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Pathology > Pre-Midterm (Post Unified) > Flashcards

Pre-Midterm (Post Unified) Flashcards

1
Q

Tissue response to fungi (type, cells)

A

Mixed PMN + lymphocytes + macrophages +/- giant cells

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2
Q

Schistosoma genus, and tissue reaction

A

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.

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3
Q

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

A

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)

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4
Q

Furuncle

A

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.

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5
Q

Lung Abscess

A

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.

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6
Q

TSS

A

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.

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7
Q

Strep Pneumoniae aka Pneumococcal pneumoniae

A

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.

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8
Q

LOBAR PNEUMONIA

A

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.

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9
Q

Bronchopneumonia

A

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.

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10
Q

Rheumatic fever

A

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).

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11
Q

Post-strep glomerulonephritis

A

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.

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12
Q

Components of pseudomembrane

A

Necrotic cells, bacteria, PMN, and exudate

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13
Q

Diphtheria toxin (Cornyebacterium diphtheria)

A

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.

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14
Q

Pseudomembranous Colitis

A

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

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15
Q

Pseudomembranous Colllitis commonly sen post use of which antibiotics

A

Clinda, cephalosporin, amoxicillin, ampicillin.

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16
Q

Clostridia Perfringens

A

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.

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17
Q

Typhoid Fever (enteric fever)

A 
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
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18
Q

Clinical features of enteric fever

A

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).

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19
Q

Causes of gram negative sepsis

A

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

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20
Q

HSV-2

A

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.

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21
Q

Cowdry A

A

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

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22
Q

Varicella Zoster virus

A

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

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23
Q

CMV infection

A

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.

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24
Q

Rabies

A

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

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25
Q

Measles (rubeola)

A

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.

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26
Q

HPV viral warts

A

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

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27
Q

Pneumocystis Jiroveci Pneumonia

A

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)

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28
Q

Cryptococcus neoformans

A

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

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29
Q

Histoplasmosis

A

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.

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30
Q

Mechanisms of Damage by foreign organisms

A

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

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31
Q

Inflammatory lesions of Staph: Lung Abscesses

A

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.

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32
Q

Most common causes of acute pyogenic meningitis by age gropu

A

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.

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33
Q

Diagnosis of Gonorrhea male v female

A

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.

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34
Q

Sickle cell and osteomyelitis

A

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

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35
Q

Gram negative septicemia

A

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.

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36
Q

Epidemic Typhus

A

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.

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37
Q

Sickle cell and osteomyelitis

A

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

38
Q

Gram negative septicemia

A

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.

39
Q

Epidemic Typhus

A

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.

40
Q

Allergic Bronchopulmonary Aspergillosis

A

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.

41
Q

Aspergilloma

A

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.

42
Q

Invasive Aspergillosis

A

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)

43
Q

Mucormycosis

A

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.

44
Q

Histoplasmosis

A

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.

45
Q

Complications of diphtheria

A

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

46
Q

Outcome of Primary TB

A

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.

47
Q

Progressive Primary Complex TB

A

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.

48
Q

Secondary TB

A

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)

49
Q

Progressive secondary TB

A

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

50
Q

Other organ involvement in TB

A

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)

51
Q

Tuberculoid Leprosy

A 
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
52
Q

Lepromatous Leprosy

A

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)

53
Q

Mercury Toxicity - Nervous System

A

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

54
Q

Mercury toxicity - kidneys

A

Inorganic Hg target (via skin and alimentary).

ACUTE due to high does - tubular necrosis
CHRONIC due to low dose - insufficiency due to eventual failure.

55
Q

Mercury effects on GI and Skin

A

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

56
Q

Berylliosis

A

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.

57
Q

Definition of AIDS (WITH lab confirmed HIV infection)

A

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.

58
Q

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

A

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

59
Q

Cocaine Toxicity

A

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

60
Q

Heroin

A

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)

61
Q

Aflatoxin B1

A

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

62
Q

AIDS defining neoplasms

A

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

63
Q

AIDs defining opportunistic infections

A

Protozoal: crytosporidiosis, isosporidiosis, toxoplasmosis

Fungal: candidiasis, cryptococcosis, coccidiomycosis, histoplasmosis, pneumocystosis

Bacterial: mycobacteriosis, nocardiosis, salmonellosis

Viral: CMV, herpes simplex, varicella-zoster, JC virus (PML)

64
Q

AIDs defining neoplasms

A

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

65
Q

Transudate

A

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.

66
Q

Exudate

A

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

67
Q

Virchow’s Triad - Endothelial Injury

A

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

68
Q

Virchow’s Trina - Loss of Laminar Flow

A

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.

69
Q

Virchow’s Triad - Hypercoagulability of Blood

A

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.

70
Q

Thrombus versus clot

A

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.

71
Q

Lines of Zhan

A

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

72
Q

Sites of thrombosis (arterial)

A

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

73
Q

Venous thrombosis

A

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)

74
Q

Sites of origin of thrombi in arterial circulation

A

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.

75
Q

Air embolism

A

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.

76
Q

Pyoderma

A

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

77
Q

Eyripelas

A

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

78
Q

Necrotizing fasciitis

A

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

79
Q

Cornyebacterium Jeikenum and minutissumum

A

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

80
Q

Diphtheria clinical importance

A

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

81
Q

HPIV-1 Infection predisposing factors and most common disease associated

A

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.

82
Q

Unstable/Vulnerable Plaque Characterisics

A

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

83
Q

Composition of vegetations in NBTE (Marantic endocarditis)

A

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

84
Q

Anti neutrophil cytoplasmic antibodies (ANCA)

A

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

85
Q

Differentiation between mycoplasma atypical pneumonia and legionella

A

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.

86
Q

B2 microglobulin

A

On MHC Class I

87
Q

Invariant chain is on which MHC type molecule

A

MHC class II

88
Q

HLA allele associated with Sjorgns

A

DR3

89
Q

HLA subtype associated with Rheumatoid Arthritis

A

DR4

90
Q

HLA with anklyoising spondylitis

A

B27

91
Q

AIDS defining neoplasms

A

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

Pathology (3 decks)

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