Pre-Midterm (Post Unified)

Question 1

Tissue response to fungi (type, cells)

Answer 1

Mixed PMN + lymphocytes + macrophages +/- giant cells

Question 2

Schistosoma genus, and tissue reaction

Answer 2

Schistosoma (genus of trematode) (blood flukes). S. Mansoni & S. Japonicum affect liver (hepatomegaly with portal HTN). S. Hematopium affects bladder (bladder cancer). Eggs induce fibrotic reaction. Chronic inflammation –> heals or resolves to scars.

Question 3

Mechanisms of decreased T cell recognition in DNA viruses and herpes, in order to evade immune response

Answer 3

DNA Viruses (eg. HSV, CMV, EBV - alter localization of MHC-1 protein, impairing CD8 presentation). Herpesviruses can degrade MHC-II - Ag presentation to CD4 Th cells)

Question 4

Furuncle

Answer 4

Skin abscess involving hair follicle and surrounding tissue. Risk: diabetes, obesity, immunocompromise, crowding with poor hygiene. Common on neck, face, buttocks, and armpit. Dx: clinical, swab for culture and sensitivity.

Question 5

Lung Abscess

Answer 5

Localized area of SUPPURATIVE necrosis (neutrophils, necrotic debris). Risk: aspiration of gastric contents, bronchial obstruction, septic emboli, complication of bac. pneum, dental extraction.
Clinical: cough productive of foul-smelling, purulent sputum, FEVER, and finger clubbing, weight loss.

Question 6

TSS

Answer 6

Intravag tampon, & others (skin wound, surgery, abortion). Longer leave in –> S. aureus growth –> release of exotoxin (superantigen) –> polyclonal T cell activation –> T cells release cytokines –> Diffuse rash, vasodilation, hypotension, death. Rash sunburn like, esp palms and soles.
Dx. Blood culture, cervical swabs.

Question 7

Strep Pneumoniae aka Pneumococcal pneumoniae

Answer 7

LOBAR PNEUMONIA. Gram +v, lancet shaped diplococci. IgA proteases. Most common cause of community acq pneumonia. Healthy adults
RIsk: DM, CHF, COPD, Absent spleen
Clinical: fever, productive cough, chest pain, bloody sputum, consolidation, bronchial breath, late insp cackles.
Inv: CXR (gold std), blood/sputum culture.
Bronchioles and alv walls NOT DMGD. SPread via PORES OF KOHN.
I. Congestion II. Red hepatization.
III. Gray hepatization IV. resolutoin.
Complications (rare) –> lung abscesses, fibrosis (org), empyema.

Question 8

LOBAR PNEUMONIA

Answer 8

Most common cause - Strep Pneumoniae
Also klebsiella and legionella
I. Congestion: exudate rich in fibrin, RBC, some PMN
II. Red hepatization: exudate RBC, fibrin, PMN. Lung consolidates
III. Gray hepatization: congestion disappears, PMN replaced by macrophages, WBCs
IV. Resolution - Macrophages clear debris.

Lobar pneumoinaL LOCALIZED to particular lobe, UNILATERAL
SEPTUM and ALVEOLAR walls are INTACT
Spreads through pores of kohn.

Question 9

Bronchopneumonia

Answer 9

Patchy, Bilateral (usually). Begins ACUTE bronchitis, spreads locally. DESTRUCTION of bronchioles and alveoli. Coon in young, edlerly, bedridden.
Cause: Haem. influena, klebsiella (alcoholics), pseudomonas (CF), staph (post viral URTI), streptococci.
May lead to abscess formation, empyema, bacteremic dissemination.

Question 10

Rheumatic fever

Answer 10

Infection with Group A, B heaeymolitic streptococci.
Type II HS reaction. Lag period 2-3 weeks post infectino - strep pharyngitis. Antibodies to M protein of bacteria cross react with tissue glycoprotein in skin, joints, heart. Deposited in tissues –> inflamm reaction.
Carditis: Aschoff Bodies in heart (granulomas with giant cells)
–> Fever, polyarthritis, carditis, chorea (syndenhams), skin nodules, erythema
ASO and ESR elevated
Rheumatic carditis –> chronic (mitral stenosis).

