= MAI /MAC

• Causes hand infection in aquarium workers= Mycobacterium marinum

-past exposure

-past BCG vaccine

-infection

-immunocompromised

-steroids

-sarcoidosis

-malnourishment

-no infection

RIPE

Rifampin

Isoniazid

Pyrazinamide

Ethambutol

What antibiotic is used for prevention of MAI in AIDS patients? (Mycobacterium Avium Intracellulare)

When?

Azithromycin

CD4 count<50

Azithromycin

Rifampin

Ethambutol

Streptomycin

Dapsone

Rifampin

Clofazamine

What is the mechanism of Isoniazid?

Toxicity?

decreases synthesis of mycolic acids

toxicity: neurotoxicity and hepatotoxicity, drug induced lupus (anti-histone ABs)

[image][image]

Pyrodoxine (B6) helps prevent toxic side effects

Isoniazid

Procainamide

Hydralazine

RNA polymerase inhibitor

Revs up microsomal cytochrome p450

Red/orange body fluids

Rapid resistance develops if used alone

[image]

TB

Leprosy

Meningococcal prophylaxis (close contacts)

H.influenzae type B prophylaxis (close contacts)

Toxicity: hepatotoxicity

[image]

decreases carbohydrate polymerization of the mycobacterium cell wall by blocking arabinocyltransferase

Toxicity: Optic neuropathy

red/green colorblindness (reversible)

[image]

BCG PQRS

Barbituates

Carbamazepine

Griseofulvin

Phenytoin

Quinidine

Rifampin

St.John's Wart

PICK EGGS

Protease Inhibitors

Isoniazid

Cimetidine

Ketoconazole

Erythromycin

Grapefruit Juice

Sulfonamides

erythema chronica migrans (bulls eye rash)

[image]

Lovely Belle Had An STD

Lyme Disease

Herpes Zoster

AIDS

Sarcoidosis

Tumors

Diabetes

Argyll Robertson Pupil

Small and irregular bilaterally

-not reactive to light

constricts with accomodation

[image]

[image]

[image]

What organism is associated with the floowing clue?

-Pet prairie dog

-Ixodes tick

-Dog bite

-Lymphadenopathy and a new kitten

-Rabbit hunter

Pet prairie dog:Yersinia pestis

Ixodes tick: Borrelia burgdorferi

Dog bite: Pasturella multocida

Lymphadenopathy and a new kitten:

Bartonella (Cat sctratch)

Rabbit hunter: Francisella tularensis

Headache

Fever

Rash

Tetracyclines or Macrolides

[image]

Chocolate Agar with Factor V (nicotinamide)

and Factor X (hematin)

[image]

Pertussis toxin: ribosylates Gi-->increases cAMP and cuases leukocytosis

Adenylate Cylcase toxin:increases cAMP (similar to edema factor of B.anthracis)

Tracheal toxin: damages cilia of the trachea

[image]

Bordatella Pertussis, H. Influenzae, Legionella

[image][image]

[image]

Borrelia (lyme disease)

Leptospirosis

Treponema Pallidum (syphillis)

[image]

[image]

[image]

Epidemic Typhus

Army recruits, prisoners, refugee camps

close quarters

rash starts at trunk and spreads out

rash spares hands, feet and head

pneumonia

myalgia

encephalitis and even coma if serious

spread via louse-->defecates-->scratch-->in blood stream

Tx: Doxycycline[image]

Rickettsia Rickettsii

[image]

eosinophils play a role in late activation

mast cells: early activation

resolution: macrophages

remodeling: epithelial cells

sensitization: dendritic and TH2 cells

What is ITP?

labs, tx,..?

