Block V

Front 1

What characterizes mucoepidermoid carcinomas?

Back 1

Malignant tumor composed of a mixture of squamous cells, mucus-secreting cells, and intermediate cells; occurs mainly in the parotids, but accounts for a large fraction of tumors in other salivary glands (esp. minor salivary glands)

Front 2

What characterizes Warthin tumors?

Back 2

2nd most common salivary gland neoplasm; almost always in parotid gland (sometimes bilateral); M>F, usually in 5th-7th decades of life; smoking increases the risk (x8); very low recurrence rate after complete resection

Front 3

When a pleomorphic adenoma undergoes malignant transformation (rare), what malignancies can arise?

Back 3

Carcinoma, Sarcoma (chondrosarcoma), True malignant mixed tumor

Front 4

What characterizes a pleomorphic adenoma?

Back 4

Most commonly seen in parotid gland (60%); contains a mixture of ductal and epithelial cells, with mixed mesenchymal and epithelial elements; painless, benign, slow-growing tumor – recurrence is rare after complete excision

Front 5

What are the malignant salivary gland tumors?

Back 5

Mucoepidermoid carcinoma (most common), adenocarcinoma NOS, acinic cell carcinoma, adenoid cystic carcinoma, and others

Front 6

What syndrome is xerostomia (dry mouth) associated with?
Sjögren syndrome

Back 6

(autoimmune destruction of exocrine glands); also seen as a complication of radiation therapy

Front 7

What characterizes mucoceles?

Back 7

Most common salivary gland lesion; result from ductal blockage or rupture with saliva leakage into surrounding stroma; most often found on the lower lip, typically result from trauma – complete excision is necessary

Front 8

What causes nonspecific (bacterial) sialoadenitis?

Back 8

Ductal obstruction by stone (sialolithiasis) is associated with bacterial overgrowth (usually Staph. aureus or Strep. viridans) which induces painful enlargement and purulent discharge

Front 9

What characterizes adenoid cystic carcinomas?

Back 9

Most often found in minor salivary glands; slow-growing by relentless/recurrent; perineural invasion is common; disseminate widely after time; early survival is good, but long-term is not

Front 10

What characterizes acinic cell carcinomas?

Back 10

Resemble normal serous acinar cells; most often in the parotid; recurrence after resection uncommon; survival rates are good

Front 11

What characterizes an olfactory neuroblastoma (esthesioneuroblastoma)?

Back 11

Neuroendocrine tumors resembling a neuroblastoma; it is a primitive neuroectodermal tumor but it does not have the 11;22 translocation of Ewing sarcoma – tumor of small cells, metastasize widely

Front 12

What characterizes an extramedullary plasmacytoma?

Back 12

Malignant plasma cells that arise in lymphoid structures adjacent to nose/sinuses – rarely progress to multiple myeloma

Front 13

What characterizes sinonasal (Schneiderian) papillomas?

Back 13

Benign neoplasms composed of squamous or columnar mucosa; caused by HPV 6 and 11 – can be septal, inverted (not exophytic), and cylindrical

Front 14

What concept is thought to be responsible for the fact that many people with oral cancer also often get laryngeal cancer?

Back 14

Field cancerization

Front 15

In what age group does otitis media most commonly occur and what are the causative agents of acute and chronic disease?

Back 15

Infants and young children – Acute: S. pneumoniae, H. influenza, M. catarrhalis;
Chronic: P. aeruginosa, S. aureus, fungus or mixed flora

Front 16

What characterizes laryngeal squamous papillomas?

Back 16

Benign neoplasms, usually on the true vocal folds; small, soft, raspberry-like excrescences that have slender, finger-like projections with fibrovascular cores and squamous epithelium; usually single in adults and multiple in children (juvenile laryngeal papillomatosis); multiple recurring papillomas are associated with HPV 6/11 (not malignant, often regress at puberty)

Front 17

What is the prognosis for a patient with laryngeal carcinoma?

Back 17

At presentation 60% are confined to the larynx; they generally spread to lymph nodes; cancer may recur at primary site or adjacent sites (field cancerization); about 1/3 die of disease (usually due to local spread of the cancer)

Front 18

Where do laryngeal cancers first metastasize to?

Back 18

Cervical lymph nodes (just like Head/Neck cancer)

Front 19

What is the treatment for laryngeal carcinomas?

Back 19

Depends on the stage: can include radiation/surgery (laryngectomy with/without ipsilateral radical neck dissection), chemotherapy/radiotherapy, or a combination of surgery/radiation/chemo

Front 20

What characterizes laryngeal carcinomas (site of origin, type)?

Back 20

Their site of origin can include the vocal cords or surrounding structure (epiglottis, aryepiglottic folds, piriform sinuses); 95% are squamous cell carcinomas; they are ulcerating/fungating lesions

Front 21

What are the most common causes of laryngitis and what are the possible consequences?

Back 21

Infection or heavy tobacco smoke exposure – β-hemolytic strep and Haemophilus influenzae can cause a lethal laryngoepiglottitis in infants/young children (may require intubation/tracheostomy); inflammation of the larynx can cause croup in children (laryngotracheobronchitis with inspiratory stridor); Laryngitis in smokers may have pre-malignant changes

Front 22

What are the major risk factors for laryngeal carcinoma?

Back 22

Cigarette smoking, alcohol exposure – minor factors: nutritional causes, asbestos, radiation, HPV

Front 23

What characterizes reactive nodules on the vocal cords?

Back 23

They most commonly occur in smokers or in those with strain on the vocal cords (singers); they occur more frequently in males than females and cause hoarseness; morphologically they are smooth rounded excrescences composed of myxoid connective tissue, covered by squamous epithelium – surgical excision is curative

Front 24

What are the most common types of ear tumor?

Back 24

Those affecting the external canal: squamous cell and basal cell

Front 25

What do carotid body tumors consist of?

Back 25

Zellballen: nests of polygonal neuroendocrine cells enclosed by fibrous trabeculae and elongated sustentacular cells

Front 26

Where are the most common paragangliomas located?

Back 26

Carotid body paraganglion, vagal paraganglia, jugulotympanic paraganglia

Front 27

What characterizes paragangliomas?

Back 27

Tumors arising in extra-adrenal paraganglia (paravertebral or associated with the great vessels of the head); often arise singly/sporadically in the sixth decade of life; may be familial, associated with autosomal dominant transmission of MEN II syndrome – they frequently recur after incomplete resection; many metastasize to local/distant sites; about half are fatal

Front 28

What characterizes a thyroglossal duct cyst?

Back 28

Midline remnants of the thyroid tract between the foramen cecum of the tongue and the thyroid;
they are 1-4 cm cysts with stratified squamous/pseudostratified columnar epithelial lining; contain lymphoid aggregates or remnants of thyroid tissue – excision with recurrence if incomplete, malignant transformation is rare

Front 29

What characterizes a branchial cleft cyst?

Back 29

Lateral remnants of the branchial arches or salivary gland inclusions in cervical lymph nodes;
they are 2-5 cm circumscribed cysts with fibrous walls, composed of stratified squamous/ pseudostratified columnar epithelial lining; they have clear, watery-to-mucinous contents or desquamated, granular cellular debris – they enlarge slowly and rarely transform to malignant

Front 30

What are the most common neck masses caused by?

Back 30

Reactive lymphadenopathy; Cysts: branchial cleft (lateral), thyroglossal duct (medial); Metastatic tumors; Lymphoproliferative disorders

Front 31

What can result from severe otitis media?

Back 31

Eardrum perforation;, Spread within ear, temporal cerebritis, abscess; Destructive necrotizing otitis media in diabetics (P. aeruginosa)

Front 32

What characterizes otosclerosis?

Back 32

Abnormal bone deposition in the middle ear, hampering stapes footplate mobility (hearing loss);
starts in young adults and is slowly developing; has an autosomal dominant pattern with variable penetrance – can be surgically corrected with a prosthesis

Front 33

What characterizes cholesteatoma?

Back 33

A non-neoplastic mass of keratinized squamous epithelium and cholesterol in the middle ear, seen with tympanic membrane perforation or chronic otitis media; complications include erosion into surrounding structures or production of a neck mass

Front 34

What are the benign salivary gland tumors?

Back 34

Pleomorphic adenoma (most common), Warthin tumor, oncocytoma, other adenomas, ductal papillomas

Front 35

What is the prognosis with mucoepidermoid carcinomas?

Back 35

Low-grade: invade locally, rarely metastasize, 5-year survival > 90%; High-grade: invasive, difficult to excise, higher recurrence rate, many disseminate, 5-year survival rate is 50%

Front 36

What characterizes periodontitis?

Back 36

Inflammatory process affecting supporting structures of the tooth (due to a shift in bacterial flora and poor oral hygiene) – can result in loss of teeth, infective endocarditis, pulmonary/brain abscesses, and adverse pregnancy outcomes (premature labor)

Front 37

What characterizes gingivitis?

Back 37

Inflammation of soft tissues around the teeth (due to a lack of oral hygiene) leading to the accumulation of dental plaque (microbes) and calculus (mineralized plaque) – most common in adolescents (but reversible)

Front 38

What characterizes hairy leukoplakia?

Back 38

White, confluent patches of fluffy (“hairy”) hyperkeratotic thickening and squamous hyperplasia found on the lateral border of the tongue – mostly associated with AID

Front 39

What pattern of metastasis is usually associated with HNSCC?

Back 39

Invades locally first (cervical lymph nodes), and then to distant sites (mediastinal lymph nodes, lungs, liver, bones)

Front 40

What are common sites for HNSCC?

Back 40

Floor of mouth, ventral surface of tongue, soft palate/gingiva, base of tongue

Front 41

What pathogenesis is associated with head and neck squamous cell carcinoma (HNSCC)?

Back 41

Most common in middle aged men who smoke or abuse alcohol; some are HPV+

Front 42

What is meant by field cancerization?

Back 42

After a primary cancer has been discovered, second primaries will often present later on – this is due to the fact that cancer causing agents are effective over a large field of distribution

Front 43

What is the most common type of head/neck cancer (95%)?

Back 43

Squamous cell carcinoma (most common in the oral cavity) – long-term survival is < 50%

Front 44

What distinguishes leukoplakia from erythroplakia?

Back 44

Leukoplakia is a white lesion without specific diagnosis (5-25% premalignant) whereas erythroplakia is a red, velvety area (level/slightly depressed) that is associated with an atypical epithelium 90% of the time (dysplasia, CIS, cancer)

Front 45

What viruses are associated with oral pathology?

Back 45

HSV-1, HSV-2, VZV, EBV, CMV, Rubeola (measles)

Front 46

What are examples of deep fungal infections?

Back 46

Zygomycosis, Aspergillosis, Coccidiomycosis, Cryptococcosis, Histoplasmosis, Blastomycosis

Front 47

In what patients is oral Candidiasis often seen?

Back 47

Immunosuppressed, diabetics, transplant patients, AIDS, patient taking chemotherapy

Front 48

What characterizes an ameloblastoma?

Back 48

Cystic, slow-growing, locally invasive, benign growth – can also occur in the paranasal sinuses

Front 49

What are mucormycosis and how are they treated?

Back 49

Spreading fungal infections (especially in diabetics) – can be treated by surgical debridement

Front 50

What can chronic tonsillitis lead to?

Back 50

Obstruction of breathing, sleep apnea

Front 51

What can an infection with β-hemolytic streptococci lead to?

Back 51

Rheumatic fever and glomerulonephritis

Front 52

What are nasal polyps?

Back 52

Edematous mucosa with a loose stroma and inflammatory cells – can occlude the nasal canal

Front 53

Which viruses are responsible for the common cold?

Back 53

Adeno-, echo-, and rhinoviruses

Front 54

What characterizes an odontoma?

Back 54

Arises from epithelium and shows extensive deposition of enamel/dentin – probably hamartomatous

Front 55

What is the most common odontogenic cyst and what characterizes it?

Back 55

Periapical cyst – inflammatory cyst found at the apex of the tooth

Front 56

What characterizes an odontoma?

Back 56

Arises from epithelium and shows extensive deposition of enamel/dentin – probably hamartomatous

Front 57

What is the most aggressive odontogenic cyst and what characterizes it?

Back 57

Odontogenic keratocyst; most common in the posterior mandible of males age 10-40;
It has well-defined rediolucencies and contains a layer of parakeratinized/orthokeratinized (“basket weave pattern”) epithelium – needs to be aggressively and completely removed

Front 58

What characterizes a dentigerous cyst?

Back 58

Unilocular cyst around the crown of an unerupted tooth; contains a thin layer of stratified squamous epithelium – complete resection is curative

Front 59

What characterizes a nasopharyngeal angiofibroma?

Back 59

Vascular neoplasm of adolescent males, can bleed profusely

Front 60

What characterizes the nasopharyngeal carcinoma?

Back 60

Associated with EBV, seen in African children and adults in S. China; EBV is associated with the undifferentiated form (lymphoepithelioma); they tend to grow silently and are very radiosensitive

Front 61

What characterizes an irritation fibroma?

Back 61

Caused by a accidental bite in the buccal mucosa leading to a nodular mass of fibrous tissue covered by squamous mucosa

Front 62

What characterizes herpes simplex virus?

Back 62

Usually HSV-1 (increase in HSV-2); primary infection occurs in children, and reactivation occurs with triggers (e.g. stress, infection); cold sores consist of vesicles with molding, intranuclear inclusion (identified by Tzanck test)

Front 63

What characterizes glossitis?

Back 63

Inflammation of the tongue, often associated with vitamin deficiencies, iron-deficiency anemia, and esophageal dysphagia

Front 64

What characterizes apthous ulcers?

Back 64

Very common shallow ulcer with this exudate and narrow erythematous border – most common in the first two decades and within families; causation is obscure

Front 65

What characterizes a peripheral giant cell granuloma?

Back 65

Multinucleate, foreign body-like giant cells in a fibrovascular stroma; similar to a pyogenic granuloma but more bluish-purple

Front 66

What characterizes a peripheral ossifying fibroma?

Back 66

Red, ulcerated, nodular, reactive growth of the gingiva (etiology unknown) – common in young and teenage females

Front 67

What characterizes a pyogenic granuloma?

Back 67

Ulcerated, red-purple vascular proliferation (form of capillary hemangioma) – common in children, young adults, and pregnant women

Front 68

What is the most common cause of tooth loss below age 35?

Back 68

Caries (focal degradation of tooth structure by bacterial acid metabolic end products)

Front 69

What is the purpose of hyphae?

Back 69

They serve to penetrate substance, translocate nutrients via coordinated cytoplasmic streaming, and produce aerial spores

Front 70

What are some nutritional characteristics of fungi?

Back 70

Grow over wide pH range (1-11); filamentous fungi are mainly aerobic, whereas yeasts are often facultative anaerobes (fungi can also be obligate anaerobes); they can grow at very low moisture levels (>50%)

Front 71

What is meant by germination of fungi?

Back 71

Hyphal growth from a spore

Front 72

What effects do the death cap/death angel and fly agaric have on the body, respectively?

Back 72

Death cap/death angel: destroys the liver; Fly agaric: muscarinic agonist (hallucinations)

Front 73

How does sexual reproduction of fungi occur?

Back 73

Via sexual spores --> fusion of nuclei from 2 haploid mating strains --> zygote --> meiosis --> recombinant haploid spores

Front 74

What fungus is commonly found in a grain silo, and causes sick building syndrome?

Back 74

Aflatoxicosis – infection can lead to liver cancer

Front 75

How are fungi identified in the lab?

Back 75

By looking at their spores (conidia)

Front 76

What are the two methods by which fungi grow and reproduce?

Back 76

Yeast: budding ; Hypha: tubules/spores (sexual/asexual)

Front 77

What substance is found in the hyphal cell walls?

Back 77

Chitin (β-1,4 N-acetyl glucosamine); may contain septa (cross-walls) or may be coenocytic (no cross-walls)

Front 78

What is meant by a fungus that is dimorphic?

Back 78

It can grow as yeast in its infective/pathogenic stage, but is capable of hyphal growth saprophytically (in lab culture at room temperature)

Front 79

By what mechanism, other than meiosis, can recombination of fungi occur?

Back 79

Mitotic recombination in multinucleated cells after hyphal anastomosis (the spindle apparatuses of two cells undergoing mitosis become confused and chromosomal material is exchanged)

Front 80

What are the various types of fungal infections (i.e. what locations/organ systems can they be associated with)?

Back 80

Systemic mycoses, CNS mycoses, opportunistic mycoses, subcutaneous mycoses (wound infections), dermatomycoses (caused by keratinophilic fungi), superficial mycoses (fungal infections of the cutaneous integument – not associated with serious complications)

Front 81

How do opportunistic mycoses relate to nosocomial infections (hospital acquired)?

Back 81

They are the third most common, but cause 50% of nosocomial mortality – also, 90% of AIDS patients are afflicted by opportunistic mycoses

Front 82

What does the Gomori Methenamine Silver (GMS) stain attach to?

Back 82

Cell wall of fungi: chitin

Front 83

What key differences are found between fungi and bacteria?

Back 83

Cell walls: chitin vs. peptidoglycan; Staining: PAS/GMS vs. Gram+/-; Cell membranes: ergosterol vs. no sterol; Spore functions: resist desiccation vs. resist heat; Secondary metabolites: FK506 vs. none – also, fungi are larger, have organelles, undergo meiosis, have longer regeneration times, have infectious airborne propagules, and more commonly form spores

Front 84

What are some examples of recombinant drugs that are developed using fungi (yeast fermentation)?

Back 84

Human insulin (humulin) and hepatitis B vaccine

Front 85

What are the most common species of Candida seen clinically?

Back 85

C. albicans > C. glabrata > C. tropicalis > C. parapsilosis > C. krusei > C. lusitaniae

Front 86

What acute and chronic adverse effects are associated with Amphotericin B?

Back 86

Acute: fever, chills, rigors, hypotension, arrhythmias, thrombophlebitis, HA;
Chronic: nephrotoxicity (!), hypokalemia, hypomagnesemia, sodium wasting, anemia

Front 87

What is the mechanism of action of Amphotericin B?

Back 87

Binds to ergosterol in fungal cell membranes and alters permeability, leading to leakage of vital cell components

Front 88

Why is Amphotericin B given with deoxycholate in systemic formulations?