Question 11

Post-strep glomerulonephritis

Answer 11

Initial strep infxn - skin or rarely sore throat.
Lag 1-4 weeks. Malaise, fever, oliguria, hematuria, azotemia (^ BUN, creatinine, v GFR ie decreased), HTN.
Immune complex (Type III HS) - ab to strep circulate, ag and ab. Deposit in BM of glomeruli. Complement activated –> actue inflamm. REsolves spont in most patients.

Question 12

Components of pseudomembrane

Answer 12

Necrotic cells, bacteria, PMN, and exudate

Question 13

Diphtheria toxin (Cornyebacterium diphtheria)

Answer 13

Gram +ve rod produces exotoxin. ADP ribosylation of EF-2, inactivating protein synthesis. Clin: Fever, dysphagia, Lymph enlargement (neck, Bull neck), laryngeal edema, gray material (pseudomembrane) covering tonsils and pharynx. = Necrotic cells, fibrin, bacteria, PMN, exudate.
From necrosis of mucosa –> pseudomembrane. Complications: myocarditis, heart failure, spinal nerve or recurrent laryngeal n. paralysis.

Question 14

Pseudomembranous Colitis

Answer 14

Antibiotic associated - destroy normal flora. Clinda, cephalosporin, amoxicillin, ampicillin.
Etiology: C. difficile (gram + bacillus, normal resident) –> enterotoxins A and B, necrosis of mucosa.
Fever, ab cramps, diarrhea (water +/ blood).
Mucosal suppurative inflamm, vascular thrombosis, necrotic mucosa –> pseudomembrane (necrotic debris, PMNs, bactria, fibrin).
Invest: C diff toxins in stool

Question 15

Pseudomembranous Colllitis commonly sen post use of which antibiotics

Answer 15

Clinda, cephalosporin, amoxicillin, ampicillin.

Question 16

Clostridia Perfringens

Answer 16

Gram pos bacilli, anaerobic, produce spores found in soil. Invade traumatic and surgical wounds - 14 toxins, Alpha toxins (Lecithinase). Degrades lecithin (cell membrane), destroys RBCs, platlets, myonecrosis. Enzymes from necrotic tissue –> degradative –> produce gas in tissues.

Question 17

Typhoid Fever (enteric fever)

Answer 17

Salmonella typhi (gram neg rod) or salmonella paratyphi (predom in travelers). Humans SOLE reservoir. Ingestion of contaminated food and water. Enters ileal wall --> M cells take up --> mononuclear cells engulf (lymphoid tissue) --> blood stream --> bacteremia. Blood --> organs. Liver - typhoid nodules with kupffer hyperplasia, hemorrhagic necrosis foci, macrophage collections (week 2). Enlarged, soft spleen - typhoid nodules. Mucosal necrosis week3
NO PMNS

Question 18

Clinical features of enteric fever

Answer 18

Anorexia, fever, headache, abdominal pain, constipation, diarrhea +- skin rash (ROSE SPOTS), toxic appearance, BRADYCARDIA (due to ENDOTOXIN decreasing HR)

DX: CBC (leukopenia endotoxin effect on bone marrow).

Question 19

Causes of gram negative sepsis

Answer 19

E. Coli (most common),H. influenza, pseudomonas auerguinosa, klebsiella, proteus and serratia

Question 20

HSV-2

Answer 20

Remains latent in sensory ganglia. Fever, malaise, recurrent vesicles –> ulcers. HSV culture and Tzanck preparation –> see multinuc giant cells and eosinophilic intranuclear inclusions (cowdry type A). Complications incl meningitis in adults, encephalitis in neonates.

Question 21

Cowdry A

Answer 21

Eosinophilic intranuclear inclusions with halo and marginated nucleus. Seen in HSV-1 HSV-2 and VZV.

Question 22

Varicella Zoster virus

Answer 22

Airborne transmission. Exposure –> IgG pdn (lifelong immunity). Also cell-mediated immunity. Remains latent in DRG (see drg necrosis lab)
VESICULAR skin rash (lesions restricted to EPIDERMIS), fever, headaches, malaise.
Lab: viral culture, Tzanck smear from vesicles.
Complications: pneumonia, herpes zoster.
Cowdry type A, nuclear moulding, fused nuclei, giant cells

Question 23

CMV infection

Answer 23

Common cause of pneumonia, in immunocopmromised. Common opportunistic viral pathogen inAIDs patients esp who get transplant (CD4 <50**)
Clin: pneumonitis (mononuclear infiltrates, foci of necrosis, and cytomegalic changes)
retinitis: blurring, double vision, cotton wool spots both eyes. Colitis: diarrhea. Esophagitis: odynophagia, fever, retrosternal chest pain
Dx. PCR assay viral culture and tissue section.enlarged alveolar macrophages, eosinophilic nuclear inclusions with halo.