Quantitative primary hemostasis disorder:

thrombocytopenia→petechiae

ITP: antibodies against Gp2b/3a;platelets are consumed by splenic macrophages; most common cause of thrombocytopenia in children(acute) and adults(chronic)

associated with SLE (secondary) IgG can cross placenta and cause short lived thrombocytopenia in newborns

Labs:

↓platelet count

normal PT/PTT

↑MEGAkaryocytes on bone marrow bx

Tx: corticosteroids (children)

IVIG (short lived defense: idea is spleen will eat up these IG instead of the platelet bound ones)

Splenectomy (site of antibody production and destruction)

__________________________________________

Qualitative:

Characterisitics of BOTH:

Quantitative platelet disorder and  Primary hemostasis disorder and hemolytic anemia

pathologic formation of platelet microthrombi in small vessels seen in TTP and HUS

RBC shearing→schistocytes→hemolytic anemia

Skin and mucosal bleeding

Fever

Renal Insufficiency

CNS abnormalities

Thrombocytopenia

↑BT

Normal PT/PTT

Anemia with schistocytes

↑megakaryocytes on bone marrow biopsy

_____________________________________

TTP: ADAMSTS13 deficiency, metalloprotease needed to chop up vWF into monomers due to autoimmune  against it

vWF accumulates→abn. platelet adhesion→microthrombi→RBC shearing→hemolysis and thrombocytopenia

commonly seen in adult females

Tx: Plasmapherisis and corticosteroids

___________________________________________

HUS: endothelial damage by drugs or infection E.Coli O157.H7 (undercooked beef) verotoxin damages endothelial cells causing platelet microthrombi→RBCs sheared→schistocytes→hemolysis and trombocytopenia

↑uremia

alpha granule of platelet

Weibel Palade bodies of the endothelial cells

What are the Qualitative primary hemostasis disorders?

What other things can case them>

Bernard-Soulier syndrome

Genetic Gp1b deficiency

mild thrombocytopenia and enlarged platelets

______________________________________

Glanzmann's Thrombasthenia

Genetic GpIIb/IIIa deficiency imparing platelet aggregation with other platelets via fibrinogen

_________________________________________

Aspirin

blocks COX2 ingibiting production of TXA2 which impairs platelet aggregation (signaling of platelets from the platelet)

_________________________________________

Uremia

poor kidney function causes a build up of nitrogenous waste products which impairs both adhesion and aggregation

deep tissue bleeding into muscles and joints

rebleeding after surgical procedures (wisdom teeth ex.)

What is the deficiency in Hemophilia A?

Labs?

Factor VIII (8) deficiency

deep tissue joint and post surgical bleeding

↑PTT

normalPT

↓Factor VIII

normal platelet count and bleeding time

remember

[image]

Factor IX deficiency

↑PTT

↓Factor IX

normal PT

Mixing study

PTT does not correct upon mixing normal plasma with patients plasma if inhibitor is present

What is the most common inherited coagulation disorder?

Tx?

vWF disorder

AD: decreased vWF→poor adhesion→mild mucosal and skin bleeding

increased bleeding time

↑PTT

(vWF stabalizes Factor 8 but no clinical problems)

normal PT

Abnormal ristocetin test

Tx: Desmopressin : increases the release of vWF from Weibel-Palade bodies of endothelial cells

disrupts the function of multiple factors:

Vitamin K is activated by epoxide reductase in the liver and the Vitamin K is needed for gammacarboxylation of Factors 10, 9, 7, 2, C and S

Pharm reminder:

(Warfarin/coumadin blocks epoxide reductase)

What causes Heparin Induced Thrombocytopenia?

How do you correct it and what are the complications?