Back 88

Amphotericin B is not water soluble and requires a water-soluble ionic detergent (deoxycholate) and must be given in dextrose 5% water in order to form a micellular dispersion so that the drug is equally spread out in the formulation

Front 89

What is the “gold standard” for fungal infections?

Back 89

Amphotericin B

Front 90

What is the most common life-threatening fungal infection in HIV-positive patients?

Back 90

Cryptococcus

Front 91

What characterizes Aspergillus clinically?

Back 91

Most common in immunodeficient/immunosuppressed patients; expensive to treat; high mortality

Front 92

Which common fungi are classified as yeasts, moulds, and dimorphic (endemic), respectively?

Back 92

Yeasts: Candida, Cryptococcus; Moulds: Aspergillus, Mucormycosis, Fusarium;
Dimorphic: Histoplasma capsulatum, Blastomyces dermatitidis, Coccidioides immitis

Front 93

What endemic areas are associated with the Dimorphic fungi?

Back 93

Histoplasma capsulatum: Ohio river valley, Mississippi river valley; Blastomyces dermatitidis: Mississippi river valley, Southern US; Coccidioides immitis: Western US (causes valley fever)

Front 94

What are the most common fungal pathogens seen clinically?

Back 94

Yeast: Candida; Mould: Aspergillus

Front 95

What is the mechanism of action of Flucytosine (5-FC)?

Back 95

It is a pro-drug that is converted into 5-FU; this is a pyrimidine analog which disrupts DNA synthesis by inhibiting thymidylate synthetase

Front 96

Which patients should be given Amphotericin B rather than Fluconazole?

Back 96

Neutropenic patients, since Fluconazole is fungistatic, and not fungicidal like Amphotericin B

Front 97

What adverse effects are associated with the older azoles?

Back 97

Although they have a good therapeutic index, there is the chance of a drug-induced hepatotoxicity and they have an inhibitory effect on the CYP450 enzymes

Front 98

How do Fluconazole and Itraconazole differ?

Back 98

Fluconazole: narrower spectrum, yeast infections; Itraconazole: broader, yeast and mould activity

Front 99

What are the older azoles and what is their mechanism of action?

Back 99

Imidazoles: Miconazole, Ketoconazole; Triazoles: Itraconazole, Fluconazole – they function by inhibiting 14-α-lanosterol demethylase (CYP51A1, normally converts lanosterol to ergosterol), leading to a more fragile cell membrane; they are fungistatic

Front 100

What adverse effects are associated with 5-FC?

Back 100

Marrow toxicity (neutropenia); also, hepatic and GI effects (same as with 5-FU)

Front 101

How and for what is 5-FC used?

Back 101

In combination with other antifungal drugs since resistance develops rapidly; its main use is in Cryptococcal infections

Front 102

What specific effect does Amphotericin B have on the kidneys?

Back 102

It damages the renal tubules, thus inhibiting the tubule’s capacity for electrolyte reabsorption; this can lead to hypokalemia, hypomagnesemia, sodium wasting, and anemia – saline-loading is done to prevent renal insufficiency

Front 103

What are the three lipid formulations of Amphotericin B and how do they differ?

Back 103

ABLC (ribbon complex): very large size; L-AMB (liposome): very small size, mildest infusion-related reactions, highest cost; ABCD (disc-like complex): intermediate size, high rate of infusion-related reactions, lowest cost – all three formulation are less nephrotoxic, but none have superior efficacy nor a survival benefit associated with them

Front 104

What drugs are given to lessen the infusion-related adverse effects of Amphotericin B, and what is given if a patient develops rigors?

Back 104

Infusion-related side effects: Acetaminophen, anti-histamines – Rigors: Meperidine

Front 105

What is the mechanism of action of the echinocandins?

Back 105

They inhibit β-D-glucan synthase which causes disruption of the enzyme complex that is responsible for the formation of glucan fibrils; a disturbance of these fibrils will cause the fungal cell wall to break down (in a similar fashion by which Penicillin disrupts bacterial cell walls)

Front 106

What is special about Posaconazole?

Back 106

It is an oral Triazole with broad-spectrum activity: approved for Candida/Aspergillus and used off-label for Zygomycosis infections (!)

Front 107

What pharmacokinetics are associated with Voriconazole?

Back 107

Oral and IV formulations; good bioavailability; food can decrease absorption; IV formulations use a carrier; large Vd and penetrates CSF (!); inter-individual pharmacokinetic variability is high (due to CYP450 variability); since it is metabolized by CYP450, drug interactions are common;
dosing is difficult

Front 108

What adverse effects are associated with Voriconazole?

Back 108

Elevated liver enzymes (has greater hepatotoxicity than Fluconazole); Skin rash;
Visual disturbances (! does mean that the drug is effective for fungal infections of the eye)

Front 109

What is characteristic about Voriconazole as compared to Fluconazole?

Back 109

Voriconazole has been engineered to be more broad-spectrum: it has enhanced activity against all Candida species and is effective against Aspergillus and some other moulds

Front 110

What issues are associated with the echinocandins?

Back 110

Although they have minimal adverse effects and drug interactions, they are very expensive and only available in IV formulation

Front 111

What fungi are affected by the echinocandins?

Back 111

Candida and Aspergillus – but NOT Cryptococcus

Front 112

Although all common forms of Candida are susceptible to Amphotericin B, which species are susceptible to Fluconazole?

Back 112

Fluconazole is effective in C. albicans/parapsilosis/tropicalis, but not in C. glabrata/krusei (in reality C. glabrata susceptibility is dose dependent whereas C. krusei is always resistant)

Front 113

What are the echinocandins?

Back 113

Caspofungin, Micafungin, Anidulafungin

Front 114

What issues are associated with Itraconazole?

Back 114

Takes a long time to get to steady-state concentrations; no good oral absorption (especially when taken with antacids); significantly more drug interactions than Fluconazole

Front 115

How does treatment of Candida differ when a patient is septic/immunocompromised vs. when they are not?

Back 115

Septic/immunocompromised: Amphotericin B, echinocandins; Not: Fluconazole, echinocandins

Front 116

What drugs are used for endemic fungal infections?

Back 116

Itraconazole and Amphotericin B

Front 117

What is the first-line treatment for Cryptococcal meningitis?

Back 117

Amphotericin B with Flucytosine, followed by Fluconazole maintenance (in HIV patients, Fluconazole treatment is continued prohylactically)

Front 118

What is the first-line treatment for invasive Aspergillosis?

Back 118

Amphotericin B or Voriconazole (second-line is Caspofungin or high-dose AmphotericinB)

Front 119

What are the Serotonin reuptake inhibitors (SRIs)?

Back 119

Fluoxetine, Fluvoxamine, Paroxetine, Sertraline, Citalopram, Escitalopram

Front 120

What is the treatment for Serotonin syndrome?

Back 120

Discontinue SRI; Treat with benzodiazepines or 5-HT2A antagonists (cyproheptadine); Use short-acting drugs to control BP, and a non-depolarizing neuromuscular blocker with intubation for severe hyperthermia

Front 121

What drug interactions are seen with SRIs?

Back 121

Never use with MAOIs: SRI must be withdrawn for a least two weeks before MAOI use (and vice versa), combined use can result in Serotonin syndrome (autonomic instability, rigidity, fever, stupor, death) – there are also concerns with other drugs that enhance serotonergic transmission

Front 122

What characterizes the pharmacokinetics of SRIs?

Back 122

Good PO absorption, long half-life (more than a day), some produce longer-lived/active metabolites, oxidized by hepatic enzymes; some have complex pharmacokinetics (CYP inhibition)

Front 123

What adverse effects are associated with SRIs?

Back 123

Initial agitation/excitation, nausea, sexual dysfunction – fewer side effects relative to other antidepressants (low incidence of cardiovascular/anticholinergic effects); little risk of overdose

Front 124

What is the primary method of inactivation of Serotonin?

Back 124

Reuptake – thus the use of SRIs

Front 125

What characterizes the SRIs?

Back 125

First-line therapy in patients diagnosed with major depression; also used to treat OCD and some eating disorders – failure of one SRI does not signal failure on another; similar efficacy to other antidepressants (may be better compliance)

Front 126

What characteristic do all antidepressants have in common?

Back 126

They show a therapeutic lag: it takes a couple of weeks for their effects to become evident, and even longer to become maximal (~8wks) – side effects are immediate

Front 127

What black box warning is associated with most antidepressants?

Back 127

Increased “suicidality” – especially in children/adolescents; more prevalent in early treatment

Front 128

What does the delay in the effects of antidepressants suggest?

Back 128

That the patient undergoes a delayed response (regulation of receptors, transporters; neurogenesis) – however, acute effects appear essential

Front 129

What characterizes Venlafaxine?

Back 129

SNRI with non-CYP metabolism; First-line agent for depression, also used for anxiety disorders;
AEs: HTN, tachycardia, nausea, anorexia, drowsiness, dry mouth, sexual effects like SRIs;
CI: HTN (not absolute); DI: Serotonin syndrome (like SRIs)

Front 130

What characterizes the pharmacokinetics of TCAs?

Back 130

Good PO absorption, long half-life (more than a day), some produce longer-lived/active

Front 131

What adverse effects are associated with TCAs?

Back 131

Orthostatic hypotension: due to antagonism of α-adrenergic receptors; Anticholinergic effects: blurred vision, worsening of narrow-angle glaucoma, dry mouth, constipation, urinary retention, tachycardia, confusion; Sedation: antagonism of histamine and α-adrenergic receptors;
Cardiovascular effects: seen with overdose, arrhythmias, direct myocardial depression, worsening of CHF, can be lethal, limit access to drug; With bipolar illness: precipitation of manic episode

Front 132

What is the mechanism of action of TCAs?

Back 132

Inhibit reuptake of Serotonin/NE; potentiate and prolong the actions of these neurotransmitters; receptor and transporter regulation with repeated treatment

Front 133

What characterizes the TCAs?

Back 133

Similar efficacy to SRIs; have been supplanted in most cases by SRIs as first-line therapy;
Generally cause weight gain; Also used to treat certain types of pain, panic disorder, ADHD

Front 134

What are the tricyclic antidepressants (TCAs)?

Back 134

Amitriptyline, Clomipramine, Desipramine, Doxepin, Imipramine, Nortriptyline, Protriptyline, Trimipramine

Front 135

What characterizes Duloxetine?

Back 135

SNRI with CYP metabolism; Used in treatment of depression itself and for the treatment of physical pain associated with depression (useful in treatment of pain from diabetic neuropathy);
AEs: nausea, anorexia, drowsiness, constipation, dry mouth, rare hepatic injury;
CI: liver disease, alcoholism; DI: Serotonin syndrome and CYP interactions

Front 136

What are some characteristics of the individual SRIs?

Back 136

Fluoxetine: potent CYP inhibitor, insomnia/anxiety more common, long T½ , active metabolites;
Sertraline: diarrhea more common; Paroxetine: potent CYP inhibitor, anticholinergic (sedation, constipation), weight gain, sexual dysfunction, ↑ risk of cardiac birth defects in 1st trimester;
Fluvoxamine: used for OCD, potent CYP inhibitor; Citalopram: faster onset of action;
Escitalopram: active stereoisomer of citalopram, more potent/more selective/faster onset

Front 137

What are the Serotonin-Norepinephrine reuptake inhibitors (SNRIs)?

Back 137

Venlafaxine, Duloxetine

Front 138

What are the effects of SRIs on the CYP enzymes?

Back 138

Strong inhibitors: Fluoxetine, Fluvoxamine, Paroxetine;
Weak inhibitors: Sertraline, Citalopram, Escitalopram

Front 139

What contraindications are associated with MAOIs?

Back 139

Alcohol abuse, cardiovascular disease, HTN, cerebrovascular disease/bleeding, renal failure, children – use with extreme caution

Front 140

What characterizes Bupropion?

Back 140

Weak blocker of DA, Serotonin, NE uptake; Can cause agitation/anxiety/restlessness; Associated with a risk of seizure (administered as divided doses or slow release formulation); Also used as aid in quitting smoking – used in patients who can’t tolerate the sexual side effects of more common antidepressants

Front 141

What are the atypical antipsychotics?

Back 141

Bupropion, Mirtazapine, Trazodone, Nefazodone

Front 142

What characterizes the reversible inhibitors of MAO (RIMAs)?

Back 142

MAO-A inhibitors: more effective antidepressants; MAO-B: used with Parkinson’s (Selegiline) – not used clinically in the US, fewer drug/food interactions

Front 143

What drug interactions are seen with MAOIs?

Back 143

Food containing high amounts of tyramine, sympathomimetic drugs (cold remedies, diet aids, stimulants), SRIs, Meperidine and some other analgesics

Front 144

What characterizes the pharmacokinetics of MAOIs?

Back 144

Good PO absorption, daily dosing required (in spite of irreversible enzyme inhibition), inactivated by acetylation (caution in slow acetylators)

Front 145

What adverse effects are associated with MAOIs?

Back 145

Orthostatic hypotension, restlessness, insomnia, sometimes fatal hypertensive crisis (when combined with drugs like sympathomimetics, and with foods containing tyramine – strict monitoring required)

Front 146

What drug interactions are seen with TCAs?

Back 146

Interactions with alcohol and other sedatives, antiparkinson drugs, antipsychotic drugs, biogenic amines – also via competition for plasma protein binding

Front 147

What characterizes the use of MAOIs?

Back 147

Only used in patients who have failed courses of treatment with other antidepressants and for whom electroconvulsive therapy is not suitable – MAO levels remain low for at least two weeks after withdrawal of an MAOI (MAO inhibition is irreversible)

Front 148

What are the MAOIs?

Back 148

Phenelzine, Tranylcypromine

Front 149

What adverse effects are seen with Trazodone, Nefazodone?

Back 149

Drowsiness, dizziness, lightheadedness, dry mouth, priapism, Serotonin syndrome with serotonergic drugs

Front 150

What atypical antipsychotics are used for the treatment of acute mania and long-term management?

Back 150

Olanzapine, Risperidone, Quetiapine, Ziprasidone, Aripiprazole

Front 151

What adverse effects are associated with Lithium?

Back 151

Mild AEs: HA, fatigue, confusion, weakness, thirst, polyuria; Severe AEs: myoclonic jerks, seizures, impaired consciousness, coma, death (levels about 3.5 mEq/L are often fatal);
Cardiac effects: ECG irregularities, cardiac arrest; Fetal/lactational effects: Ebstein anomaly, fetal goiter, floppy baby syndrome, arrhythmias in nursing infants

Front 152

What characterizes Lithium?

Back 152

Mechanism of action poorly understood: inhibits inositol phosphate signalling, inhibits neurotransmitter-stimulated adenylyl cyclase; Low therapeutic index: monitor plasma concentrations; Renal clearance: sensitive to diuretics and anti-inflammatory drugs

Front 153

What characterizes the pharmacotherapy of bipolar depression?

Back 153

Mood stabilizers: Lithium, Carbamazepine, Valproate, other anticonvulsants, atypical antipsychotics; Acute anti-mania effects: benzodiazepines, antipsychotics

Front 154

What are the stages of treatment of MDD?

Back 154

Acute treatment (1-3 months): decrease symptoms; Continuation treatment (4-9 months): prevent relapse; Maintenance treatment (12+ months): used for high risk patients

Front 155

What contraindications are associated with Bupropion?

Back 155

Patient with seizure disorders, during lactation – can see Serotonin syndrome with serotonergic drugs

Front 156

What characterizes Trazodone, Nefazodone?

Back 156

Moderate inhibition of Serotonin reuptake, Serotonin-2 receptor antagonist – useful in the treatment of depression characterized by anxiety and sleep disturbances

Front 157

What adverse effects are seen with Mirtazapine?

Back 157

Drowsiness/fatigue (H1 receptor antagonist), appetite stimulation, weight gain, elevated blood lipids, rare blood dyscrasia; CI in severe liver disease and blood dyscrasia – do not use with MAOIs, watch for signs of neutropenia, caution due to sedation

Front 158

What characterizes Mirtazapine?

Back 158

Enhances the release of Serotonin and NE by antagonizing presynaptic α2-adrenergic receptors; also antagonizes 5-HT2/3 receptors – relative to SRIs, there is a reduced incidence of GI and sexual side effects

Front 159

What characterizes the phases of treatment with bipolar illness?

Back 159

Acute phase: control symptoms of mania (with an antipsychotic); Continuation phase: remission (mood stabilization with Lithium, anticonvulsants, atypical antipsychotics) and maintenance (lifetime therapy may be necessary)

Front 160

What are the different ways in which the viral genome can be protected?

Back 160

Via an icosahedral capsid or a helical capsid; and with or without a membrane present

Front 161

What are the stages of the virus life cycle?

Back 161

Initiation of infection: adsorption and penetration; Synthesis of viral proteins and genetic material: genome replication and transcription/translation of viral proteins; Maturation: assembly and release

Front 162

What is the key difference between a virus containing +RNA and one containing –RNA?

Back 162

The virus containing +RNA can immediately be translated by host ribosomes, whereas the virus containing only –RNA must first be transcribed to a +RNA by an RNA-dependent RNA polymerase before viral proteins can be synthesized

Front 163

How does a virus containing a single strand of +RNA create many more of that same +RNA?

Back 163

It uses an RNA-dependent RNA polymerase to create a –RNA (i.e. it is in 3` to 5` orientation instead of the normal 5` to 3` orientation); this –RNA serves as a template to create a large number of +RNA

Front 164

What are the parameters for viral classification?

Back 164

Nucleic acid structure and composition (e.g. RNA vs. DNA, ss vs. ds); Nucleocapsid symmetry (e.g. icosahedral vs. pleomorphic vs. filamentous); Presence/absence of an envelope

Front 165

Which viral enzyme is an attractive drug target since the enzyme is not produced by humans?

Back 165

RNA-dependent RNA polymerase (creates an mRNA transcript from RNA)

Front 166

What structures are associated with viral membranes and what is their clinical significance?

Back 166

Membrane-spanning glycoproteins that are specific to a particular virus and function in their adhesion to host cells; these glycoproteins can be the target of antibodies, thus preventing adhesion (e.g. hemoglutinin of influenza)

Front 167

What determines the specificity of a virus?