Question 24

Rabies

Answer 24

Raccoons, bats, wild dogs
Incubation period - depends on site of bit. Faster if closer to brain. Virus vinds preipheral nerves then by retrograde transport (dynein) enters DRG. and spinal cord -> brain. Encephalitis.
Prodrome: 2-10 daysadvanced infxn: CNS excitability, paral, hypersalivation, hydrophobia, convulsion.
Negri bodies: intracytoplasmic inclusions

Question 25

Measles (rubeola)

Answer 25

RNA paramyxovirus. Inhalation of droplets -- virus enters lymph then enters blood. Fever, coryza (runny nose), conjunctivitis, koplik spots and cough. uncomplicated: lasts 7-10 days. Dx: serology for IgG or IgM Measles giant cells (esp in lung) Complciation: pneumonia, otitis media, encephalitis.

Question 26

HPV viral warts

Answer 26

Viral warts. Exophytic, papillary architecture. Hyperkeratosis , acanthosis. Verruca vulgaris

Question 27

Pneumocystis Jiroveci Pneumonia

Answer 27

P. Jiroveci: Risk factor advanced HIV infectino (<200 CD4), may affect severely malnourished children, organ transplant pts, chemotherapy. SOB, dry cough, hypoxia. DX: chest x ray, BAL (most accurate)

Question 28

Cryptococcus neoformans

Answer 28

Budding yeast with narrow based buds, surrounded by thick capsule. Pigeon excreta. Risk: HIV, organ transplant, leukemia, lymphomas. Virulence: Polysacch capsule (inhibits phago, leukocyte migration, inflamm recruitment) Primary lung disase (40%) - granulomatous inflamm with caseation. Do NOT have to be immunocompromised Dissemination: meningitis and meningoencephalitis Clin: fever, dry cough

Question 29

Histoplasmosis

Answer 29

Histoplasma capsulatum. Most common systemic fungal infxn. Construction sites (ohio & mississippi). Spores in dust with excreta from bats, starlings, chickens. Weak immunity --> inhalation --> multiplication within macrophages --> organ spread via lymphatics. Usually asymptomatic, flue like. Fever, fatigue, night sweats, dry cough. SIm to TB. Acute primary pulmonary infxn, chronic granulomatous pulmonary disease, disseminated miliary disease. D: CXR, CT, serology, BAL with comori methenamine silver tain, fine needle asp.

Question 30

Mechanisms of Damage by foreign organisms

Answer 30

Direct tissue injury - impetigo Exotoxins - enzymes (exfoliative toxin protease from S .aureus),A B toxins (diphtheria), superantigens (TSS), neurotoxins (C. Tétani), enterotoxins (C. Diff) Endotoxins: LPS, LOS --> septic shock (DIC) Vascular damage: ischemic injury (Rickettsia and fungi) Indirect tissue injury: cells eath via host immune response ie Rheumatic heart disease

Question 31

Inflammatory lesions of Staph: Lung Abscesses

Answer 31

Localized, suppurative necrosis. Risks: aspiration of gastric contents, bronchial obstruction, septic emboli, complication of necrotizing bac pneumonia, dental extraction Clinical: productive cough - foul smelling, purulent sputum, FEVER, finger clubbing, weight loss DX: CXR, BAL.

Question 32

Most common causes of acute pyogenic meningitis by age gropu

Answer 32

Neonate: Group B strep and E. Coli Adolescents and young adults: neisseria meningitis Older adults: strep pneumoniae and listeria monocytogenes Chronic meningitis: Mycobacterium TB and fungi. Previously H. Influenza in children and young adults - rare bc of vaccinations.

Question 33

Diagnosis of Gonorrhea male v female

Answer 33

Male: microscopy of exudate. PMN and gram negative diplococci Females: Culture of exudate - essential because gram negative diplococci normal part of flora. Could yield false negative.

Question 34

Sickle cell and osteomyelitis

Answer 34

Complication of enteric./typhoid fever (salmonella typhi, paratyphi) in sickle cell patients is osteomyelitis. In general population staph aureus is major cause of osteomyelitis.