Heparin can form complexes with platelet factor 4 which causes an IgG response causing the destruction of platelets by the spleen

Fragments of destroyed platelts can stay in blood stream and activate remaining platelets leading to thrombosis

Tx, stop heparin

treat with another anticoagulant (not coumadin bc of risk for skin necrosis)

[image]

Pathologic activation of coagulation cascade→widespread micothrombi→ischemia and infarction and overtime thrombocytopenia resulting in bleeding

Bleed from IV sites

mucosal surfaces

↓platelet count

↑PT/PTT

↓Fibrinogen

Microangiopathic hemolytic anemia

elevated fibrin split products (D-dimer)

best screening test

Tx: address underlying cause and perhaps transfuse blood

converts plasminogen to plasmin so fibrin and fibrinogen can be cleaved to reduce fibrinolysis

breaks down clots

prevents clots from forming

prevents platelet aggregation

MORE INFO: a protein involved in the breakdown of blood clots. It is a serine protease found on endothelial cells,lining blood vessels. As an enzyme, it catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown. Because it works on the clotting system, tPA is used in clinical medicine to treat embolic or thrombotic stroke. Use is contraindicated in hemorrhagic stroke and head trauma. The antidote for tPA in case of toxicity is aminocaproic acid.

Disorder of Fibrinolysis

(NOT DIC bc you see D-dimers with DIC)

Lines of Zahn and attachment to vessel wall

[image]

PGI2

HLM

(Heparin Like molecules->activates antithrombin III)

NO

(Nitric Oxide)

tPA

(converts plasminogen to plasmin which has many functions)

Thrombomudulin

(modulates thrombin activity to activate Protein C which is an inhibitor to the coagulation cascade)

atherosclerosis

vasculitis

high levels of serous homocysteine

(Vitamin B12 or Folate deficiency which inhibits the conversion of homocysteine to methionine

Deficiency in CBS causing homocystinuria)

NO! They are at an increased risk for skin necrosis

When you give warfarin, the new factors will be degraded (2,7,9,10,C,and S) but Protein C and S will degrade first (and these pts are already deficient) and there will be 2,7,9,10 that will still be active for a period of time and they will be at an increased risk for hypercoaguable state and thrombosis in the skin

warfarin skin necrosis

Factor V Leiden

mutated Factor V that isn't shut off by Proteins C and S causing a hypercoaguable state

vessels of the lung

patient may presen with dyspnea and petechia onthe chest

[image][image]

when you dive, the increased pressure causes nitrogen to dissolve into the blood

If you ascend to quickly the nitrogen can precipitate out of blood as gas bubbles and these bubbles get lodged in places

bends: joint and muscle pain

chokes: respiratory symptoms

Chronic: Caisson's disease: multifolcal ischemic necrosis of bone

[image]

Amniotic emblous

 very serious bc often go to the lungs and can cause SOB-->Neurologic symptoms-->DIC and death

the cells in the emboli from he fetus can cause DIC

Spiral CT

also...

Lower extremeity doppler to image DVT

D-dimer elevation

GM-CSF

G-CSF

Bacterial infection

Tissue necrosis

will see a less shift, with immature neutrophils lacking an Fc receptor (decreased CD16)

High cortisol state

causes marginated pool of neutrophils to drop into circulation this is why pts on cortisol a\have an increased WBC

Allergic reactions

Parastitic infection

Hodgkin lymphoma (mediated by IL-5)

CML

Philadelphia cream cheese with Basol

Bordetella pertussis (lymphocytosis promoting factor)

&

Viral infections

Infectious mononucleosis

pharynx, liver, spleen

LAD-paracortex hyperplasia

increased CD8 T cells

high white count of atypical lymphocytes (CD8 T cells)

splenomegaly (PALS --risk for rupture:no contact sports for a year)

screening: monospot test detecting IgM heterophile antibodies

sheep/horse agglutination

negative test: think CMV

confirm: EBV capsid antigen

Rash if exposed to penicillin

MPO+/ Auer rods

(myeloperoxidase)

B-ALL

lymphoblasts express:

CD10, CD19, CD20

associated with Trisomy 21 (after age of 5)

t(12;21)

excellent repsonse to chemo

common in kids

requires prophylaxis to scrotum and CSF

chemo has to be directly injected there

_______________________________

t(9;22)

poor prognosis

more commonly seen in adults

(Ph+ALL)