Back 167

The organ that contains the protein that is recognized by a particular virus

Front 168

What are the functions of the

Back 168

viral capsid?
Packaging/condensation; Protection of nucleic acid; Transport of nucleic acid from cell to cell; Provide specificity for attachment

Front 169

What is a virion?

Back 169

Viruses released from cells after the initial infection

Front 170

What occurs during the eclipse period of the viral life cycle?

Back 170

It replicates its genome

Front 171

What characterizes the picornaviruses?

Back 171

Icosahedral, no envelope present, ss-linear, nonsegmented, +RNA; includes poliovirus (gut/brain), rhinovirus (upper respiratory tract), Hepatitis A (liver), meningitis, hand-foot-mouth disease

Front 172

Which type of RNA does not bring in the RNA-dependent RNA polymerase and why?

Back 172

+RNA, since it can immediately be translated and start producing RNA-dependent RNA polymerase; –RNA has to bring the enzyme with it since host ribosomes cannot read the –RNA, so the initial +RNA will have to made by the virus itself

Front 173

What are plaque assays used for?

Back 173

To quantify the number of viral particles in a particular sample

Front 174

What are the three main host responses in regards to viral particles?

Back 174

Humoral response: antibodies; Cell mediated response: T-cells; Interferons: sense double-stranded RNA and block viral replication

Front 175

What happens in certain viruses when the host cell reaches yield?

Back 175

It bursts and releases all intracellular virions

Front 176

What occurs at the end of the latent period of the viral life cycle?

Back 176

Intracellular virions are released into the extracellular environment

Front 177

By what two mechanisms can viral particles gain entry into the cell?

Back 177

It can directly fuse with the host cell membrane (e.g. HIV); It can gain entry through a host endocytic vesicle (e.g. West Nile)

Front 178

What is a mechanism by which virus assembly and release occurs?

Back 178

Viral glycoproteins insert themselves into the host cell membrane --> viral matrix proteins associated with the intracellular portion of these glycoproteins --> when the viral genome comes in contact with the matrix proteins, it induces folding and budding of the viral particle (some host cell proteins may become part of the virus)

Front 179

Why do viruses have to regulate what genes are transcribed when?

Back 179

So that they produce their replication machinery first, before producing the capsid

Front 180

What characterizes the flaviviruses?

Back 180

Identical morphology to alphaviruses (icosahedral, envelope present, ss-linear, nonsegmented, +RNA), but different replication strategy; includes West Nile virus (transmitted by mosquitoes), Yellow fever (mosquitoes, liver), Dengue fever (hemorrhagic-type fever), Hepatitis C

Front 181

What characterizes paramyxovirus?

Back 181

Helical, envelope present, ss-linear, nonsegmented, –RNA; includes measles (very infectious, encephalitis), mumps (parotid gland, encephalitis, sterility), parainfluenza (croup), respiratory syncitial disease

Front 182

What characterizes orthomyxovirus?

Back 182

Helical, envelope present, ss-linear, segmented (8 strands), –RNA; includes influenza, common cold (influenza C)

Front 183

What characterizes the retroviruses?

Back 183

Icosahedral, envelope present, 2 strands of ss-linear +RNA with a reverse transcriptase attached; includes HIV, HTLV-I, HTLV-II

Front 184

What characterizes the coronaviruses?

Back 184

Helical, envelope present, ss-linear, nonsegmented, +RNA; includes SARS, common cold

Front 185

What makes Hepatitis C a difficult virus to treat?

Back 185

It has a RNA-dependent RNA polymerase that makes many mistakes, which means it has a high rate of mutation

Front 186

What characterizes the calciviruses?

Back 186

Icosahedral, no envelope preset, ss-linear, nonsegmented, +RNA; includes Norwalk virus (“cruise ship diarrhea, self-limting/acute), Hepatitis E

Front 187

What characterizes the alphaviruses (arboviruses/togaviruses)?

Back 187

Icosahedral, envelope present, ss-linear, nonsegmented, +RNA; includes Western equine encephalitis (also Venezuelan equine encephalitis and Eastern equine encephalitis, all are transmitted by mosquitoes), and Rubella virus (especially harmful in first trimester)

Front 188

What characterizes the reoviruses?

Back 188

Icosahedral, double-shelled capsid, no envelope present, ds-linear, segmented; includes reovirus, rotavirus (diarrhea), Colorado Tick Fever

Front 189

Which class of viruses is very similar to the calciviruses and usually affects children?

Back 189

Astroviruses

Front 190

What characterizes the arenaviruses?

Back 190

Helical, envelope present, 2 strands of circular –RNA, ambisense (contains both – and + RNA characteristics); includes Lassa fever (hemorrhagic), Lymphocytic choriomeningitis (hamsters)

Front 191

What characterizes herpesviruses?

Back 191

Icosahedral, envelope present, ds-linear, complex genome; includes Herpes I (cold sores), Herpes II (genital herpes), Herpes III (chicken pox, shingles), Herpes IV (Epstein-Barr, mononucleosis), Herpes V (roseola, child with fever/rash), Herpes VI-VIII (less characterized, although VIII is associated with Kaposi’s sarcoma)

Front 192

What characterizes adenovirus?

Back 192

Icosahedral with pentons, no envelope present, ds-linear; includes common cold

Front 193

What characterizes papovaviruses?

Back 193

Icosahedral, no envelope present, ds-circular DNA, supercoiled; includes papillomavirus (chondylomas, warts, cervical cancer)

Front 194

What characterizes hepadnaviruses?

Back 194

Icosahedral, envelope present, partially ds-circular DNA, spherical to filamentous, contain reverse transcriptase; includes Hepatitis B

Front 195

What characterizes parvoviruses?

Back 195

Icosahedral, no envelope present, ss-linear, +DNA; includes B19 (“slapped cheek disease”), Fifth disease

Front 196

What characterizes bunyaviruses?

Back 196

Helical, envelope present, 3 strands of circular –RNA, ambisense; includes Lacrosse fever (epilepsy-like symptoms), Rift valley fever, Hantavirus (Hanta pulmonary syndrome, upper respiratory tract)

Front 197

What characterizes rhabdoviruses?

Back 197

Helical, envelope present, ss-linear, nonsegmented, –RNA; includes rabies virus (slow virus)

Front 198

What characterizes the filoviruses?

Back 198

Helical, envelope present, ss-linear, nonsegmented, –RNA, filamentous virus; includes Ebola, Marburg virus (these are hemorrhagic)

Front 199

What characterizes poxviruses?

Back 199

Complex capsid structure, envelop present, ds-linear; includes smallpox, vaccinia, monkeypox

Front 200

How is acute MI diagnosed?

Back 200

With a diagnostic ECG (about half of patients) or if the patient has a non-diagnostic ECG, through the use of cardiac markers

Front 201

What changes in cardiac Troponin are seen with unstable angina?

Back 201

A small increase (peaks in the gray zone: 0.050-0499) that is not sufficient for a diagnosis of AMI

Front 202

How is BNP metabolized?

Back 202

It is rapidly removed from the blood through clearance receptors on the endothelial cells and degraded by neutral endopeptidases

Front 203

What are the important natriuretic polypeptides and where are they produced?

Back 203

Atrial natriuretic peptide (ANP): produced and stored in atria granules; B-type natriuretic peptide (BNP): produced in ventricles, but not stored – ANP/BNP secretion increases when the ventricular myocardium is overloaded (BNP is secreted in much greater quantities)

Front 204

What is the purpose of natriuretic polypeptides?

Back 204

They counter the effects of the renin-angiotensin-aldosterone system by acting on guanylyl cyclase A receptors and NPR (natriuretic polypeptide receptor)

Front 205

What are the early and definitive markers for MI?

Back 205

Early: myoglobin, CK-MB; Definitive: cTnT, cTnI

Front 206

What are causes of elevations in Troponin levels?

Back 206

Cardiac contusions, trauma (e.g. steering-wheel injuries), acute heart failure, pulmonary embolism, inflammatory diseases, extreme exertion

Front 207

What can cause a false elevation of cTnI?

Back 207

Heterophile antibodies; Rheumatoid factor; Human anti-mouse antibodies (as seen with some anti-cancer and anti-viral mouse monoclonal antibodies); and other animal antibodies (e.g. in people who work with animals)

Front 208

How is myoglobin used to diagnose MI?

Back 208

It is a small molecule that leaks easily out of damaged cells; this makes it very sensitive for MI, but not very specific – 1-3 hours: rise; 6-9 hours: peak; 12-24 hours: normal

Front 209

What levels of cTnI are expected post-MI?

Back 209

3-4 hours: rise; 24-48 hours: first peak (due to cytosolic pool); 72-100 hours: second peak (due to structural pool); 4-7 days: normal (10-14 days for cTnT)

Front 210

What is the standard cardiac marker used for the diagnosis of MI?

Back 210

Troponin: Troponin T and Troponin I have specific cardiac forms (cTnT, cTnI) whereas Troponin C is structurally identical in cardiac and skeletal muscle

Front 211

What is hs-CRP?

Back 211

High sensitivity C-reactive protein; it is an acute phase reactant released during acute inflammation (i.e. it is a marker of low-grade inflammation seen in unstable atherosclerotic plaques) – it is useful to help assess risk of an initial acute coronary event in apparently healthy individuals

Front 212

What are the classes and levels defined in the NACB practice guidelines?

Back 212

Class I: treatment/procedure should be used; Class II(a/b): reasonable/may be considered;
Class III: should not be used – each treatment/procedure also has a level associated with it:
Level A: recommendation based on multiple randomized trials/meta-analyses;
Level B: based on one randomized trial or non-randomized studies;
Level C: based on expert opinion, case studies

Front 213

What is Myeloperoxidase?

Back 213

An ischemia marker involved in the inflammatory process (released from neutrophils); may identify Troponin-negative patients at risk for MI

Front 214

What does the Albumin Cobalt Binding Test detect?

Back 214

Cobalt binding to Albumin, which is decreased in ischemia (due to Ischemia Modified Albumin – IMA); IMA rises within minutes of an ischemic event and returns to baseline within 6 hours; very effective when used in conjunction with Troponin

Front 215

What is the clinical use of LP(a)?

Back 215

Higher levels of LP(a) correlate with an increased risk of coronary heart disease; Niacin can be used to lower LP(a) levels

Front 216

What is Lipoprotein(a) (LP(a))?

Back 216

Acute phase reactant that promotes atherogenesis and thrombogenesis (via inhibition of fibrinolysis and by increasing cholesterol deposition in arterial walls, amongst other effects)

Front 217

What drugs have an effect on hs-CRP?

Back 217

Estrogen therapy increases hs-CRP, whereas low-dose aspirin and “statin” drugs decrease it

Front 218

What is the precursor of BNP?

Back 218

ProBNP; it is cleaved into NT-proBNP and BNP

Front 219

What are the differences between BNP and NT-proBNP?

Back 219

BNP has a shorter half-life, can detect a treatment response rapidly, is biologically active, and cannot be used to monitor response to Nesiritide therapy; both compounds will be increased in renal failure (due to increased secretion and slower removal)

Front 220

What is the most important use of BNP, clinically?

Back 220

It is a marker for the diagnosis and assessment of severity associated with CHF (NT-proBNP is similarly useful); It can be used in risk stratification for future cardiovascular events; It is a screening tool in patients with known risk factors; And, it can be used to monitor the effectiveness of drug therapy

Front 221

What happens to CK-MB levels when a MI is reperfused?

Back 221

A wash-out effect takes place where CK-MB levels rise rapidly, and return to normal more rapidly – in a patient who underwent reperfusion, infarct size cannot be assessed using CK-MB levels

Front 222

What does the MB index elicit?

Back 222

Whether an elevated CK is due to skeletal muscle injury (if value is < 2.0) or due to MI/necrosis (if value is > 5.0)

Front 223

What are the causes of an elevated CK and what causes an elevated CK-MB, specifically?

Back 223

Elevated CK: acute MI, heart surgery/trauma, skeletal muscle breakdown (for various reasons);
Elevated CK-MB: acute MI, cardiac ischemia, chronic renal failure, heart surgery/trauma, electrical injury, extreme exercise, muscle disease (polymyositis, Duchenne’s MD)

Front 224

What levels of CK are expected post-MI?

Back 224

4-6 hours: rise; 22-24 hours: peak; 48-72 hours: normal

Front 225

How is Creatinine Kinase (CK) measured?

Back 225

By immunoassay (called mass CK-MB)

Front 226

How soon should thrombolytic treatment be administered for maximal benefit?

Back 226

Within the first 2 hours post-MI (since myocardial necrosis begins within 30 minutes)

Front 227

What is acute coronary syndrome (ACS) and what are the two associated categories?

Back 227

Symptoms due to acute myocardial ischemia – STEMI: ST elevation MI; NSTEACS: non-ST elevation ACS, consists of NSTEMI (MI with myocyte necrosis) and UA (unstable angina, no necrosis)

Front 228

What ECG changes are seen with MI?

Back 228

ST segment elevation (hours after MI), inverted T waves (hours to days), enlarged Q waves (hours to days) – in days to weeks, ST segment returns to near normal; in weeks to months, the T waves becomes upright again, but the large Q wave may remain (and the R wave may disappear)

Front 229

What describes the “textbook” MI?

Back 229

Male, >65, chest pain

Front 230

What treatments/procedures are considered Class I in regards to the diagnosis of MI?

Back 230

In conjunction with the clinical history and ECG, cardiac Troponin is the preferred marker (although CK-MB may be used when Troponin is not available); Troponin should be measured on presentation and during the 6-9 hour period (need >99th percentile = >0.500)

Front 231

With what patient are natriuretic peptides considered Class I?

Back 231

The patient who present with SOB of unclear cause

Front 232

What treatments/procedures are considered Class I/IIa/III in early risk stratification?

Back 232

Class I: cardiac Troponin by serial sampling; Class IIa: hs-CRP/BNP;
Class III: the use of biomarkers in patients with a low clinical probability of ACS

Front 233

What treatments/procedures are considered Class III in regards to the diagnosis of MI?

Back 233

Total CK, AST, LDH; also in patients with a diagnostic ECG, they should be treated immediately instead of waiting for cardiac marker tests to come back

Front 234

What treatments/procedures are considered Class IIa/b in regards to the diagnosis of MI?

Back 234

Class IIa: Myoglobin; Class IIb: frequent early sampling of markers (e.g. every 2-3 hours)

Front 235

What pathological mechanisms are associated with parasites?

Back 235

Toxic products: hydrolytic enzymes, proteinases, collagenases, endotoxins; Mechanical tissue damage: blockage of internal organs, pressure atrophy, migration through tissue (larval stage);
Immunopathology (damage done by our immune system)

Front 236

Which amoebae can be pathologic to humans?

Back 236

Parasitic: Entamoeba histolytica; Free-living: Acanthamoeba, Naegleria (all have pseudopodia)

Front 237

What are the four medically-important protozoa?

Back 237

Amoebae, Flagellates, Ciliates, Sporozoans/Apicomplexans

Front 238

What characterizes the protozoa?

Back 238

Unicellular eukaryotes; Have organelles which serve in locomotion (used for categorization); Glucose is their chief source of energy and ATP (glycolysis, Krebs cycle)

Front 239

What are the two main groups that parasites can be divided

Back 239

up in?
Protozoa, Helminths

Front 240

What evasion mechanisms of host defenses are employed by parasites?

Back 240

Antigenic variation; Molecular mimicry; Concealment of antigenic site (masking); Intracellular location; Immunosuppression

Front 241

What immunopathologic responses are associated with parasites?

Back 241

Anaphylactic shock, local inflammation; Lysis of cell bearing microbial antigens (e.g. RBCs); Immune complex deposition; Chronic inflammation, mononuclear accumulation, macrophage activation

Front 242

What occurs in the definitive host and what in the intermediate host?

Back 242

Definitive host (human): the parasite passes its adult existence and/or sexual reproductive phase;
Intermediate host: animal in which a parasite passes its larval stage or asexual reproductive phase

Front 243

What are the ports of entry by which parasites gain access to their host?

Back 243

Ingestion by host; Direct penetration: arthropod bite, transplacental penetration, organism-directed penetration (e.g. penetration through intact skin)

Front 244

What is the difference between the direct and indirect life cycle of parasites?

Back 244

Direct: involves one host that passes cysts in feces which then contaminate food/water sources;
Indirect: involves multiple hosts, in which the definitive host passes eggs in feces which produce larvae, which are subsequently eaten by the intermediate host (this intermediate host can then be eaten by other intermediate hosts), which is then eaten by the host

Front 245

What are reservoirs associated with amoebae and what symptoms are often seen with an infection of amoebae?

Back 245

Reservoirs: humans and animals; Symptoms: usually diarrhea

Front 246

What are the stages associated with Leishmania?

Back 246

Promastigote stage (infective stage): flagellated, transmitted from insect to human; Amastigote stage (diagnostic): non-flagellated, found in tissue

Front 247

What stage can certain types of Trypanosoma be found in when they enter the tissue?

Back 247

Amastigote stage (diagnostic stage): non-flagellated

Front 248

What are the stages associated with Trypanosoma?

Back 248

Trypomastigote (infective and diagnostic stage): flagellated, found in blood/lymph, transmitted from insect to human, back to insect

Front 249

How are hemoflagellates transmitted into their host?

Back 249

Via an arthropod vector (specific arthropod varies between genera)

Front 250

What stages are associated with the intestinal/urogenital flagellates?

Back 250

Trophozoite and cyst stages; although Trichomonas vaginalis only has a trophozoite stage

Front 251

What characterizes the flagellates and what main categories are they separated in to?

Back 251

They have flagella – Intestinal/urogenital flagellates: Giardia lamblia, Trichomonas vaginalis;
Hemoflagellates: Trypanosoma brucei, Trypanosoma cruzi, Leishmania species

Front 252

What are the stages of amoebae?

Back 252

Trophozoite (troph): vegetative state of organism (active/feeding/motile), pseudopodia are temporary cytoplasmic extensions, very fragile organisms; Cyst: nonfeeding/nonmotile, stage infective for humans, passed from host in feces and can remain active for long periods of time

Front 253

How do the free-living amoebae gain access to their host?

Back 253

Through direct penetration: Naegleria in a host with meningeal encephalitis, and Acanthamoeba in a host with keratitis

Front 254

What happens when an amoeba in the cyst stage is consumed by an appropriate host?