Question 35

Gram negative septicemia

Answer 35

E. Coli the most common cause (E. coli normal commensal, but pathogenic in immune compromise and mucous membrane breakage) Other causes: H. Influenzaand, pseudomonas aeruginosa, klebsiellla, proteus and serratia. Clinicals: High grade fever, DIC, hypotension --> Death.

Question 36

Epidemic Typhus

Answer 36

Etiology: R. Prowazeki (gram negative bacillus) Spread by: LICE Penetrate skin/mucous memb --> blood --> endothelial cells of small vessels --> perivascular Inflammation --> vasculitis, thrombosis, hemorrhage. Fibrin thrombi, sparse mononuclear response. Headaches, aches, high fever. MACULOPAPULAR RASH on TORSO. Can cause pneumonia, hepatitis. CNS involvement (typhus nodule). If severe ---> necrosis of earlob, scrotum, nose, finger. DX: Weil Felix (ab with proteus ag), Complications: interstitial pneumonia, myocarditis, encephalitis.

Question 37

Sickle cell and osteomyelitis

Answer 37

Complication of enteric./typhoid fever (salmonella typhi, paratyphi) in sickle cell patients is osteomyelitis. In general population staph aureus is major cause of osteomyelitis.

Question 38

Gram negative septicemia

Answer 38

E. Coli the most common cause (E. coli normal commensal, but pathogenic in immune compromise and mucous membrane breakage) Other causes: H. Influenzaand, pseudomonas aeruginosa, klebsiellla, proteus and serratia. Clinicals: High grade fever, DIC, hypotension --> Death.

Question 39

Epidemic Typhus

Answer 39

Etiology: R. Prowazeki (gram negative bacillus) Spread by: LICE Penetrate skin/mucous memb --> blood --> endothelial cells of small vessels --> perivascular Inflammation --> vasculitis, thrombosis, hemorrhage. Fibrin thrombi, sparse mononuclear response. Headaches, aches, high fever. MACULOPAPULAR RASH on TORSO. Can cause pneumonia, hepatitis. CNS involvement (typhus nodule). If severe ---> necrosis of earlob, scrotum, nose, finger. DX: Weil Felix (ab with proteus ag), Complications: interstitial pneumonia, myocarditis, encephalitis.

Question 40

Allergic Bronchopulmonary Aspergillosis

Answer 40

Aspergillus fumigatus --> opportunistic fungi. Ubiquitous in nature (isolated from anywhere). Causes allergic bronchopulmonary commonly in patients with ASTHMA. Presents as worsening asthma sxs (cough, wheezes, SOB). Is a type I HS reaction (IgE mediated), and can lead to COPD if untreated.

Question 41

Aspergilloma

Answer 41

Ie. Fungal balls. Occurs after aspergillus fumigatus (opportunistic, ubiquitous) colonizes pre-existing lung cavities (TB, old abscesses). Can cause massive hemoptysis in 60-80% of patients.

Question 42

Invasive Aspergillosis

Answer 42

Aspergillus fumigatus (opportunistic, ubiquitous). In severely immunosuppressed patients --> necrotizing pneumonia with VASCULAR invasion. Cough, dyspnea, pleuritic chest pain, sometimes hemoptysis. Vascular involvement --> hemorrhagic infarcts Can disseminate --> heart, brain, kidney. DX: PAS, Silver stain. Hyphae have frequent septal, narrow angled (<45degrees)

Question 43

Mucormycosis

Answer 43

Opportunistic infection, caused by zygomycetes (rhizopus and mucor). Common in immunosuppressed and DM Type I (DKA). Inhale, ingest, or spores enter through skin. Colonise nasal cavity, extend to brain, orbit, head and neck structures. Also colonise lungs causing cavitation, and gut (malnourished). Vascular involvement --> necrosis, infarcts. Clinical RHINOCEREBRAL: headache, nasal contest, black pus, fever. Later: diplopia, vision loss, proprotiss, confusion PULMONARY> cough, hemoptysis, SOB GI: abdominal pain, blood stool, diarrrhea.

Question 44

Histoplasmosis

Answer 44

Histoplasma Capsulatum. Most common systemic fungal infxn (Ohio and Mississippi River valleys). Exposure in construction sites, caves. Inhalation of spores contam. with bat, starling, chicken excreta. Weakened immunity --> inhalation --> multiply in macrophages --> spreads via lymphatics Usually asymptomatic, nonspecific flu like sxs. Similar to TB -- Acute primary pulmonary infection, Chronic granulomatous pulmonary disease, disseminated miliary disease. CXR, CT, Serology, BAL with Gomori Methenamine silver, fine needle aspiration.