CD2-CD8

presents as mediastinal mass

seen in teenagers

Based on:

cytogenic abnormalities

lineage of myeloblasts

surface markers

classic type t(15;17) disrupts retinoic acid receptor RAR

promyelocytes accumulate with numerous Auer rods-->increased risk for DIC

Tx: ATRA

binds RAR causing promyelobasts to mature

Acute Monocytic Leukemia

lack MPO

AML assoc. with Downs Syndrome (before the age of 5)

REMEMBER!:

ALL (after the age of 5)

Cytopenias with hypercellular bone marrow and abnormal maturation with increased blasts

most pts die from infection or bleeding

may progress to acute leukemia

Hematopoietic stem cell

naive B cells that co-express CD5 and CD20

also see smudge cells on histology

Hypogammaglobulinemia

Autoimmune hemolytic anemia

transformation to diffuse large B cell lymphoma

neoplastic proliferation of mature B cells

hairy cytoplasmic processes

positive for TRAP

dry TAP with bone marrow aspiration

NO LYMPADENOPATHY

Tx: 2-CDA

Adenosine deaminase inhibitor

[image]

ATLL

associated with HTLV-1

neoplastic proliferation of mature CD4 T cells

Rash (Pautrier microabscesses)

Generalized LAD

Hepatosplenomegaly

Seazry syndrome if spread to the blood (cerebriform nuclei)

Lytic bone lesions with hypercalcemia

don't automatically think multiple myeloma if you see lytic bone lesions, read and look for rash and other stuff..

JAK2 kinase mutation

symptoms of hyperviscosity

blurry vision and headache

Bud-Chiari:thrombosis in hepatic vein causing infarction

flushed face due to congestion

itching after bathing

decreased EPO

normal SaO2

tx- phlebotomy and hydroxyuea

t(14,18)

BCL2 on 18 translocates to Ig heavy chain locus on 14

results in overexpression of bcl2 which inhibits apoptosis

Tx-cxt or rituximab

IL-6

IL-6 is not only a growth factor, but also a survival factor in MM, inhibiting apoptosis in myeloma cells. IL-6 interacts with several factors which are involved in the pathogenesis of MM, such as adhesion molecules, tumour suppressor genes and oncogenes. Considering the essential role of IL-6, it could serve as a target for new therapeutic interventions. Neutralizing the effect of IL-6 may result in a regression of tumour progression.

reversible ischemic heart disease due to >70%stenosis due to atherosclerosis that causes ischemia during exertion or emotional stress

hallmark: cellular swelling

presents: chest pain

for less than 20 minues that radiates to left arm or jaw

diaphoresis

shortness of breath

EKG: ST-segment depresion(subendocardial ischemia)

relived by rest or nitroglycerin (vasodilates arteries and veins)

[image]

chest pain that occurs at rest

due to ruptures atheosclerotic plaque with thrombosis and incomplete occlusion of coronary artery

reversible injury to myocytes (cellular swelling)

ST-segment depression

relieved by nitroglycerin

High risk of progression to MI

[image]

reversible chest pain due to coronary artery spasm

episodic chest pain unrelated to exertion

reversible injury (cellular swelling)

EKG shows ST-segment elevation due to transmural ischemia

Relieved by Nitroglycerin or calcium channel blockers

[image]

necrosis of cardiac myocytes due to rupture of atherosclerotic plaque with thrombosis and complete occlusion of the coronary artery

other causes are coronary artery vasospasm, emboli and vasculitis (Kawasakis)

presents: sever crushing chest pain that radiates to left arm or jaw for greater than 20 min.

diaphoresidyspnea

symptoms are NOT RELIVED BY NITROGLYCERIN

Left anterior descinding is most commonly involved (infarction of anterior left ventricle and anterior portion of septum)

Right coronary artery is second most common site

(Posterior left ventricle and posterior ventricular septum)

Left circumflex is the third most common artery

First phase:

first subendocardial infarction (<50% of the wall) (EK:ST DEPRESSION)