Back 254

It becomes a trophozoite – the trophozoite will once again convert to a cyst when the required signals are present (i.e. it is close to exiting the intestinal tract)

Front 255

What characterizes sporozoans/apicomplexans and what are some examples of associated species?

Back 255

They are intracellular parasites; Contain an apical complex for penetration into the host cell;
Life cycle consists of a sexual phase (sporogony) and an asexual phase (schizogony);
Examples include Plasmodium species and Cryptosporidium species

Front 256

What reservoirs are associated with Sporozoans?

Back 256

Plasmodium: humans, mosquitoes; Cryptosporidium: humans, animals

Front 257

What symptoms are associated with a Cryptosporidium infection?

Back 257

In healthy individuals, usually little to none (possible self-limiting diarrhea); but in immunocompromised patients they can have a life-threatening diarrhea

Front 258

What describes the life cycle of Cryptosporidium?

Back 258

It is direct: fecal contamination and ingestion of oocyst --> sexual part of life cycle in intestinal wall --> asexual part of life cycle in lumen --> oocyst elimination in fecal material

Front 259

What are the diagnostic stages associated with Plasmodium?

Back 259

In blood: trophozoite, schizont (merozoites), gametocyte; Exoerythrocytic: schizont in liver (merozoite) – merozoites reproduce in schizonts and are released when the schizont bursts (this is what causes the symptoms of fever, chills, sweating in malaria)

Front 260

What are the names of the stages associated with Plasmodium that transmits from insect to human, and vice versa?

Back 260

Insect to human: sporozoite; Human to insect: gametocyte

Front 261

What vector is associated with Plasmodium and what characterizes its metabolism?

Back 261

Vector: female Anopheles mosquito; Metabolism: facultative anaerobe, degradation of glucose to lactate, usually no pentose phosphate pathway, use host hemoglobin as a source of nutrition, cannot assimilate folic acid

Front 262

What reservoirs are associated with flagellates/hemoflagellates?

Back 262

Humans, animals, arthropods

Front 263

What is the only ciliate that is pathological to humans and what characterizes it?

Back 263

Balantidium coli: possess cilia for a pulsing locomotion, goes through trophozoite and cyst stages, associated with fecal contamination, associated with pigs

Front 264

What modes of transmission are associated with Nematodes?

Back 264

Ingestion of eggs: Ascaris, pinworm, whipworm; Penetration of larvae: Hook worm, Strongyloides; Ingestion of larvae: Trichinella

Front 265

What is the first intermediate host in the life cycle of trematodes?

Back 265

Snails (a miracidium is released from the host and taken up by the snail --> inside the snail it is known as a sporocyst/redia --> once eliminated from the snail, it is known as a cercaria --> the cercaria can live on vegetation or enter a second intermediate host before returning to the definitive host) – in schistosomes, the cercaria do not require vegetation or a second intermediate host, but can penetrate the definitive host directly

Front 266

What differentiates the hermaphroditic trematodes from the schistosomes?

Back 266

Hermaphroditic: associated with a single organ system (intestine, liver, lung), complex life cycle;
Schistosomes: blood flukes, associated with the veins of a particular organ (intestine, bladder), complex life cycle

Front 267

What characterizes the flukes?

Back 267

Dorsoventrally flattened, non-segmented, leaf-/lancet-shaped, smaller in size; They have 2 suckers: oral sucker and ventral sucker (acetabulum, used to attach itself to the host);
Outer covering is called tegument: very absorptive for nutrient acquisition

Front 268

What pathology/symptoms are associated with filarial worms and what is the treatment?

Back 268

Blockage of the lymphatics (elephantiasis when chronic); Treatment: Diethylcarbamazine and Ivermectin (microfilariae), prevention – there is no treatment for adult worms

Front 269

What characterizes the filarial worms?

Back 269

Arthropod borne (mosquito, fly, midge): varies from worm to worm; Stages found in human: adult and microfilariae (larvae found in blood, produced after sexual reproduction); Often found in tropical locations (geographic distribution can be very diagnostic)

Front 270

What characterizes the roundworms?

Back 270

Direct life cycle; Widespread geographical distribution; Pathology/symptoms are associated with adult and larval stages; Prevention is stressed

Front 271

What are the three different classes of Helminths

Back 271

Nematodes: roundworms and filarial worms; Trematodes: flukes; Cestodes: tapeworms

Front 272

What are the three stage associated with the Nematodes?

Back 272

Adult stage; Egg stage (contains larvae); Larvae stage (once they hatch out of the egg)

Front 273

Which are the most complex class of Helminths and what describes them?

Back 273

Nematodes: round in cross-section, complete digestive tract, have separate sexes with male/female reproductive organs

Front 274

What modes of transmission are associated with Nematodes?

Back 274

Ingestion of eggs: Ascaris, pinworm, whipworm; Penetration of larvae: Hook worm, Strongyloides; Ingestion of larvae: Trichinella

Front 275

What is the first intermediate host in the life cycle of trematodes?

Back 275

Snails (a miracidium is released from the host and taken up by the snail --> inside the snail it is known as a sporocyst/redia --> once eliminated from the snail, it is known as a cercaria --> the cercaria can live on vegetation or enter a second intermediate host before returning to the definitive host) – in schistosomes, the cercaria do not require vegetation or a second intermediate host, but can penetrate the definitive host directly

Front 276

What differentiates the hermaphroditic trematodes from the schistosomes?

Back 276

Hermaphroditic: associated with a single organ system (intestine, liver, lung), complex life cycle;
Schistosomes: blood flukes, associated with the veins of a particular organ (intestine, bladder), complex life cycle

Front 277

What characterizes the flukes?

Back 277

Dorsoventrally flattened, non-segmented, leaf-/lancet-shaped, smaller in size; They have 2 suckers: oral sucker and ventral sucker (acetabulum, used to attach itself to the host);
Outer covering is called tegument: very absorptive for nutrient acquisition

Front 278

What pathology/symptoms are associated with filarial worms and what is the treatment?

Back 278

Blockage of the lymphatics (elephantiasis when chronic); Treatment: Diethylcarbamazine and Ivermectin (microfilariae), prevention – there is no treatment for adult worms

Front 279

What characterizes the filarial worms?

Back 279

Arthropod borne (mosquito, fly, midge): varies from worm to worm; Stages found in human: adult and microfilariae (larvae found in blood, produced after sexual reproduction); Often found in tropical locations (geographic distribution can be very diagnostic)

Front 280

What characterizes the roundworms?

Back 280

Direct life cycle; Widespread geographical distribution; Pathology/symptoms are associated with adult and larval stages; Prevention is stressed

Front 281

What are the three different classes of Helminths

Back 281

Nematodes: roundworms and filarial worms; Trematodes: flukes; Cestodes: tapeworms

Front 282

What are the three stage associated with the Nematodes?

Back 282

Adult stage; Egg stage (contains larvae); Larvae stage (once they hatch out of the egg)

Front 283

Which are the most complex class of Helminths and what describes them?

Back 283

Nematodes: round in cross-section, complete digestive tract, have separate sexes with male/female reproductive organs

Front 284

What is the geographical distribution, pathology/symptoms, and treatment of cestodes?

Back 284

Geographical distribution is widespread; Pathology/symptoms: blockage, diarrhea, constipation, pernicious anemia (with Diphyllobothrium latum, since it absorbs Vitamin B12);
Treatment: praziquantel, niclosamide, prevention (cooking meat thoroughly)

Front 285

What are virulence factors associated with adherence/colonization?

Back 285

Pili; Motility/chemotaxis (flagella); Outer membrane proteins (for adhesion/invasion)

Front 286

What are some examples of tissue damaging/cytolytic exotoxins?

Back 286

Tissue damaging: enzymes (proteases, DNases); Phospholipase C (with C. perfringens);
Surfactant (with S. aureus); Cholesterol-dependent cytolysins (with Streptolysin O)

Front 287

What are diseases caused by exotoxins?

Back 287

Diphtheria, Tetanus, Botulism, Anthrax, Cholera, Pertussis (“whooping cough”), Gas gangrene, Toxic Shock Syndrome, Enterohemorrhagic E. coli, Necrotizing fasciitis (“flesh-eating bacteria”)

Front 288

How does the cell wall of Gram– organisms activate the immune systems?

Back 288

Via LPS which functions as an endotoxin (PAMP interacting with a TLR)

Front 289

How does the cell wall of Gram+ organisms activate the immune system?

Back 289

The lipoteichoic acid found on the cell wall functions as a pathogen-associated molecular pattern (PAMP) which activates toll-like receptors (TLRs) of the innate immune system

Front 290

What are virulence factors associated with the infectious process?

Back 290

Cell wall/endotoxin; Exotoxins; Secretion systems (type III); Intracellular growth

Front 291

What are the three types of bacterial-host interactions?

Back 291

Symbiotic (both benefit), commensal (association that causes no harm), parasitic (association where one organism gains benefit from the other without compensation)

Front 292

What are the types of disease caused by bacteria?

Back 292

Localized infection produces toxins that are release systemically (e.g. Clostridium tetani);
Disseminated infection in which organisms themselves invade the blood stream (Staph aureus);
Intoxication in which spores multiply and produce toxin outside of the body, which is subsequently ingested (e.g. Clostridium botulinum)

Front 293

By what two mechanisms can bacteria cause disease?

Back 293

Release of factors (cell wall/endotoxins), direct host cell manipulation (intracellular/extracellular)

Front 294

What is the measurement used to check virulence?

Back 294

ID50: number of bacteria necessary to infect 50% of animals exposed to bacterium

Front 295

What are the Type II secretion effectors in Gram– bacteria?

Back 295

AB toxins, proteases

Front 296

How is the function of microbial communities in biofilm analyzed?

Back 296

Via metagenomics: analyze complete genetic information of community using pyrosequencing

Front 297

What technique is used in research to determine to composition of a particular biofilm?

Back 297

Bacterial 16S RNA sequences

Front 298

What are examples of biofilm infections?)

Back 298

Chronic infections, catheter-related infections, soft contact lens infections, dental carries/ periodontal disease (most common disease in humans

Front 299

What is a biofilm composed of?

Back 299

Living, 3-D community of microorganisms, adherent to a surface and enclosed within a polysaccharide matrix (highly resistant to antibiotics)

Front 300

What are some examples of ways that bacteria protect against host defenses?

Back 300

Antigenic variation (e.g. of pili), capsule (highly antigenic protective shell – used in vaccines), biofilm formation

Front 301

What molecule is often used by bacteria to get into host cell and sometime to move around inside the cell?

Back 301

Actin

Front 302

What are some examples of cell receptor interaction toxins?

Back 302

Heat-stable toxins (e.g. from E. coli): activate guanylate cyclase which causes an increase in cGMP  this creates an ion flux which causes diarrhea; Superantigens (e.g. Toxic Shock Syndrome)

Front 303

How do the Type III secretion effectors differ from the AB toxins?

Back 303

They do not have a leader sequence – they do contain a GAP protein which is a GTPase-activating protein (can turn host G-proteins on and off)

Front 304

What is the largest group of exotoxins and how do they function?

Back 304

AB toxins: consist of an A subunit (contains a leader sequence which moves the protein outside of the bacterial cell, a particular enzyme, and a signal sequence that traffics the protein to a location inside the target cell) and a B subunit (contains a receptor binding region and internalization domain) – both subunits are required for toxicity to occur

Front 305

What are examples of transmissible spongiform encephalopathies in animals?

Back 305

Scrapie, Bovine spongiform encephalopathy (mad cow disease), Chronic wasting disease of deer and elk

Front 306

What genetic characteristic do people who have developed vCJD in common?

Back 306

They have all been homozygous for the methionine amino acid (pos. 129) of PrPc due to polymorphisms in the PRNP gene (found in 40% of population)

Front 307

How does brain tissue differ between patients with sCJD and vCJD?

Back 307

In sCJD there is fine spongiform degeneration that is evenly distributed, whereas in vCJD the spongiform degeneration is clustered around a plaque surrounded by a vacuole (“florid”/”daisy” plaques)

Front 308

How can vCJD be transmitted?

Back 308

Via blood and blood products (which is why people who have visited the UK can’t donate blood), whereas conventional/sporadic CJD (sCJD) cannot

Front 309

By what mechanisms can iatrogenic CJD come about?

Back 309

Improperly sterilized equipment, corneal/dura matter transplant, contaminated human growth hormone (not an issue anymore)

Front 310

What are examples of transmissible spongiform encephalopathies in humans?

Back 310

Kuru (ceremonial cannibalism), Creutzfeldt-Jakob disease (CJD), variant CJD (vCJD, human form of Mad cow disease)

Front 311

What is the pathogenesis of transmissible spongiform encephalopathy?

Back 311

Uniformly fatal disease of CNS with a long incubation period, characterized by development of vacuolization of neurons and accumulation of amyloid-like plaques

Front 312

How are transmissible spongiform encephalopathies most commonly diagnosed?

Back 312

On autopsy, by finding the characteristic “spongy” brain appearance

Front 313

What symptoms are associated with transmissible spongiform encephalopathy?

Back 313

Loss of muscle control, shivering, dementia, tremors

Front 314

What are some key differences between sCJD and vCJD?

Back 314

vCJD is found in young adults (vs. older people in sCJD), the median duration of the illness is much longer, and it can be found in the lymphatics and blood (not seen in sCJD)

Front 315

What are some key differences between sCJD and vCJD?

Back 315

vCJD is found in young adults (vs. older people in sCJD), the median duration of the illness is much longer, and it can be found in the lymphatics and blood (not seen in sCJD)

Front 316

What are some key differences between prions and viruses?

Back 316

Prions do not contain nucleic acid and they do not have a defined morphology on EM; they are also more difficult to kill in sterilization procedures (i.e. they are not sensitive to ionizing radiation, formaldehyde, and steam heat)

Front 317

What is the concern regarding chronic wasting disease in deer?

Back 317

The possibility of transmitting this prion disease across species barriers to infect humans who hunt and eat deer

Front 318

What is the proposed mechanism by which PrPsc can infect the brain after ingestion?

Back 318

They travel to Peyer’s patches in the intestine where the follicular dendritic cells contain PrPc; here they convert those normal prions to PrPsc at which point they propagate via nerve fibers in order to enter the brain

Front 319

What is the proposed mechanism for prior replication?

Back 319

PrPsc has enzymatic activity by which it converts normal prions into PrPsc; these PrPscs then accumulate in the neuronal cytoplasm and cause neuronal death

Front 320

What are some key differences between normal and aberrant prion proteins?

Back 320

Aberrant prion proteins (PrPsc)have a globular structure (with characteristic β-pleated sheets) that is resistant to protease degradation, are found in the cytoplasm (vs. plasma membrane) and turn over in days (vs. hours for normal prions)

Front 321

How is the diagnosis of a Babesia microti infection made and what is the treatment?

Back 321

By Giemsa-stained thin and thick smears (or by Wright stain) of blood;
Treatment: clindamycin/oral quinine or azithromycin/quinine (or atovaquone)

Front 322

What geographical distribution is associated with Leishmania species and what are its reservoirs?

Back 322

Mediterranean, SW Asia, central/NW Africa, central/S America – reservoirs: human, rodents, dogs, other animals

Front 323

What class of parasites do Leishmania species belong to and what are its definitive/intermediate hosts?

Back 323

Hemoflagellates – the intermediate host is an arthropod (e.g. sand fly) that injects the flagellated promastigote into the definitive host during a blood meal; once inside the human host, the promastigote is ingested by macrophages at the bite site and converted to an amastigote (loses its flagella)

Front 324

How is the diagnosis of a Toxoplasma gondii infection made and what is the treatment?

Back 324

↑ IgM titer to Toxoplasma gondii; also, appearance of neurological symptoms, multiple ring-enhancing lesions on CT/MRI, detection of tachyzoites in brain biopsy using fluorescently-labeled antitoxoplasma antibodies – Treatment: pyrimethamine with either sulfadiazine/clindamycin

Front 325

What pathology/symptoms are associated with Toxoplasma gondii?

Back 325

Immunocompetent: usually asymptomatic or mild mononucleosis-like syndrome; Immunocompromised: encephalitis with severe tissue damage in brain, lesions in heart/lungs;
Developing fetus: stillbirth, hydrocephalus, chorioretinitis, liver damage, deafness, MR

Front 326

By what three ways can humans become infected by Toxoplasma gondii?

Back 326

Ingestion of oocysts in cat feces; Ingestion of bradyzoites in undercooked/rare meat; Tachyzoites cross placenta of primarily-infected mother during pregnancy (not an issue with bradyzoites)

Front 327

What class of parasites does Toxoplasma gondii belong to and what are its definitive/intermediate hosts?

Back 327

Coccidian (sporozoans) – Definitive host: feline, sexual life cycle in gut --> release of oocyst;
Intermediate host: other vertebrates (incl. humans) --> tachyzoite stage in tissue/fluids --> formation of cysts containing bradyzoites in tissue (after the immune system has walled it off)

Front 328

What class of parasites does Babesia microti belong to and what are its definitive/intermediate hosts?

Back 328

Sporozoans – Definitive host: Ixodes tick (deer tick), sexual life cycle;
Intermediate host: White-footed mouse, human (accidental), asexual life cycle

Front 329

What pathology/symptoms are associated with Babesia microti?

Back 329

In the immunocompetent: asymptomatic/mild flu-like illness, parasitemia <2%;
Splenectomized person: parasitemia = 10%, symptoms include HA/fatigue/fever/shaking chills/ joint and muscle aches/hemolytic anemia (pathology due to infection and lysis of RBCs)

Front 330

What is the geographical distribution associated with Babesia microti?

Back 330

Northeast, Pacific coast, Missouri, Georgia, Wisconsin

Front 331

What class of parasites does Trypanosoma cruzi belong to and what are its definitive/intermediate hosts?

Back 331

Flagellate – the intermediate host is the reduviid bug (Triatoma) that releases the trypomastigote in its feces while taking a blood meal on the definitive host (usually on the face around moist areas)

Front 332

What class of parasites does Trypanosoma brucei belong to and what are its definitive/intermediate hosts?

Back 332

Flagellate – the intermediate host is the tsetse fly (Glossina) that transmits trypomastigotes from its saliva as it takes its blood meal; the definitive hosts include humans, wild game, cattle

Front 333

What is the treatment for Trypanosoma cruzi?