Question 45

Complications of diphtheria

Answer 45

Myocarditis (heart failure 3 weeks), spinal nerve paralysis.

Question 46

Outcome of Primary TB

Answer 46

Heals in most people --> fibrosis, calcification. Some bacteria can remain dormant in lungs or distant organs and become reactivated to secondary TB Or, in immunosuppressed patients, can lead to primary progressive complex and miliary TB.

Question 47

Progressive Primary Complex TB

Answer 47

Failure of primary lesion to heal (rare) --> progressive involvement of surrounding lung --> invades BVs and spreads all over body --> miliary TB lungs liver spleen kidney brain gut --> may end fatally. Millet sized granulomas everywhere.

Question 48

Secondary TB

Answer 48

Reinfection (already had primary but reinfected), or dormant bacteria reactivated due to lowered immunity. Pre-developed cell mediated immunity --> Rapid development of caseation (few days) --> CAVITY formation. Lesions usually at lung APEX. Fibrosis, quick healing, and calcification. Productive cough +/ hemoptysis. Chest pain, SOB (pleural effusion)

Question 49

Progressive secondary TB

Answer 49

Less than 5%, no healing. Spread to lung, pleura, LN. Pneumonia, bronchiectasis, pleural effusion, Boood --> miliary TB.

Question 50

Other organ involvement in TB

Answer 50

GIT - ileocecal ulcers, intestinal obstruction, peritonitis Vertebra: Pott's disease - cold abscesses of the spine, cord compression, rupture into paravertebral soft tissue LN: axillary, cervical, mesenteric Kidney hematuria, pyuria. Heart: constrictive pericarditis CNS: chronic meningitis, tuberculoma (acts ike brain tumour) Organometallic of liver, spleen Endometrium - infertility (salpingitis --> healing by fibrosis) Adrenals: Addision's disease (insufficiency)