_________________________________

2nd phase:

THEN transmural infarction (EKG: ST ELEVATION)

EKG:

test for cardiac enzymes:

Troponin I (most sensitive and specific)

CK-MB (useful for detecting reinfarction days after MI)

Rises 4-6 HRS after infarction

PEAKS AT 24

Returns to normal by 72 hours

Tx:

ASA/heparin

supplemental O2

Nitrates

Beta blocker

ACE inhibitor

also: fibrinolysis or angioplasty

can cause

contraction band necrosis

repurfusion injury (O2 causes free readicals which further damage tissue)

What happens to a heart within the first month after an MI?

complications?

 ---coagulative necrosis----

1 day

---(day 1-3) inflammation (neutrophils)

fibrinous pericarditis *chest pain w/ friction rub(only with transmural infarction)*---

 ---(day 4-7) more inflammation ( macrophages)

rupture of ventricular wall which causes tamponade

rupture of IV septum which leads to shunt  rupture of papillary muscle which causes mitral insufficiency---

1 week

-----Granulation tissue: red border emerging from infarct, plump foibroblas, collagen and blood vessels--

1 month

---scar (dense type I collagen)-----aneurysm, mural thrombus or Dressler syndrome

unexpected death due to cardiac disease

occurs without symptoms or within les than an hour of symptoms

usually due to a fatal ventricular arrhythmia usually

>90% preexisiting atherosclerosis

other causes:

mitral valve prolapse

cardiomyopathy

cocaine abuse (vasospasm)

ischemia

hypertension (hypertrophy)

dilated cardiomyopathy

myocardial infarction

restrictive cardiomyopathy

because a failing heart will not pump blood out effectively, the RAAS will percieve the low blood pressure and release renin to activate angiotensin and eventually aldosterone

collectively this system will increase vascular resistance and increase blood volume further excacerbating the CHF

What is the most common cause of right sided heart failure?

clinical features?

Left heart failure

others:

left to right shunt

chronic lung disease (cor pulmonale)

clinincal features:

JVD

Painful hepatosplenomegaly (nutmeg liver)

cardiac cirrhosis

dependent pitting edema

DOE(dyspnea on exertion)

Cardiac dilation

Pulmonary congestion (crackles heard)

Paroxysmal Nocturnal Dyspnea

Orthopnea

L,M,N,O,P

Lasix

Morphine

Nitrates

Oxygen

Positioning/pressors

ACE Inhibitors

Digoxin

Beta blockers

Diuretics

inhibit the Na/K ATPase

decrease extracellular Na which increased untracellular calcium which increases contractility

No vector

No rash

causes interstiital pneumonia

negative weil-felix

aerosol transmission

endospore

palpable olve

infant doesnt feed well

hyperchloremic metabolic alkalosis

nonbilious projectile vomiting

2 weeks of age

[image]

Basalis

loss of basalis is called Asherman Syndrome

due to overagressive dilation and curettage(D&C)

Endometrial polyp

antiestrogenic in breast

weakly proestrogenic in the uterus

endometrial glands and stroma outside the uterin endometrial lining

presents with dysmenorrhea and pelvic pain

may cause infertility

can see involvement in many places

ovary:chocolate cyst

fallopian tube: scarring

myometrium: adenomyosis

etc..

cause:

retrograde menstruation theory

metaplastic theory

lymphatic dissemination theory

endometrial tissue outside of the endometrium excluding the ovary (ovary is the chocolate cyst)

increased risk of carcinoma at these locations especially the ovary

psammoma bodies can arise in mesothelioma and cystadenocarcinoma of the uterus

meningiomas

cystadenocarcinoma of the ovary

medullary (papillary) thryroid cancer

leiyomyoma

 asymptomatic usually (can cause bleeding, infertility and pelvic mass if presents)

usually pre-menopausal women

leiomyosarcoma

(post menopausal women)