Back 333

Early: nifurtimox or benznidazole; Chronic: treat symptoms (e.g. for heart condition, megacolon)

Front 334

How is the diagnosis of Trypanosoma cruzi made?

Back 334

Early: check for trypomastigotes in blood or through xenodiagnosis (let reduviid bug take a blood meal on a potentially infected patient, then observe the bug over the following weeks for changes);
Later: amastigotes in tissue or serological tests for antibodies to T. cruzi

Front 335

What pathology/symptoms are associated with Trypanosoma cruzi?

Back 335

Chagas’ disease --> Chagoma (chancre) at site of bite; Acute phase: fever, weakness, enlarged lymph nodes/liver/spleen with a Romaña’s sign (unilateral swelling of the face, if bitten on face, especially seen in children; Chronic phase: destruction of ganglia of the ANS (megacolon, megaesophagus, can be fatal, also possible to see chronic heart disease in young adults)

Front 336

How are Trypanosoma cruzi and Trypanosoma brucei distinguished in a blood smear?

Back 336

T. cruzi is small and will form C-shapes in the blood, whereas the larger T. brucei forms S-shapes

Front 337

What is the geographical distribution of Trypanosoma cruzi?

Back 337

Central/S America, maybe southern US

Front 338

What are the two forms of Leishmaniasis?

Back 338

Cutaneous Leishmaniasis: L. tropica, L. major, L. mexicana, L. brasiliensis;
Visceral Leishmaniasis: L. tropica, L. donovani (bone marrow)

Front 339

How is the diagnosis of Leishmaniasis made and what is the treatment?

Back 339

Biopsy of skin lesion/bone marrow/lymph node followed by Giemsa stain or PCR to look for amastigotes in macrophages – Treatment: antimony-containing compounds (sodium stibogluconate or meglumine antimonate)

Front 340

What pathology/symptoms are associated with the two forms of Leishmaniasis?

Back 340

Cutaneous: dry/long-lasting lesion (12-18 months), moist/short-term lesion (3-6 months);
Visceral: cutaneous lesion followed by chills, fever, sweating, diarrhea, weight loss, splenomegaly, hepatomegaly, hyperplasia of tissue/organs, anemia, death within 2 years

Front 341

What are the causative agents of lymphatic filariasis and what is their geographical distribution?

Back 341

Nematodes --> Wuchereria bancrofti: tropic/subtropics; Brugia malayi: Asia and South Pacific

Front 342

What is the geographical distribution of Onchocerca volvulus?

Back 342

Mostly in central Africa, but also some foci in central/South America

Front 343

What class of parasites does Onchocerca volvulus belong to and what are its definitive/intermediate hosts?

Back 343

Nematodes – Arthropod intermediate host (Simulium fly/black fly) transmits infective larvae into definitive host (human) during blood meal; Simulium fly prefers to breed near fast flowing water

Front 344

How is the diagnosis of lymphatic filariasis made and what is the treatment?

Back 344

Detection of microfilariae in blood smears using Giemsa/Wright stain (blood sample taken at night since this is when microfilariae are released) – Treatment: diethylcarbamazine/ivermectin (for microfilariae, not adults), vector control (kill mosquitoes)

Front 345

What pathology/symptoms are associated with lymphatic filariasis?

Back 345

Early: low grade fever and inflammation of lymphatics/lymph nodes due to adult worms;
Late: lymphatics become occluded, fluids leak into tissues, severe swelling --> elephantiasis

Front 346

What distinguishes between Wuchereria bancrofti and Brugia malayi, morphologically?

Back 346

Wuchereria bancrofti: nuclei end before the tail tip; Brugia malayi: nuclei extend into the tail tip

Front 347

What intermediate host is associated with lymphatic filariasis?

Back 347

Arthropods: Anopheles/Culex/Aedes mosquitoes (transmit the infective larvae during blood meal)

Front 348

What is the geographical distribution of Trypanosoma brucei?

Back 348

African continent --> western part: T.b. gambiense (less virulent); eastern part: T.b. rhodesiense (more virulent)

Front 349

How is the diagnosis of Trypanosoma brucei made and what is the treatment?

Back 349

Detection of trypomastigote in blood or CSF by Giemsa stain; Treatment --> blood: pentamidine isethionate or suramin; CSF: melarsoprol or eflornithine

Front 350

What pathology/symptoms are associated with Trypanosoma brucei?

Back 350

African sleeping sickness --> Initially, high fever and swollen postcervical lymph nodes (Winterbottom’s sign) every 10 days to 2 weeks (due to antigenic switching of variable surface glycoprotein); Once the parasite gets into the CNS, patients will suffer from meningitis, lethargy, motor changes, staggered gait, loss of balance, coma, and eventually death

Front 351

What class of parasites does Schistosoma mansoni belong to and what are its definitive/intermediate hosts?

Back 351

Trematode (blood fluke, schistosomes – not hermaphroditic); the intermediate host is the fresh water snail which releases free-swimming cercariae that then penetrate intact skin of the definitive host (human); once in the host, the flukes resides in the veins of the large intestine

Front 352

What pathology/symptoms are associated with Schistosoma hematobium infection?

Back 352

Onset of symptoms is delayed: painful urination, hematuria; chronic infection is correlated with bladder cancer

Front 353

What is the geographic distribution of Schistosoma hematobium?

Back 353

Africa and Middle East

Front 354

What class of parasites does Schistosoma hematobium belong to and what are its definitive/intermediate hosts?

Back 354

Trematode – same life cycle as Schistosoma mansoni, although S. hematobium has a predilection for the veins of the bladder, not the large intestine

Front 355

How is the diagnosis of Schistosoma mansoni infection made and what is the treatment?

Back 355

Finding eggs in stool exam or biopsied tissue (eggs are oval with large lateral spine);
Treatment: praziquantel

Front 356

What pathology/symptoms are associated with a Schistosoma mansoni infection?

Back 356

Initially: rash at the site of cercarial entry a few days after penetration (ground itch);
4-6 weeks later: Schistosomiasis, Katayama fever --> Typhoid fever-like symptoms (cough, malaise, myalgias), hepatosplenomegaly, cirrhosis of the liver (with chronic infection), bloody diarrhea, hypertension, toxic reactions due to granuloma formation around eggs (all of the symptoms are in response to the eggs, not the adults)

Front 357

What is the geographical distribution of Schistosoma mansoni?

Back 357

Africa, South/Central America, Caribbean area (incl. Puerto Rico and the West Indies)

Front 358

Where in the human body are the adult worms and microfilariae of Onchocerca volvulus found?

Back 358

Adults: subcutaneous tissue in nodules; Microfilariae: in skin

Front 359

How is the diagnosis of Onchocerca volvulus infection made and what is the treatment?

Back 359

Detection of microfilariae in skin snip; Treatment: remove skin nodules to kill adults, give ivermectin to kill microfilariae, also vector control

Front 360

What pathology/symptoms are associated with Onchocerca volvulus?

Back 360

Skin nodules where the adult reside; females travel through the skin causing chronic dermatitis, severe itching, and discoloration of the skin; Migrating microfilariae cause blindness (thus the name river blindness)

Front 361

How is the diagnosis of Schistosoma hematobium infection made and what is the treatment?

Back 361

Detection of eggs in sedimented urine or bladder biopsy (eggs are oval with a large terminal spine, peak egg excretion is noon to 3pm); Treatment: praziquantel

Front 362

What is the rate-limiting step in the phosphorylation of Acyclovir?

Back 362

The first phosphorylation, performed by herpes thymidine kinase (for HSV, Varicella Zoster Virus) or by phosphotransferase (CMV)

Front 363

What adverse effects are associated with Ganciclovir?

Back 363

Bone marrow suppression (!): neutropenia, anemia, thrombocytopenia; Renal insufficiency (uncommon); Contraindicated in pregnancy (teratogenic) – if used for more than 3 months, 10% of patients will excrete resistant strains; More toxic than Acyclovir

Front 364

What is the “gold standard” for CMV?

Back 364

Ganciclovir

Front 365

What adverse effects are associated with Acyclovir?

Back 365

n/v/d, nephrotoxicity (especially when given IV and in high doses, due to crystallization), HA, CNS effects/hallucinations/seizures – category B in pregnancy

Front 366

If a patient has a strain of herpesvirus that is resistant to Acyclovir and Ganciclovir due to resistance in thymidine kinase, what alternatives can be given?

Back 366

Foscarnet and Cidofovir

Front 367

What are the inhibitory concentrations of Acyclovir regarding the different herpes viruses?

Back 367

HSV-1 < HSV-2 < VZV < CMV (the dose needs to go up considerably to treat VZV and the dose to treat CMV would be too high to tolerate)

Front 368

Although Acyclovir resolves symptoms and prevents shedding of the virus, what does it not do?

Back 368

It does not terminate herpesvirus latency

Front 369

What is the “gold standard” antiviral for herpes simplex viruses?

Back 369

Acyclovir

Front 370

What mechanism of action do most anti-herpes virus agents have in common?

Back 370

They mimic natural deoxynucleosides (purines, esp. guanine) and in this fashion become phosphorylated and inhibit DNA polymerase, stopping viral DNA synthesis

Front 371

What are the anti-herpes virus agents and which are effective

Back 371

against CMV?
Acyclovir, Valacyclovir, Famciclovir, Ganciclovir, Foscarnet, Cidofovir, Valganciclovir (the latter 4 are effective against CMV) – Famciclovir has the greatest bioavailability (78%) and Acyclovir has a bioavailability of 20-30%

Front 372

What is the mechanism of action of Foscarnet?

Back 372

It is a pyrophosphate compound that functions as a non-competitive inhibitor of viral RNA and DNA polymerases

Front 373

What viral surface proteins define the strain of the virus?

Back 373

Neuraminidases, Hemagglutinins

Front 374

What is the treatment for VZV?

Back 374

Normal adult: Acyclovir, Valacyclovir; Immunocompromised: higher dose Acyclovir

Front 375

What adverse effects are associated with Cidofovir?

Back 375

Nephrotoxicity (administer with probenecid and saline hydration), neutropenia, uveitis, decreased intraocular pressure, neuropathy

Front 376

Besides Foscarnet, what other drug can be used in the treatment of acyclovir/ganciclovir-resistant strains and what is its mechanism of action?

Back 376

Cidofovir (nucleotide monophosphate): it is somewhat similar to acyclovir/ganciclovir but it already has the first phosphate (rate-limiting) attached, so it will function in resistant stains

Front 377

What adverse effects are associated with Foscarnet?

Back 377

Severe nephrotoxicity, hypocalcemia, hypo-/hyperphosphatemia, hypomagnesemia, hypokalemia, n/v, penile ulcers (unique)

Front 378

What strains of herpesvirus are affected and why?

Back 378

Since it does not have to be phosphorylated by thymidine kinase or phosphotransferase, it affects all herpesviruses (HSV, CMV, VZV) and even most acyclovir/ganciclovir-resistant strains

Front 379

Why is oral Ganciclovir not used much anymore?

Back 379

Its bioavailability is 5-10%, so the pro-drug Valganciclovir is used instead (bioavailability 60%, used in the treatment of several types of CMV)

Front 380

What is special about the dosing of Ganciclovir?

Back 380

There is an initiation dose (high) and a consolidation dose (lower) – also requires renal adjustment

Front 381

What are the approved indications for Ganciclovir?

Back 381

CMV retinitis, prevention of CMV in transplant patients

Front 382

In what case would influenza antivirals not be recommended?

Back 382

If a patient recently had a live flu virus vaccine; this is not an issue with killed vaccine

Front 383

What are the selective neuraminidase inhibitors?

Back 383

Oseltamivir, Zanamivir – both are indicated for the prophylaxis and treatment of influenza; they both have action on Type A and B influenza

Front 384

What is the purpose of neuraminidase?

Back 384

It allows the viral particles to break free from the host cell in which they were synthesized;
It prevents aggregation of newly formed viral particles by removing sialic acid on the viral particles and the infected cells; It allows for penetration of the respiratory tract

Front 385

What class of drugs is used currently for influenza infections?

Back 385

Neuraminidase inhibitors:

Front 386

What adverse effects are associated with Amantadine and Rimantadine?

Back 386

Amantadine: (90% excreted in urine) n/v, CNS (>5-10%), insomnia, altered concentration, seizures, suicidal ideation; Rimantadine: (20% excreted in urine), n/v, CNS (<3-6%), insomnia, altered concentration, seizures – contraindicated in pregnancy

Front 387

What are the effects of giving someone an influenza antiviral?

Back 387

Post-exposure: decrease symptom duration by 1-2 days (and decrease viral shedding);
Pre-exposure: 70% decrease in symptomatic influenza infection

Front 388

What structures, found on the surface of cell membranes (especially RBCs and cell membranes of the upper respiratory tract), are recognized by the hemagglutinins?

Back 388

Sialic acid

Front 389

What is the mechanism of action of the influenza antivirals Amantadine and Rimantadine?

Back 389

They inhibit the M2 ion channel functioning, thus blocking the uncoating of the viral genome and viral entry – active against Influenza Type A only (since M2 ion channel is not as important in Types B and C)

Front 390

What are the different types of influenza viruses classified as?

Back 390

Type A: potentially severe illness, cause of epidemics/pandemics, rapidly changing form;
Type B: usually less severe illness, has caused some epidemics, more uniform antigens;
Type C: Usually mild/asymptomatic illness, minimal public health impact

Front 391

What is responsible for influenza’s year-to-year bypassing of human immunity?

Back 391

Antigenic drift: makeup of the hemagglutinin changes every year so antibodies become ineffective

Front 392

What is the difference in dosing regarding Oseltamivir and Zanamivir?

Back 392

Oseltamivir is an oral dosing whereas Zanamivir is inhaled

Front 393

Which influenza type has been responsible for the avian flu?

Back 393

Type A, H5N1

Front 394

When should neuraminidase inhibitors be given for the treatment of influenza?

Back 394

Within 1-2 days after the onset of symptoms (if given at this time, there is a reduction in the duration of uncomplicated illness by 1-2 days)

Front 395

What adverse effects are often seen with dry powder inhalers (i.e. Zanamivir)?

Back 395

Cough and bronchospasm (watch in patients with COPD, asthma) – Zanamivir is also Category C

Front 396

What adverse effects have been found with Oseltamivir?

Back 396

n/v, neuropsychiatric events (self-injury, delirium) – Category C in pregnancy

Front 397

What should use of the neuraminidase inhibitors be avoided with?

Back 397

Patients who have recently taken the live flu vaccine

Front 398

What characterizes a congenital pulmonary airway malformation?

Back 398

Hamartomatous lesion of the lung;
Type 1: most common, large cysts, good prognosis;
Type 2: medium-sized cysts, poor prognosis

Front 399

What conditions are associated with ARDS?

Back 399

Infection: sepsis, diffuse pulmonary infections, gastric aspiration; Physical injury: mechanical trauma; less commonly: inhaled irritants, chemical injury, hematologic conditions, others

Front 400

What characterizes ARDS?

Back 400

Rapid onset of severe life-threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia that is refractory to oxygen therapy (must balance therapy carefully) – CXR will show diffuse alveolar infiltration

Front 401

What are the various names for adult respiratory distress syndrome (ARDS)?

Back 401

In the wards: ARDS; Internationally: acute interstitial pneumonia; Autopsy: diffuse alveolar damage (DAD) – other synonyms: shock lung, acute alveolar lung, acute lung injury

Front 402

What are causes of pulmonary edema and what

Back 402

characterizes each?
Hemodynamic: increased hydrostatic pressure, edema seen in basal portions of lower lobes (dependent edema), presence of frothy pink fluid in alveoli;
Injury to capillaries: leakage of fluids due to injury to vascular endothelium or alveolar epithelial cells, seen with pneumonia and adult respiratory distress syndrome

Front 403

What are the three types of atelectasis (collapse)?

Back 403

Resorption atelectasis: due to complete airway obstruction causing resorption of oxygen in alveoli (causes mediastinum to shift towards the affected lung); Compression atelectasis: pleural cavity become partially/completely filled with fluid, tumor, or air (e.g. pulmonary edema, pneumothorax) causing elevation of the diaphragm and a mediastinal shift away from the affected lung;
Contraction atelectasis: local/generalized fibrosis prevent full lung expansion (not reversible)

Front 404

What characterizes pulmonary sequestration?

Back 404

Lung tissue without any normal connection to the airway system; can be extralobar (external to lung in thorax/mediastinum) or intralobar (within lung substance – often presents with recurrent localized infection or bronchiectasis)

Front 405

What distinguishes the bronchi from the bronchioles?

Back 405

Bronchioles have no cartilage

Front 406

What characterizes foregut cysts?

Back 406

Abnormal detachment of primitive foregut; most commonly bronchogenic cysts lined by ciliated, pseudostratified epithelium; they are usually an incidental finding in children/young adults;

Front 407

What characterizes pulmonary hypoplasia?

Back 407

Defective development of both lungs (found in 10% of neonatal autopsies); can be caused by space-occupying lesions in the uterus, oligohydramnios, congenital diaphragmatic hernia, renal cystic disease, anencephaly – microscopically there will be a lack of alveolar development

Front 408

What histologic features are seen with DAD?

Back 408

Diffuse distribution, uniform temporal appearance, alveolar septal thickening, hyaline membranes! – pertinent negatives include lack of granulomas, lack of infectious agents, and negative cultures

Front 409

What distinguishes centriacinar from panacinar emphysema?

Back 409

Centriacinar: destruction of the respiratory bronchioles (mostly in upper lobes – apices), occurs in heavy smokers and often associated with chronic bronchitis;
Panacinar: destruction of the entire alveolus (mostly in lower lobes – bases)

Front 410

What characterizes emphysema?

Back 410

Abnormal enlargement of airspaces distal to the terminal bronchiole due to destruction of walls without obvious fibrosis; Types of emphysema are classified according to their anatomical distribution: centriacinar, panacinar, paraseptal, irregular

Front 411

What is the pathogenesis of COPD?

Back 411

Mild, chronic inflammation throughout the lung, characterized by increased macrophages T cells, and neutrophils as well as increased inflammatory mediators (IL-8, TNF, etc.)

Front 412

What characterizes COPD?

Back 412

Chronic bronchitis (disease of bronchi) and emphysema (disease of acinus); 4th leading cause of morbidity/mortality in US; 90% of patients with COPD smoke

Front 413

How do lung test values differ between obstructive and restrictive lung disease?