Question 51

Tuberculoid Leprosy

Answer 51

``` Mycobacterium leprae (foot pads of mice and armadillos) Granuloma formation with intact cellular immunity , few bacteria. POSITIVE LEPROMIN test, localized skin lesions with nerve involvement ```

Question 52

Lepromatous Leprosy

Answer 52

Depressed cell mediated immunity (no Th1 response) --> absence of granuloma. NEGATIVE lepromin test. Numerous bacteria in foamy macrophages (macrophage ingest lipids) Modular lesions, classic leonine facies (lion-like)

Question 53

Mercury Toxicity - Nervous System

Answer 53

Target of elemental Hg (via respiratory sx) paresthésie, tremors, Neuropsych (insomnia, memory loss, depression, instability), ataxia, vasomotor distrubance ie excessive perspiration, blushing.

Question 54

Mercury toxicity - kidneys

Answer 54

Inorganic Hg target (via skin and alimentary). ACUTE due to high does - tubular necrosis CHRONIC due to low dose - insufficiency due to eventual failure.

Question 55

Mercury effects on GI and Skin

Answer 55

Mucosal injury and necrosis in GI, discolouration and desquamation of skin

Question 56

Berylliosis

Answer 56

Chronic exposure to fumes/dust -- DTH (Type IV) Response (infrequent, 1-10%) Industrial exposure: metal machining, aerospace, nuclear power, electronics. GRANULOMATOUS inflammatory response, similar to sarcoidosis. Granuloma --> fibrotic nodules BeLPT (beryllium lymphocyte proliferation test) - peripheral blood, BAL fluid.

Question 57

Definition of AIDS (WITH lab confirmed HIV infection)

Answer 57

WIth lab confirmed HIV infection AND either <200 CD4+ T cells/uL or <14% of lymphocytes CD4 T cells, or any of the following: coccidiomycosis, histoplasmosis, ... kaposi's sarcoma, primary CNS lymphoma, non-hodgkin lymphoma, mycobacterium other than TB, candidiasis, pneumocystis jiroveci, HIV encephalopathy... etc.

Question 58

Definition of AIDS withOUT confirmation of HIV, but no other cause of immunodeficiency

Answer 58

Any of the following conditions: Candidiasis of esoph etc, cryptococcosis extrapulm, cryptosporidium, CMV except of liver spleen lymph, HSV of lungs etc, Kaposi's or primary CNSl y Phome in pts less than 60yo, Mycobacterium avium disseminated/extrapulmonary, pneumocystis carinii, multifocal leukoencephalopathy, toxoplasmosis of brain

Question 59

Cocaine Toxicity

Answer 59

Tachy, HTN, vasoconstriction. Myocardial ischemia - coronarty artery constriction, accel arteriosclerosis, cardiac arrhythmia, dilated cardiomyopathy. CNS: Hyperpyrexia (fever), seizures, paranoiia.

Question 60

Heroin

Answer 60

Diacetylmorphine. Relaxation, euphoria, analgesia. Toxicity: resp. depression, pulmonary oedema, cardiac arrhythmia. Sudden death. Substances mixed in, Quinine. Complications of injection --> infections, FOREIGN body reaction. Secondary RENAL lesions - focal glomerulosclerosis, amyloidosis (secondary to chronic infections due to IVDU)

Question 61

Aflatoxin B1

Answer 61

Byproduct of fungal contamination, example of metabolic activation, highly toxic with carcinogenic potential, (Aspergiullus flavus). Can grown on contaminated food, metabolized in and toxic to LIVER

Question 62

AIDS defining neoplasms

Answer 62

Kaposi sarcoma (HHV8), non-hodgkin lymphoma (EBV), Primary CNS lymphoma (EBV), invasive cervical carcinoma (HPV)

Question 63

AIDs defining opportunistic infections

Answer 63

Protozoal: crytosporidiosis, isosporidiosis, toxoplasmosis Fungal: candidiasis, cryptococcosis, coccidiomycosis, histoplasmosis, pneumocystosis Bacterial: mycobacteriosis, nocardiosis, salmonellosis Viral: CMV, herpes simplex, varicella-zoster, JC virus (PML)

Question 64

AIDs defining neoplasms

Answer 64

Kaposi sarcoma (HHV 8), Non-hodgkin lymphoma (EBV), pimary CNS lymphoma (EBV), invasive cervical carcinoma (HPV)

Question 65

Transudate

Answer 65

PASSIVE (increased pressure) processes, normal vascular permeability, no plasma proteins, protein content <1.5 g/dL, Low S.G (<1.012), NO fibrin, NO inflammatory cells.

Question 66

Exudate

Answer 66

ACTIVE processes (inflammation), increased vascular permeability, plasma protein leak present, high SG >1.020, proteins >1.5 g/dL, presence of FIBRIN and INFLAMMATORY cells

Question 67

Virchow's Triad - Endothelial Injury

Answer 67

Endothelial Injury - Important in ARTERIAL thrombi. Stress induced by HTN, bacterial toxins, hypercholestérolémie, homocystinuria, Cigarette smoking. Atherosclerosis, LVF after MI, myocarditis.

Question 68

Virchow's Trina - Loss of Laminar Flow

Answer 68

Stasis: endothelial cell hypoxia, allows platelets to contact endothelium, local activation of coag factors, buildup of platelets/fibrin, prevents dilution of clotting factors, reduces flow of clotting inhibitors. Stasis in aneurysms, leg veins Turbulence: Structural damage to vasculature ie atherosclerotic plaques, platelets contact damaged endothelium.

Question 69

Virchow's Triad - Hypercoagulability of Blood

Answer 69

Inherited: Factor V leiden, Protein C and S deficiency, Antithrombin III deficiency. Acquired: Trousseau syndrome in terminal cancer - thrombogenic substances released from necrotic tumour cells. Cardiac failure: anoxic dmg to tissues, release of thrombo substances Severe trauma, burns Oral contraceptives - increased pdn. Of clotting factors.

Question 70

Thrombus versus clot

Answer 70

Thrombus: platelet aggregation, endothelial interaction, blood coagulation and fibrin deposition. Attached to bv wall and friable. Clotting: ONLY fibrin + trapped cells. Post-mortem, test tube, hematoma. NOT attached to vessel wall.

Question 71

Lines of Zhan

Answer 71

Seen in THROMBI , NOT clots. Alternating pale and dark lines - light: platelets and fibrin, Dark: RBCs

Question 72

Sites of thrombosis (arterial)

Answer 72

Heart (mural), aorta (on atherosclerotic plaque), aneurysm (mural), other arteries (occlusive) - coronaires, carotids, cerebral, femoral, mesenteric

Question 73

Venous thrombosis

Answer 73

Takes the shape of the vessels in which it forms. REDDER than arterial. Superficial veins rarely embolise (varicosities) Deep veins: 90% - deep calf at or above knee - femoral, popliteal, iliac. Edema of ankle. Asymptomatic in 50% due to collaterals. high risk of embolus. Trousseau;s syndrome: unexplained, moving thrombophlebitis - look for underlying abdominal malignancy (pancreatic cancer, release of procoagulants)

Question 74

Sites of origin of thrombi in arterial circulation

Answer 74

Heart (mural thrombus, 80%), aorta (ulcerated atherosclerotic plaque), venous circulation (paradoxical via ASD, VSD). --> embolize to lower extremities (75%) and brain (10%) --> block end arteries leading to infarction.

Question 75

Air embolism

Answer 75

Introduced into venous circulation through neck wounds, thoracocentesis, cut IJ, hémodialyses, Child birth, abortion. 150mL of air causes death. Coalesce and physically obstruct flow of blood in right ventricle, lungs, and brain.

Question 76

Pyoderma

Answer 76

Localized skin infection with vesicles progressing to pustules, NO systemic disease. Caused by Group A streptococcus (Pyogenes)

Question 77

Eyripelas

Answer 77

Localized skin infection with pain, inflammation, lymphadenopathy, and systemic sxs. Due to Group A strep (Strep pyogenes)

Question 78

Necrotizing fasciitis

Answer 78

Deep infection of skin involving destruction of muscle and fat layers. Can be due to Group A strep infection (Strep pyogenes)

Question 79

Cornyebacterium Jeikenum and minutissumum

Answer 79

Other clinically relevant cornybacterium. Jeikenum: associated with bacteriema, IV catheter colonisation Minutissimum: RTI’s, wound infections

Question 80

Diphtheria clinical importance

Answer 80

Respiratory diphtheria - sudden onset exudative pharyngitis, sore throat, fever, malaise, dysphagia. Thick pseudomembrane over pharynx —> obstruction. Carditis, neuro complications ( recurrent laryngeal palsy) if severe Cutaneous diphtheria (low yield) —> papule on skin —> non-healing ulcer, systemic signs can develop

Question 81

HPIV-1 Infection predisposing factors and most common disease associated

Answer 81

Lack of breast feeding, Vitamin A deficiency, overcrowding, malnutrition, and environmental smoke or toxins predispose to infection with HPIV. HPIV-1 most common cause of CROUP. Respiratory secretions are source of infection - fomites, person to person, droplets. Can survive in aérosoles for >1 hour.

Question 82

Unstable/Vulnerable Plaque Characterisics

Answer 82

Moderate stenosis (50-75% bc no sxs), thinner fibrous cap, core rich in lipids, macrophages, T cells, LESS smooth muscle proliferation, markedly eccentric.

Question 83

Composition of vegetations in NBTE (Marantic endocarditis)

Answer 83

=eosinophilic material (fibrin) and delicat layer of aggregated platlets. NO inflammation or fibrosis, loosely attached to the cusps

Question 84

Anti neutrophil cytoplasmic antibodies (ANCA)

Answer 84

Hetero group of auto-antibodies against enzymes mainly found in primary granules in neutrophils, in lysosomes of monocytes, and in endothelial cells.

Question 85

Differentiation between mycoplasma atypical pneumonia and legionella

Answer 85

Legionella - GI symptoms, confusion, or bloody mucoid sputum Mycoplasma - scratchy sore throat, mild pharyngeal injection, skin rash. Rest of the stuff is same, milder symptoms than typical pneumonia ie fever with chills, shortness of breath on exertion, dry cough, persistent, pleuritic chest pain, headaches, myalgies, arthralgies, loss of appetite, low energy, fatigue.

Question 86

B2 microglobulin

Answer 86

On MHC Class I

Question 87

Invariant chain is on which MHC type molecule

Answer 87

MHC class II

Question 88

HLA allele associated with Sjorgns

Answer 88

DR3

Question 89

HLA subtype associated with Rheumatoid Arthritis

Answer 89

DR4

Question 90

HLA with anklyoising spondylitis

Answer 90

B27

Question 91

AIDS defining neoplasms

Answer 91

Kaposi sarcoma (HHV8), nonhodgkin lymphoma (EBV) rpimary CNS lymphoma (EBV), invasive cervical carcinoma (HPV)