Back 413

Obstructive: decreased FEV1 (seen in chronic bronchitis, emphysema, asthma, brochiectasis);
Restrictive: decreased FEV1 and FVC leading to a normal or increased FEV1/FVC (seen in ARDS and chest wall disorders – polio, obesity)

Front 414

What is the difference between obstructive and restrictive lung disease?

Back 414

Obstructive: increased resistance to airflow due to partial/complete obstruction in airway;
Restrictive: reduced expansion of lung parenchyma causing a decreased total lung capacity

Front 415

What is the pathogenesis associated with ARDS?

Back 415

Damage to alveolar capillary walls leading to increased vascular permeability, alveolar flooding, loss of diffusion capacity, widespread surfactant abnormalities (due to type II pneumocyte damage), and scarring (may not cause any functional consequences) – during this process pro-inflammatory mediators are expressed (NF-κB and IL-8) and inflammatory cells (neutrophils, macrophages) cause damage and maintain the inflammatory cascade

Front 416

What is the clinical course associated with ARDS?

Back 416

Usually occurs in hospitalized patients; they will experience profound dyspnea/tachypnea although an early CXR is normal; there will be increasing cyanosis/hypoxemia, respiratory failure and diffuse bilateral infiltrates; hypoxemia can become unresponsive to oxygen and respiratory acidosis can develop – 60% mortality rate

Front 417

What enzymatic deficiency can lead to emphysema?

Back 417

PiZZ: α1-antitrypsin deficiency (protease inhibitor); patients are more likely to develop panacinar emphysema at a young age (especially when they smoke)

Front 418

What characterizes irregular emphysema?

Back 418

Acinus involvement is irregular (many parts are involved); associated with scarring and coal workers pneumoconiosis

Front 419

What clinical features are associated with chronic bronchitis?

Back 419

Persistent productive cough, dyspnea on exertion, eventual hypercapnia/hypoxemia/cyanosis;
often seen in conjunction with emphysema; can lead to cor pulmonale and cardiac failure;
death is often due to pulmonary infection

Front 420

What is the pathogenesis of chronic bronchitis?

Back 420

It is a protective metaplastic response to tobacco smoke/pollutants, leading to hypertrophy of the submucosal glands in the trachea/bronchi; will see an increase in goblet cells of the small airways and hypersecretion of mucus

Front 421

What characterizes chronic bronchitis?

Back 421

Associated with tobacco smoke and other substances (grain, cotton, silica dust); infections may trigger acute exacerbations; most frequent in middle-aged men

Front 422

How is chronic bronchitis defined?

Back 422

Persistent cough with sputum for >3 months in 2+ years, in the absence of other causes

Front 423

What are some rare types of emphysema?

Back 423

Compensatory hyperinflation: dilation of alveoli without septal destruction; Obstructive overinflation: due to airtrapping; Interstitial emphysema: air in connective tissue stroma

Front 424

What characterizes bullous emphysema?

Back 424

Any form of emphysema that produces large subpleural blebs; often seen at the apex of the lung, and rupture can cause pneumothorax

Front 425

How does smoking affect the protease-antiprotease balance in the lungs?

Back 425

Smoke attracts neutrophils and causes the formation of ROS; these two factors will cause an increase in lung degradation leading to centriacinar emphysema

Front 426

What characterizes paraseptal (distal acinar) emphysema?

Back 426

Preferential destruction of the distal airway structures (starting around the septae of the lungs and affecting the alveolar sacs/ducts first); often forms adjacent to fibrosis/scarring; more severe in the upper half of the lung; can cause spontaneous pneumothorax (seen especially in young adults)

Front 427

What is the clinical course associated with emphysema?

Back 427

Clinical manifestations occur once >1/3 of the pulmonary parenchyma is damaged; symptoms start with a progressive insidious dyspnea (may have cough/wheezing), followed by weight loss, cor pulmonale and eventual CHF – death due to respiratory acidosis, right heart failure, and pneumothorax

Front 428

What is seen on CXR with COPD?

Back 428

Increased vascular markings (with bronchitis); Hyperinflation (emphysema)

Front 429

What is the clinical course associated with bronchiectasis?

Back 429

Severe, persistent cough; foul-smelling expectoration (often bloody); dyspnea/orthopnea; occasional life-threatening hemoptysis;

Front 430

What characterizes bronchiectasis?

Back 430

Permanent dilation of bronchi/bronchioles due to destruction of the muscle and elastic tissue;
can result in chronic necrotizing infections; also associated with CF, intralobar sequestration, immunodeficiency, tumor, foreign body, mucus impaction, autoimmune disease

Front 431

How does the appearance bronchitis patient differ from a patient with emphysema?

Back 431

Bronchitis: blue bloater; Emphysema: pink puffer – *check table in slide show

Front 432

What causes the rigor/crises of Malaria?

Back 432

The RBCs are lysed in a synchronous fashion by the parasites; once this occurs Merozoites will be free in the blood, causing an immune response which will present as rigor/crises

Front 433

Why are most African blacks not affected by P. vivax?

Back 433

They lack the Duffy antigen on their RBCs

Front 434

Which strain of Plasmodium is known to cause benign tertian malaria?

Back 434

Plasmodium vivax (40% of world-wide malaria cases) – infects only young RBCs

Front 435

What is Plasmodium falciparum very lethal?

Back 435

It attacks RBCs of all ages, causing them to form knobs that block capillaries, especially those in the brain (cerebral malaria) and kidneys (black water fever)

Front 436

Which strain of Malaria is responsible for 40-50% of the world’s Malaria cases and around 95% of total mortality?

Back 436

Plasmodium falciparum (malignant tertian malaria); it also has the most drug resistance

Front 437

What is the vector associated with Malaria and when does it feed?

Back 437

Anopheles mosquito, feeds after dusk

Front 438

What are the classic Malaria symptoms?

Back 438

Prodrome: malaise, myalgia, HA, fever (also cough, diarrhea, vomiting, abdominal pain);
Abrupt paroxysms of rigor (violent chills) followed by high fever, HA, sweating;
Fever periodicity is often absent initially, but indicates severe illness when present;
Other symptoms: nausea, jaundice (hemolysis), delirium, low glucose, splenomegaly

Front 439

What are the resistance zones associated with Malaria drugs?

Back 439

A: sensitive to chloroquine, includes central America, Middle East, temperate China;
B: partially chloroquine resistant, includes India, Western Indonesia;
C: significant chloroquine resistance, includes Amazon, SE Asia, PNG, sub-Saharan Africa

Front 440

What are Hypnozoites?

Back 440

Dormant form of the Malaria life cycle which can cause relapses in the disease (only in Vivax/Ovale species)

Front 441

What are the stages of the Malaria life cycle?

Back 441

Sporozoite (injected into human host during blood meal) --> travel to the liver which functions as a nursery bed --> after leaving the liver the infective organisms are called Merozoites --> they will enter the RBCs to feed and reproduce at which point they are known as Trophozoites --> once they have multiplied enough, the RBC will lyse and release more Merozoites (since now they are infective again) --> some of these Merozoites can enter the reproductive stage and become Gametocytes --> the Gametocytes can then be taken up again by another intermediate host

Front 442

Which type of malaria do humans share with primates?

Back 442

P. malariae (benign quartan): oldest/least virulent form, 1% of world malaria, infects oldest RBCs, persists in blood without the use of Hypnozoites – associated with transfusions malaria and nephrotic syndrome

Front 443

What adverse effects are associated with Chloroquine?

Back 443

GI upset, itching (especially in African blacks since they have slower metabolism), psoriasis exacerbation, intradermal HDCRV (rabies vaccine) interference; safe for retina at prophylactic doses (avoid of diseased), but requires annual eye exam if life dose is exceeded – safe in pregnancy, avoid with epilepsy, pills taste very bitter

Front 444

What is the mechanism of action of Chloroquine?

Back 444

It inhibits the enzyme heme polymerase; this enzyme normally functions in the biocrystallization of hemozoin molecules (heme --> hemozoin), thus removing toxic heme from infected RBCs; however, Chloroquine caps the hemozoin molecules, preventing further biocrystallization, and in effect causing a lethal buildup of heme

Front 445

What are the oral treatment options for malaria?

Back 445

Chloroquine (only in central America); Quinine sulfate/doxycycline (cinchonism);
Mefloquine (neuropsych reactions); Pyrimethamine-sulfa (Fansidar, resistance problems); Atovaquone/proguanil (Malarone, expensive)

Front 446

What are the ABCDs of malaria prevention?

Back 446

be Aware of malaria risk at destination; avoid being Bitten by mosquitoes; take Chemoprohylaxis when appropriate; immediately seek Diagnosis/treatment if fever develops (within 1 year)

Front 447

What are the four drugs used for the prophylaxis of malaria?

Back 447

Mefloquine (weekly dosage); Chloroquine (weekly); Doxycycline (daily); Malarone (daily, expensive, shortest post-trip course)

Front 448

What should be done if malaria is suspected?

Back 448

Treat immediately; don’t wait for test results

Front 449

Why must a P. vivax infection also be treated with Primaquine?

Back 449

Because it infects the host’s liver as Hypnozoites, causing the infection to relapse (P. vivax adapted to this mechanism in order to survive the cold winters in temperate climates)

Front 450

What form of malaria is P. ovale malaria most like?

Back 450

P. vivax malaria – infects only young RBCs, makes Hypnozoites; <10% of world malaria, most common in W Africa; usually Chloroquine sensitive

Front 451

Which antimalarial drugs are effective against the blood stage, and which against the liver stage (Hypnozoites)?

Back 451

Blood: Quinine, Chloroquine, Mefloquine; Liver: Primaquine

Front 452

What adverse effects are associated with Mefloquine?

Back 452

Sleep disturbance, vivid dreams, GI upset (take with water), dizziness, panic attacks, cardiac conduction problems; rarely: hallucinations, seizures – OR for psych reactions is 3.56

Front 453

What is Doxycycline usually taken with and why?

Back 453

Quinine, since Doxycycline is slow-acting (effective in chloroquine-resistant malarias)

Front 454

What is the mechanism of action of Doxycycline?

Back 454

Ribosomal inhibition (in pre- and erythrocytic phases)

Front 455

What contraindications and drug interactions are associated with Doxycycline?

Back 455

Contraindications: pregnancy, children<9 yo, allergy, liver disease; Drug interactions: antagonized by seizure meds (barbiturates, phenytoin, carbamazepine), avoid with Pepto-Bismol/iron/antacids, oral contraceptive become less effective, monitor PT (INR) if on Coumadin;
Doxycycline is cheap and effective, but has poor adherence

Front 456

What does Doxycycline also protect against (besides Malaria) and what adverse effects are associated with it?

Back 456

Also protects against Leptospirosis – Adverse effects: photosensitivity, esophagitis (take with water and keep upright!), Monilia (yeast-like fungus)

Front 457

What contraindications are associated with Mefloquine?

Back 457

Seizure disorders, h/o psychosis/depression, cardiac conduction defects (!); avoid use with quinine, quinidine, halofantrine (due to conduction defects, but BB/CCB use is OK) –
relative contraindications: 1st trimester pregnancy, people who perform tasks involving fine motor coordination (airline pilots), infants (unless high risk case)

Front 458

What can be problematic regarding the pharmacokinetics of Mefloquine?

Back 458

It has a very long half-life (21 days), meaning that adverse effects continue for a long time

Front 459

What dosage is associated with Chloroquine and Mefloquine?

Back 459

Once weekly, starting one week prior to departure and continuing 4 weeks after return

Front 460

How has Chloroquine resistance come about?

Back 460

Plasmodium has developed the ability to pump Chloroquine out of its food vacuoles where hemozoin biocrystallization occurs

Front 461

What is the purpose of Nivaquine?

Back 461

It is a syrup of Chloroquine that does not taste as bitter (not sold in US since it can cause a lethal overdose in children)

Front 462

How does Quinine affect blood glucose levels?

Back 462

It can exacerbate the hypoglycemia already caused by P. falciparum (can mimic changes of cerebral malaria)

Front 463

What adverse effects are associated with Primaquine?

Back 463

n/v, HA, methemoglobinemia

Front 464

What must be screened for before giving a person Primaquine?

Back 464

G6PDH deficiency (could be fatal due to hemolysis)

Front 465

What is the treatment of choice in the US for malaria?

Back 465

Primaquine phosphate – can also be used prophylactically

Front 466

What drug interactions are associated with Proguanil?

Back 466

It interacts with Coumadin, Rifampin, Tetracycline

Front 467

What adverse effects are associated with Atovaquone/Proguanil?

Back 467

Very few: GI upset, HA, mouth sores – not yet approved for pregnancy (use Mefloquine instead)

Front 468

What drug is the best choice for short-term effective Chloroquine-resistant P. falciparum prophylaxis?

Back 468

Atovaquone/Proguanil (Malarone)

Front 469

What is the most common adverse effect associated with Quinine?

Back 469

Cinchonism (flushing, ringing of ears, hearing loss, dizziness), may necessitate discontinuation;

Front 470

Where should Quinine never be administered?

Back 470

In the buttocks of a child, since it can cause sciatic nerve paralysis (use thigh injection)

Front 471

What is the mechanism of action of Quinine?

Back 471

Inhibits hemozoin biocrystallization

Front 472

Why should long-term treatment with Fansidar (Pyrimethamine/Sulfadoxine) be avoided?

Back 472

Since it has a sulfa drug in it, long-term treatment can lead to Stevens-Johnson syndrome – also avoid in 1st trimester and in last 2 weeks of pregnancy (due to kernicterus)

Front 473

What homeopathic preparations are not effective against malaria?

Back 473

Demal 200, Papaya leaf tea, Sweet wormwood home-brewed tea, Thiamine, ultrasound devices, repellant-impregnated wristbands

Front 474

How is Artemisinin best used?

Back 474

In combination with a long-acting antimalarial (e.g. Lumefantrine, which is the safer alternative to Halofantrine = no QT prolongation)

Front 475

What is the mechanism of action of Artemisinin?

Back 475

As the parasite consumes hemoglobin, it frees up the heme which releases iron --> the iron can then reduce a peroxide bond in Artemisinin, generating high-valent iron-oxo species --> these species result in a cascade of reactions that produce oxygen radicals which kill the parasite

Front 476

What new drug is reserved for severe cases of Malaria in the US?

Back 476

Artemisinin (derived from Sweet Wormwood or Artemesia annua) – has a very short half-life

Front 477

What is used in the US as an alternative to IV Quinine treatment?

Back 477

IV Quinidine

Front 478

What is the adverse effect associated with Halofantrine?

Back 478

QT prolongation – also, avoid with Mefloquine

Front 479

What distinguishes Tafenoquine from Primaquine?

Back 479

It has a longer half-life

Front 480

What does Maloprim (Deltaprim) consist of, where is it used, and what adverse effects are associated with it?

Back 480

Pyrimethamine and Dapsone; used overseas as an affordable alternative for malaria prophylaxis; not used in US/Europe due to adverse effects: agranulocytosis, thrombocytopenia

Front 481

What is the treatment for Babesia microti?

Back 481

Clindamycin with quinine (same treatment as for malaria in pregnant women)

Front 482

What is the treatment for Trichinella spiralis (Trichinosis)?

Back 482

Albendazole and steroids

Front 483

How does Trichinella spiralis cause disease?

Back 483

Worms enter the body in undercooked meat (pork/bear meat), mature in the GI tract, and their progeny encyst in host muscle; It causes painful, tender muscles and fever, as well as eyelid edema, diarrhea, and high eosinophil counts

Front 484

What characterizes Albendazole?

Back 484

MOA: interferes with microtubule assembly and impairs glucose uptake; PK: part of the Benzimidazole class, it is metabolized in the liver to Albendazole sulfoxide which is the most active form;

Front 485

What is the treatment for cutaneous larva migrans?

Back 485

Albendazole or Ivermectin; can also use ethyl chloride or freezing ahead of the advancing margin

Front 486

What is cutaneous larva migrans also known as and what characterizes it?

Back 486

Creeping eruption: causes uncontrolled itching and a characteristic skin track (serpiginous)

Front 487

What characterizes Clindamycin?

Back 487

MOA: attaches to ribosomes; Uses: Gram+/anaerobes/anti-malarial/oral and bone infections;
AE: can cause C. difficile colitis (since it is resistant), as well as diarrhea and a rash

Front 488

What are tissue helminth infections often associated with?

Back 488

Eosinophilia – whereas protozoan infections usually do not develop eosinophilia

Front 489

What characterizes Babesia microti?

Back 489

It can appear as a malaria-like blood infection, but is distinguished by RBCs containing tetrads (or “Maltese cross”); it is spread by ticks or via transfusion, and is endemic to the NE and Midwest US (also globally)

Front 490

What is the danger with Naegleria?

Back 490

They live in warm springs and can attack the human brain by traveling through the cribriform plate - can be treated with Amphotericin B

Front 491

What is the pathology of Onchocerciasis (river blindness)?

Back 491

adasd

Front 492

What characterizes Diethylcarbamazine (DEC)?

Back 492

Used in the treatment of filarial infections (available only from CDC); MOA: damages surface of microfilariae, allowing the host immune system to kill it; AE: Mazzotti reaction = host immune reaction due to dying microfilarial antigens (itching, rash, fever, edema, conjunctivitis, encephalitis) – often given with corticosteroids to prevent these adverse effects

Front 493

What is the pathology of Loa loa?

Back 493

How is Loa loa diagnosed?
Take a blood sample during the day (since that’s when the vector is active) and look for microfilariaeIt is a filarial worm; the adults migrate through the tissue and may travel to eye (causing conjunctivitis); wherever the worms are, it can create an inflammatory swelling (Calabar swelling); the microfilariae live in the blood where it can be picked up by the deer fly during daylight hours

Front 494

What is the treatment for Strongyloides?

Back 494

Ivermectin (or Albendazole)

Front 495

What is the pathology of Strongyloides?

Back 495

It is a parasitic/free-living nematode that can invade humans, especially when immunocompromised (in this case it can cause a hyper-infection syndrome which is fatal in 80% of cases) – symptoms include a rash due to migrating larvae in the skin (larva currens)

Front 496

What side effects are important for Ivermectin?

Back 496

Although it kills the microfilariae, it does not kill the adult Oncocerca worms (it is curative for Strongyloides and Mansonella); most side effects are due to the dying microfilariae (itching, rash, edema, eye inflammation); there is a risk of fatal encephalitis if co-infected with Loa loa

Front 497

What is the treatment for Onchocerciasis and how does it work?

Back 497

Ivermectin – derived from Streptomyces avermitilis; MOA: opens chloride channels in invertebrates (but not in mammals); it is also used for Strongyloides, Mansonella, and scabies

Front 498

What is the pathology of visceral larva migrans?

Back 498

Dog/cat roundworm eggs are deposited in soil/sandbox; dirt can then be ingested (often by a child < 3yo) causing nausea, fever, hepatomegaly, edema, urticaria, and seizures

Front 499

What is the treatment for visceral larva migrans?

Back 499

Albendazole or Mebendazole

Front 500

What parasites can be responsible for Filariasis/Elephantiasis, what is the vector, and what is the treatment?

Back 500

Wuchereria bancrofti, Brugia malayi, Mansonella – vector: mosquitoes (feed at night); treatment: DEC

Front 501

What is the treatment for Leishmaniasis?

Back 501

Cutaneous lesions: infiltrate lesion with stibogluconate/liquid nitrogen, or give oral antimony/fluconazole; For L. braziliense or recalcitrant infections, pentavalent antimony is given IV/IM (i.e. sodium stibogluconate/meglumine antimonate)

Front 502

What can Schistosomiasis lead to?

Back 502

Liver cancer

Front 503

What are the three species that cause Schistosomiasis and what is the treatment?

Back 503

S. mansoni (inferior mesenteric vessels, terminal spine on side); S. haematobium (bladder vessels, terminal spine on end); S. japonicum (superior mesenteric vessels) – treatment is praziquantel

Front 504

What can be a complication of visceral leishmaniasis?

Back 504

Post Kala Azar Dermal Leishmaniasis – causes hypopigmented macules (usually occurs up to several years after treatment); may require pentavalent antimony treatment

Front 505

What characterizes Miltefosine?

Back 505

Used for visceral Leishmaniasis in India; Category X in pregnancy; investigational treatment in HIV

Front 506

What adverse effects are associated with pentavalent antimonials?

Back 506

Cardiac arrhythmias, chest pain, pancreatitis, very painful when given IM

Front 507

What is the treatment for visceral Leishmaniasis?

Back 507

Pentavalent antimonials, although resistance in India has required replacement by Miltefosine; in the US, treatment is L-AMB (less nephrotoxicity)

Front 508

What is the treatment for Dracunculiasis (Guinea worm infection)?

Back 508

Mechanical removal of worm (found in Southern Sudan and war-torn areas of Africa)

Front 509

What form of Leishmaniasis is responsible for Espundia?

Back 509

L. braziliense

Front 510

What are the three types of Leishmaniasis and what is the vector?

Back 510

Cutaneous, Mucosal (Espundia), Visceral (Kala Azar/black fever – common in India) – all are caused by the sand fly

Front 511

What are the different types of Trypanosomal infections?

Back 511

South American Trypanosomiasis: Chagas disease (caused by Reduviid bug);
African Trypanosomiasis: African sleeping sickness (W. African variety – T. brucei gambiense, slow course; E. African variety – T. brucei rhodesiense, fast course)

Front 512

What is the usual treatment for PCP pneumonia?

Back 512

Bactrim – however in AIDS patients, the adverse sulfa reaction can be too severe, so alternative treatments may have to be used

Front 513

What adverse effects are associated with Pentamidine?

Back 513

Hypoglycemia; later on, diabetes

Front 514

What is the treatment for African sleeping sickness?

Back 514

West African --> early: pentamidine (also used for PCP pneumonia); late: eflornithine
East African --> early: suramin; late: melarsoprol (arsenic)

Front 515

What is an important symptom of African sleeping sickness?

Back 515

Winterbottom’s sign (posterior cervical lymph node enlargement); also Tsetse bite chancre with lymphadenitis

Front 516

What is the treatment of choice for Chagas disease?

Back 516

Benznidazole

Front 517

What is an important symptom of Chagas disease?

Back 517

Romana’s sign (unilateral swelling of the face)

Front 518

What is the treatment for non-intestinal flukes?

Back 518

Praziquantel – does not work for F. hepatica (use Triclabendazole)

Front 519

What characterizes Praziquantel?

Back 519

Best treatment for most flukes and tapeworms; MOA: penetrates integument of worms causing tetanic contraction and paralysis; AE: dizziness (don’t drive), interacts with Rifampin, Category B in pregnancy

Front 520

What can be a complication of ingestion a pork tapeworm eggs?

Back 520

Neurocysticercosis (common cause of seizures in the developing world) – treatment is praziquantel or albendazole (sometimes seizure medication)

Front 521

What is an unusual side effect of eflornithine?

Back 521

Retards facial hair growth in women

Front 522

How do people often get infected with Toxoplasma gondii?

Back 522

By cleaning out the litter box and inhaling the parasite

Front 523

What is the treatment for Toxoplasmosis and when is it used?

Back 523

Pyrimethamine and sulfadiazine (work by folic acid synthesis inhibition) – only used in pregnant women, acute neonatal toxicity, and immunocompromised patients

Front 524

What are the various ways in which Toxoplasmosis can present?

Back 524

Congenital toxoplasmosis: seizures, intracerebral calcifications, MR, microcephaly, blindness;
Mono-like presentation: in adults; Meningoencephalitis: in AIDS patients – however, most patients will be asymptomatic

Front 525

What are examples of antigen-specific mechanism for mucosal host defense?

Back 525

Lymphoid elements associated with internal surfaces of the body; Exocrine secretory glands (e.g. salivary, lacrimal, pancreas, mammary glands)

Front 526

What is the difference between monomeric and dimeric IgA?

Back 526

Monomeric: produced mostly in bone marrow and found in the blood; Dimeric: produced mostly in lamina propria of mucosal tissues and found mainly in external secretions, also dimeric IgA is actively transported into external secretions via the polymeric immunoglobulin receptor (Pig-R)

Front 527

By what mechanism does migration of mucosal-derived lymphoblasts to distant mucosal sites take place?

Back 527

By the interaction of lymphocyte adhesion receptors (integrins) and vascular addressin

Front 528

What can happen when an antigen-response is generated in the gut?

Back 528

It can generalize to other mucosal surfaces (e.g. bronchial tract, mammary glands) – mediated by lymphoblast trafficking

Front 529

How does the MALT differ from lymph nodes?

Back 529

MALT is associated with T cells that preferentially support a B cell class switch to IgA

Front 530

Where are M cells located and what is their function?

Back 530

They are part of the specialized epithelium that overlies Peyer’s patches and function in the facilitation of antigen uptake

Front 531

What are examples of mucosa-associated lymphoid tissue (MALT)?

Back 531

Nasal-associated lymphoid tissue (NALT): tonsils, adenoids; Gut-associated lymphoid tissues (GALT): Peyer’s patches; Bronchus-associated lymphoid tissues

Front 532

What are examples of non-antigen specific mechanisms for mucosal host defense?

Back 532

Nasal function (e.g. being able to clear particulates), cough reflex, gag reflex, mucociliary clearance

Front 533

What problems can lead to dysfunction of mucociliary clearance and what can this result in?

Back 533

Improperly functioning cilia, abnormally thick mucus (with CF) --> stasis --> bronchiectasis (abnormal enlargement of conducting airways) due to recurrent infection

Front 534

What can an impaired cough/gag reflex lead to?

Back 534

Aspiration --> pneumonia, lung abscess

Front 535

How does IgA2 differ from IgA1?

Back 535

IgA2 is more resistant to bacterial proteases, thus more IgA2 is secreted than IgA1

Front 536

What binds two IgA monomers together to form the dimeric IgA?

Back 536

J chain – B cells can be either J chain-positive or J chain-negative; this will determine whether they secrete monomeric or dimeric IgA

Front 537

What is the purpose of the secretory component of secretory IgA?

Back 537

It provides the secretory IgA with some form of protection against enzymatic cleavage, thus prolonging its half-life

Front 538

How does dimeric IgA cross the mucosal epithelial cell layer?

Back 538

After being secreted from B cells, they bind to the poly-Ig receptor found on the basal surface of mucosal cells --> this causes them to be taken up via endocytosis, after which they are transported to the apical surface of the cell --> once they are released from the apical surface into the lumen, a secretory component from the poly-Ig receptor remains attached to the dimeric IgA

Front 539

Why is IgA better suited for mucosal immunity than IgG?

Back 539

It does not activate inflammatory systems to the same extent as IgG (i.e. it can block infection without inducing an inflammatory response that damages the surface)

Front 540

By what mechanism can TH2 cells cause suppression of TH1 cells?

Back 540

TH2 can secrete IL-10 which interferes with the co-stimulator function of APCs to TH1 cells

Front 541

What is the purpose of oral tolerance to antigens and how is this thought to be achieved?

Back 541

Its purpose is to prevent a harmful immune response to harmless antigens/foods – it is thought to be achieved through clonal deletion, clonal anergy, or active suppression by T cells

Front 542

What is the significance of the presence of TCRγδ/CD8+ T cells as part of the intra-epithelial lymphocytes?

Back 542

They are thought to play an important role in immunoregulation and epithelial renewal during infection or enteropathy

Front 543

How do intra-epithelial lymphocytes differ from lamina propria lymphocytes?

Back 543

Intra-epithelial lymphocytes contain more of the TCRγδ-type whereas those of the lamina propria are almost exclusively the TCRαβ-type – also, the intra-epithelial lymphocytes are mostly CD8+. Whereas those of the lamina propria are mostly CD4+

Front 544

What type of infection is common in people who have low T cell counts (e.g. AIDS patients)?

Back 544

Fungal infections (e.g. Candida, Pneumocystis)

Front 545

What is the effect of having HIV on malarial infections?

Back 545

Increased incidence and increased mortality

Front 546

What describes the clinical symptoms of malaria?

Back 546

Non-specific (must take epidemiological history)

Front 547

How does Plasmodium falciparum affect RBCs and what are the consequences?

Back 547

They make them less deformable and more sticky causing them to form knobs --> knobs block capillaries and small blood vessels in essential organs --> impaired oxygen/substrate delivery, focal ischemia, anaerobic glycolysis, lactic acidosis --> cellular injury

Front 548

How do Plasmodia derive energy from their host?

Back 548

By anaerobic glycolysis of glucose to lactic acid

Front 549

What causes the symptoms of malaria?

Back 549

Rupture of schizont in RBC with release of merozoites

Front 550

What form of malaria has recently been found to transmit to humans (formerly only seen in primates)?

Back 550

Plasmodium knowlesi

Front 551

What are modes of malaria transmission besides via the Anopheles vector?

Back 551

Sharing of needles (drug abuse), blood transfusion, mother to infant transmission, organ transplantation

Front 552

What does it mean when a patient with malaria has crescent/banana-shaped gametocytes in their blood?

Back 552

They are infected with Plasmodium falciparum

Front 553

What is meant by airport malaria?

Back 553

Mosquitoes around international airports pick up Plasmodium from travelers and spread it to other human hosts

Front 554

What is seen in a blood smear from a patient infected with P. vivax/ovale?

Back 554

Enlarged RBCs containing small, red dots

Front 555

What are the quinolone derivatives used for malaria treatment?

Back 555

Chloroquine, quinine, quinidine (IV), mefloquine, halofantrine, primaquine

Front 556

What must be done before giving primaquine?

Back 556

Check for G6PDH deficiency

Front 557

What is the main treatment for P. vivax/ovale?

Back 557

Chloroquine and primaquine; if patient from PNG/Indonesia, use quinine with doxycycline and primaquine

Front 558

What is the main treatment for P. falciparum with chloroquine-resistance?

Back 558

Quinine with doxycycline (if pregnant: quinine with clindamycin)

Front 559

What type of treatment is given in patients with an extremely high parasitemia?

Back 559

Exchange transfusion (replace plasma)

Front 560

What are the ribosomal inhibitors used for malarial treatment?

Back 560

Tetracycline, clindamycin – used in combination with other drugs (e.g. Quinine)

Front 561

What are the antifolates used for malaria treatment?

Back 561

Pyrimethamine, sulfonamides

Front 562

How is malaria diagnosed?

Back 562

By thick and thin smears; thick smear is more sensitive, thin smear allows for species identification – also useful for quantifying the degree of parasitemia

Front 563

What is an example of a substance detected by rapid diagnostic tests for malaria?

Back 563

Histidine-rich protein (from P. falciparum infected RBC)

Front 564

What are the pros and cons of PCR testing for malaria?

Back 564

Can find very small number of parasites, but cannot tell whether they are dead or alive

Front 565

What antimalarial is used prophylactically when traveling to areas with no drug-resistance?

Back 565

Chloroquine – treatment must be started earlier and continued longer

Front 566

What is a problematic side effect associated with mefloquine prophylaxis?

Back 566

Neuropsychiatric and cardiac issues – cheaper and weekly dosing

Front 567

What is a problematic side effect associated with doxycycline prophylaxis?

Back 567

Photosensitivity (easy to get burned in areas where malaria is endemic)

Front 568

Why are chemoprophylaxis antimalarials started prior to travel?

Back 568

Determine whether drugs are tolerated (also, to build up steady-state levels of drugs)

Front 569

What antimalarial is used prophylactically when traveling to areas of drug-resistance?

Back 569

Malarone (atovaquone/proguanil) – treatment is quite expensive, but has short post-trip dosage; other options include doxycycline or mefloquine

Front 570

When is vaccination against Strep pneumo especially important?

Back 570

In the elderly and pre-splenectomy

Front 571

What characterizes community-acquired atypical pneumonia (CAAP)?

Back 571

Pathy inflammatory changes in the lung, mostly interstitial; Little/no sputum; No physical signs of consolidation; Little/no elevation of WBCs; Extrapulmonary signs

Front 572

Which bacteria often cause pneumonia in patients with CF?

Back 572

Pseudomonas aeruginosa (also seen with nosocomial pneumonia)

Front 573

What is the most common cause of Gram-negative pneumonia?

Back 573

Klebsiella: causes formation of thick/gelatinous sputum; often seen in debilitated/malnourished people (e.g. chronic alcoholism)

Front 574

What bacteria often cause pneumonia following a viral infection?

Back 574

Staph aureus

Front 575

What characterizes Moraxella catarrhalis?

Back 575

Mostly seen in elderly; common cause of acute exacerbation of COPD; common cause of otitis media in children

Front 576

What disease is associated with H. flu?

Back 576

Children: lower respiratory tract infection, meningitis, epiglottitis, conjunctivitis (“pink eye”); Adults: CAP; Elderly: septicemia, endocarditis, pyelonephritis, cholecystitis, suppurative arthritis

Front 577

What are the key distinctions between lobar pneumonia and bronchopneumonia?

Back 577

Lobar pneumonia: consolidation of a large part of a lobe/the entire lobe (4 stages: congestion, red hepatization, gray hepatization, resolution); Bronchopneumonia: patchy consolidation, consolidated areas of acute suppurative infection, multilobar/bilateral/basal

Front 578

What (soft) radiologic findings are associated with pneumonia?

Back 578

Lobar distribution --> RLL (S. pneumo/H. flu), Upper lobe (Klebsiella); Effusions --> H. flu/streptococcal, not S. pneumo; Cavitation --> Klebsiella, not S. pneumo/H. flu

Front 579

What physical exam findings are associated with pneumonia?

Back 579

Dullness to percussion, crackles/rales, bronchial breath sounds, egophony

Front 580

What is absolutely necessary for the diagnosis of CAAP?

Back 580

CXR – since physical exam is not as helpful

Front 581

What clinical signs are associated with a lung abscess?

Back 581

Foul-smelling purulent/sanguineous sputum; Fever, chest pain, weight less; Clubbing

Front 582

What characterizes SARS?

Back 582

Coronavirus; First found in China; Lower respiratory tract syndrome; Diagnosis by PCR or detection of antibodies; 10% mortality rate; No treatment, supportive care only

Front 583

What type of infection are immunosuppressed patients especially vulnerable to?

Back 583

CMV(e.g. CMV pneumonia, CMV retinitis)

Front 584

What extrapulmonary signs are associated with CAAP?

Back 584

Ear/throat lesions: mycoplasma; Diarrhea: mycoplasma, legionella; Abdominal pain: legionella;
Skin rash: mycoplasma, psittacosis

Front 585

What are disadvantages of combination therapy?

Back 585

Cost, IV lines, drug interactions, adverse effects, difficulty in identifying single agent effects (both positive and negative effects), antagonism, superinfection (antibiotics kill natural flora, allowing opportunistic infection to take root)

Front 586

What is meant by the terms inappropriate/inadequate therapy?

Back 586

The drugs that were used initially to treat the infection are shown to be ineffective for the organisms later found to be causative – a change of therapy is required

Front 587

What is the procedure for nosocomial pneumonia or intraabdominal infections?

Back 587

Multi-drug therapy based on a variety of potential pathogens

Front 588

Why do bacteria respond differently to gentamicin/tobramycin and streptomycin?

Back 588

They are affected by different aminoglycoside-modifying enzymes

Front 589

In what clinical setting are synergistic drug combinations a must?

Back 589

Serious infections, like endocarditis

Front 590

What combination of drug has been shown to be synergistic against enterococcal infections?

Back 590

Aminoglycosides and ampicillin/vancomycin; this combination can make two bacteriostatic drugs bactericidal (ampicillin/vancomycin break up the cell wall so that aminoglycosides can get in and inhibit the 30S bacterial ribosomes)

Front 591

What class of drugs are enterococcal infections inherently resistant to?

Back 591

Cephalosporins

Front 592

What is the major reason why combination therapy is used?

Back 592

Empiric therapy to cover all most likely pathogens

Front 593

How is synergism defined, in vitro?

Back 593

As a greater than 2 log10 reduction in bacterial count when comparing combination treatment with a single agent (e.g. Enterococcus time-kill study)

Front 594

What indications for combination therapy have not yet been established to a great extent?

Back 594

Prevention of the emergence of resistance, disease severity/organisms with high/rapid mortality

Front 595

How often does inappropriate therapy take place?

Back 595

about 30% of the time – often due to antibiotic-resistant pathogens

Front 596

How does outcome differ between combination therapy vs. appropriate monotherapy (i.e. bug is susceptible to monotherapy drug)?

Back 596

It does not; there is no difference in mortality rates

Front 597

What drug combinations have not been shown to be synergistic in the treatment of Pseudomonas aeruginosa?

Back 597

Ciprofloxacin + aminoglycosides; Double β-lactams

Front 598

What drug combinations have been shown effective in treating Pseudomonas aeruginosa?

Back 598

Antipseudomonal β-lactam + aminoglycosides (gold standard); also antispseud β-lactam + ciprofloxacin or aztreonam; other options include carbapenems + aminoglycosides or ciprofloxacin, or also aztreonam + aminoglycosides

Front 599

Why is combination therapy important in treating Pseudomonas aeruginosa?

Back 599

It is a common nosocomial pathogen with a high mortality rate; it has multiple mechanisms for attaining drug-resistance

Front 600

What is the significance of the SPACE organisms?

Back 600

Two antibiotics should be used for Serratia, Pseudomonas, Acinetobacter, Citrobacter, Enterobacter – unless the exact species is known (monotherapy is sufficient)

Front 601

What organisms are known to be resistant/difficult to treat?

Back 601

MRSA, Pseudomonas aeruginosa, Acinetobacter, Klebsiella pneumoniae, Enterobacter, Enterococcus, Candida

Front 602

What describes the activity of barbiturates?

Back 602

Sedation to coma/death; Induces a state resembling normal sleep (decreases REM; at hypnotic doses can see distortion of mood, impairment of judgment, impairment of fine motor coordination); No analgesia; Anticonvulsant activity

Front 603

What characterizes the clinical use of benzodiazepines in the treatment of anxiety?

Back 603

Most effective in patients showing high levels of emotional and somatic symptoms, and low levels of depression; Some use in patients showing anxiety associated with other disease states; Improvement usually seen within the 1st week or two of treatment

Front 604

What activity is seen with benzodiazepines?

Back 604

Sedative/hypnotic, anxiolytic, anticonvulsant (not used prophylactically), muscle relaxant, amnestic

Front 605

What advantages do benzodiazepines have over barbiturates?

Back 605

Do not induce liver enzymes, have very little effect on REM sleep, have a much wider margin of safety, withdrawal is mild

Front 606

When is giving a barbiturate contraindicated?

Back 606

When the patient has a family or personal history of acute intermittent porphyria: overproduction and excretion of porphyrins and their metabolites, causes severe abdominal pain and neurological disturbances; barbiturates increase the production of porphyrins

Front 607

What is the treatment for barbiturate overdose?

Back 607

Maintain respiration, rule out narcotics (e.g. Naloxone), treat symptoms (maintain respiration and perfusion, gastric lavage [?], administer bicarbonate, hemodialysis)

Front 608

What are adverse effects of barbiturates?

Back 608

Symptoms of overdose incl. comatose state, marked respiratory depression (immediate cause of death in overdose), shortened REM sleep, marked hypotension, weak/rapid pulse; Induces P450; Can see physical/psychological dependence – At one time barbiturates were the most common drug class used in suicide

Front 609

What is the mechanism of action of benzodiazepines?

Back 609

Bind between the gamma and alpha subunits on the GABAA receptor, thus increasing the influx of Cl-, causing hyperpolarization of the cell

Front 610

What are barbiturates used for clinically?

Back 610

Induction in general anesthesia; Seizure disorders

Front 611

What are examples of barbiturates and their half-life?

Back 611

Long-acting: Phenobarbital; Intermediate-acting: Pentobarbital, Secobarbital;
Short-acting: Thiopental, Methohexital

Front 612

What side effects and toxicities are seen with benzodiazepines?

Back 612

Drug interactions: do not induce P450, combination with other CNS depressants can be lethal;
Adverse effects: very few, safe, toxic doses treated with supportive care, caution in 1st trimester;
At time of peak plasma levels: marked effects on driving, patients underestimate impairment;
Tolerance: develops to many effects, but not to antianxiety effects;
Physical dependence: abrupt discontinuation of chronic administration leads to withdrawal

Front 613

What characterizes Temazepam?

Back 613

Oral absorption slow and erratic; No active metabolites

Front 614

What characterizes Lorazepam?

Back 614

Absorbed slowly when administered orally; Well absorbed following IM administration; No active metabolites; Proper dose adjustment can give a good night’s sleep with minimal residual effects

Front 615

What characterizes Flurazepam?

Back 615

Metabolized to active metabolites; peak concentration of active metabolites reached in 1-3 hrs after oral intake; good BA; Proper dose can give 8hrs of sleep with minimal residual effects the next day

Front 616

Which benzodiazepines are used as sedatives/hypnotics?

Back 616

Flurazepam, Lorazepam, Temazepam, Triazolam

Front 617

What characterizes Flumazenil?

Back 617

It is a benzodiazepine antagonist: used for overdose to reverse respiratory depression; it will precipitate withdrawal so don’t give to patients with a history of seizures or to patients with barbiturate/tricyclic antidepressant overdose – variable effects with ethanol intoxication; it has a rapid onset and short duration

Front 618

What is the best way to avoid side effect when withdrawing benzodiazepines?

Back 618

Gradually taper the dose

Front 619

Besides treating anxiety, what other uses do benzodiazepines have?

Back 619

Sleeping disorders, convulsive disorders, neuromuscular disorders, preoperative medication, treatment of withdrawal from CNS depressants

Front 620

What characterizes the metabolism of benzodiazepines?

Back 620

Many are metabolized to active metabolites with longer half-lives and possibly more activity; Only Lorazepam, Oxazepam, Temazepam, and Triazolam have no active metabolites

Front 621

What characterizes the absorption and distribution of benzodiazepines?

Back 621

Oral absorption within 1-3 hours; Only Lorazepam is absorbed following IM injection; Apparent volume of distribution is 1-3L/kg; Typically have 80% of dose protein-bound

Front 622

What characterizes Oxazepam?

Back 622

Slow oral absorption; T½: 5-10hrs; No active metabolites

Front 623

What describes the absorption, distribution, and metabolism of Buspirone?

Back 623

Rapid and complete absorption following oral administration; Extensive first-pass effect;
T½: 2-3hrs, active metabolite half-life is twice as long

Front 624

What characterizes Buspirone?

Back 624

May act through serotonin systems; possibly has some effect on dopamine systems;
CNS activity: anxiolytic, delayed effects (4-6wks), not as effective in patients with prior history of benzodiazepine use, may be drug of choice in patients with history of sedative/hypnotic abuse;
Does NOT have sedative, anticonvulsant, or muscle relaxant properties (may be helpful in treating elderly patients) – minimal adverse effects, no dependence/cross-tolerance

Front 625

What type of drug class are the azaspirodecanediones?

Back 625

Non-benzodiazepine anxiolytic; prototypical drug is Buspirone

Front 626

What are the advantages of benzodiazepines in sleep disorders?

Back 626

Safety, do not disrupt REM, do not induce P450, milder withdrawal syndrome

Front 627

What characterizes Alprazolam?

Back 627

Oral absorption slower than Diazepam (like Chlordiazepoxide); T½: 10-14hrs; Metabolized to active metabolite (significant levels of active metabolite are not observed at therapeutic doses)

Front 628

What characterizes Chlordiazepoxide?

Back 628

Slower oral absorption than Diazepam; T½: 7-13hrs; Metabolized to Desmethyldiazepam and Oxazepam

Front 629

What characterizes Triazolam?

Back 629

Well absorbed orally; peak plasma levels 1 hr after oral administration; No active metabolites; May have higher abuse potential and more withdrawal with chronic use; Reported higher incidence of adverse behavioral reactions

Front 630

What characterizes Diazepam?

Back 630

Well absorbed orally; Elimination is biphasic and variable; Metabolized to Desmethyldiazepam which is further metabolized to Oxazepam (both metabolites are active)

Front 631

Which benzodiazepines are used as anxiolytics?

Back 631

Diazepam, Chlordiazepoxide, Oxazepam, Alprazolam

Front 632

What is the mechanism of action of GABAA-α1 agonists?

Back 632

Non-benzodiazepines; bind to with high affinity to α1 receptor subtype, but with much lower affinity to the other subtypes

Front 633

What are the spasmolytic drugs?

Back 633

GABA agonists (e.g. Diazepam and other benzodiazepines)

Front 634

What drug interactions are seen with GABAA-α1 agonists?

Back 634

Additive effects with ethanol and other CNS depressants; Inhibitors of CYP enzymes can increases serum concentrations of Eszopiclone

Front 635

What can occur at high doses of Zaleplon?

Back 635

Rebound insomnia

Front 636

What adverse effects are seen with GABAA-α1 agonists?

Back 636

Respiratory depression is NOT a major problem; Hypoxia/hypercarbia may be seen in patients with obstructive sleep apnea; All have some residual daytime sedation

Front 637

What characterizes the absorption, distribution, and metabolism of GABAA-α1 agonists?

Back 637

Rapid onset with short duration of action; well absorbed orally; T½: Zolpidem --> 2-2.5hrs, Zaleplon --> 1hr, Eszopiclone --> 6hrs; Metabolized by liver to inactive metabolites; Need to lower dose for elderly and patients with liver disease; All are metabolized by P450

Front 638

What are the clinical uses of GABAA-α1 agonists?

Back 638

Sedative/hypnotic: decrease sleep latency, little effect on sleep cycles at low doses; Zaleplon has a shorter duration of action than Zolpidem/Eszopiclone – compared to benzodiazepines they have less anti-anxiety effect, less anti-convulsant effects, and less muscle relaxant effects

Front 639

What drug interaction is found with Buspirone?
binding sites

Back 639

Displaces Digoxin but not Warfarin from plasma protein

Front 640

What are the GABAA-α1 agonists?

Back 640

Zolpidem, Eszopiclone, Zaleplon

Front 641

What is the key difference between viral and bacterial sinusitis?

Back 641

Viral sinusitis does not last as long as bacterial sinusitis (and it is not associated wit pus formation)

Front 642

What is the most common cause of pneumonia?

Back 642

Bacterial infection (Strep pneumo)

Front 643

What characterizes the lower respiratory tract infections?

Back 643

The etiologic agents for these infections vary widely

Front 644

What causes the most severe type of epiglottitis?

Back 644

Bacterial infection (mainly H. flu) – not seen much anymore due to H. flu vaccine

Front 645

What is almost always the underlying cause of laryngitis?

Back 645

Viral infection

Front 646

What is the most important organism causing otitis media?

Back 646

Strep pneumonia (also H. flu)

Front 647

What type of bacterial infection can be a complication of a viral infection?

Back 647

Infection due to bacteria that comprise the normal flora of the nasopharynx; the viral infection causes swelling and inflammation which prevents normal drainage, thus giving the normal flora an opportunity to cause overgrowth and infection

Front 648

What are considered upper respiratory infections?

Back 648

Any infection affecting the larynx or structures above it

Front 649

What is the most important microbe responsible for pharyngitis?

Back 649

Group A Strep (Strep pyogenes)

Front 650

What is the most common cause of rhinitis?

Back 650

Viral infection

Front 651

What is the most common cause of bronchitis?

Back 651

Viral infection (presents as a lingering cough/cold), although Mycoplasma is also common

Front 652

Why does rhinovirus mostly affect the upper respiratory tract?

Back 652

Because it is transmitted in larger particles (>10 microns)

Front 653

What type of atelectasis can be caused by an empyema?

Back 653

Compressive atelectasis

Front 654

What can atelectasis (collapse of a segment of lung) lead to?

Back 654

Pneumonia (since normal functioning is impaired)

Front 655

Why are patients with COPD more likely to get pneumonia?

Back 655

They have a reduced capacity to expel organisms from the lungs; they also often smoke, which further impairs host defense mechanisms

Front 656

What host defense mechanisms are specific to the respiratory tract?

Back 656

Clearance: mucous layer, cilia, macrophages, cough – these mechanisms can be impaired by smoking

Front 657

What can result from aspiration of food?

Back 657

Anaerobic bacteria are carried along with the food and can create a lung abscess (seen as a cavity on x-ray) – location of aspiration depends on position of patient while aspiration occurred (lower lobes are more common)

Front 658

What is the most common cause of bronchiolitis?

Back 658

Viral infection (most common in children, can be very serious)

Front 659

How can a patient with an empyema present?

Back 659

Patient being treated in the hospital for pneumonia appear to be getting better but is still febrile and CXR shows a pleural effusion

Front 660

What does the term empyema mean?

Back 660

A collection of pus in a potential space (e.g. located around the lung) – can be due to a complication of pneumonia, often requires surgical drainage

Front 661

What is the classic virus that is considered intermediate size (2-10 microns)?

Back 661

Influenza virus (can damage cilia thus increasing the chances for secondary bacterial pneumonia – this is a major reason why people die from influenza virus)

Front 662

What can be a distinguishing factor between bacterial pharyngitis and viral pharyngitis?

Back 662

If the patient has a concomitant rhinitis, the cause is most likely viral

Front 663

What organisms are part of the differential diagnosis for pharyngitis?

Back 663

Viral: rhinovirus, EBV (mono); Bacterial: group A strep, diphtheria; also, deep neck abscess

Front 664

What organism can be responsible for pneumonia in the bronchioles and alveoli?

Back 664

A very small organism (1-5 microns); e.g. Mycobacterium tuberculosis

Front 665

What circadian-specific physiologic events occur during sleep?

Back 665

GH secretion spikes during first bout of Delta sleep (stage III/IV); Cortisol secretion is maximal at dawn; Body temperature falls until 5AM; REM propensity is maximal between 3-5AM; Sleepiest times of the day are between 2-4PM and 3-5AM

Front 666

What occurs during Stage II sleep?

Back 666

Sleep spindles, K complexes; bodily movements continue; lasts 10-25 minutes during first sleep cycle; constitutes ~50% of sleep

Front 667

What occurs during Stage I sleep?

Back 667

Transition from Alpha to Theta waves; easily responsive to sounds; lasts 1-7 min.; Hypnic myoclonus may occur

Front 668

During which states of sleep does arousal cause only a limited confusional state?

Back 668

Stage I, II, REM

Front 669

How long does it take on average to enter REM sleep?

Back 669

Hour and a half (in narcolepsy, 20 min)

Front 670

What results from a chronic lack of sleep?

Back 670

Being tired/fatigued; Kids are hyperactive; Impaired performance at work/school/sports; Reduced alertness/attention; Mood swings, irritability; Impaired social interactions; Decreased creativity

Front 671

What are the major chief complaints in sleep medicine?

Back 671

Insomnia, excessive daytime sleepiness (EDS), unusual movements/behaviors/sensations while asleep or attempting to sleep

Front 672

How much sleep is necessary?

Back 672

Infants: 16-20 hours (half in REM), Adults: 8 hours

Front 673

What percent of sleep is taken up by REM sleep?

Back 673

~20%

Front 674

What are reasons that sleep is important?

Back 674

Restore wakefulness, tissue growth/repair/cellular division/protein synthesis

Front 675

What are the three subtypes of insomnia?

Back 675

Delayed sleep onset, impaired sleep continuity, early morning awakenings

Front 676

What characterizes the Multiple sleep latency test?

Back 676

Patients are given ~5 nap opportunities; time to sleep onset and REM is measured for each nap; can measure narcolepsy

Front 677

What characterizes the Epworth Sleepiness Scale?

Back 677

Consists of 8 questions that assess sleepiness under varying conditions; >10 is a significant score

Front 678

What are tests that objectively measure sleepiness?

Back 678

Multiple sleep latency test (MSLT), Maintenance of Wakefulness Test (MWT), Epworth Sleepiness Scale (ESS)

Front 679

What characterizes narcolepsy?

Back 679

REM sleep onset, cataplexy, hypnagogic/hypnopompic hallucinations, disturbed nocturnal sleep, excessive daytime sleepiness

Front 680

What are the main causes of excessive daytime somnolence?

Back 680

Insufficient sleep, sleep disordered breathing, restless leg syndrome overlapping with nocturnal myoclonus or PLMS, narcolepsy

Front 681

In what groups of people is insomnia more commonly seen?

Back 681

Women, elderly, thin; Chronic illness, pain; Anxiety, depression, stress; Drug/alcohol use/abuse

Front 682

What occurs during Stage III/IV sleep?

Back 682

High voltage Delta waves predominate; high stimulus threshold for arousal; important stages for feeling well-rested in the morning; skeletal muscles relaxed by still active

Front 683

What characterizes REM Behavior Disorder?
REM sleep activity without

Back 683

skeletal muscle atonia

Front 684

What occurs during REM sleep?

Back 684

Brain is active and EEG resembles awake state; Body is paralyzed except for diaphragm/eyes; REM is “dream sleep time”

Front 685

What are physiologic consequences of sleep apnea?

Back 685

Systemic/pulmonary hypertension, cardiac dysfunction, polycythemia

Front 686

What should be considered in the patient with restless leg syndrome?

Back 686

Renal failure, iron deficiency anemia

Front 687

What are the main causes of central sleep apnea?

Back 687

Stroke, CHF

Front 688

How is OSA treated?

Back 688

Positive airway pressure

Front 689

What is a common cause of obstructive sleep apnea (OSA)?

Back 689

Cranio-facial abnormalities

Front 690

What are the main complications of sleep apnea?

Back 690

MVA, CVA, MI, arrhythmias, airway obstruction/pulmonary edema after general anesthesia

Front 691

What characterizes the Multiple sleep latency test?

Back 691

Patients are given ~5 nap opportunities; time to sleep onset and REM is measured for each nap; can measure narcolepsy

Front 692

What are risk factors for sleep apnea?

Back 692

Small airway, Cushing’s, hypothyroidism, acromegaly, morbid obesity

Front 693

What is sleep apnea?

Back 693

Ability to maintain the patency of the upper airway during sleep

Front 694

What is the treatment for narcolepsy?

Back 694

CNS stimulants, SSRIs/antidepressants, scheduled naps

Front 695

What sleep disorder sometimes precedes Parkinson’s disease?

Back 695

REM behavior disorder

Front 696

What are the most common sleep disorders in children?

Back 696

Night terrors, nightmares, insomnia

Front 697

What are examples of parasomnias?

Back 697

REM behavior disorders, sleep walking, night terrors, PLMS, head banging

Front 698

What is the treatment for AOM?

Back 698

Analgesics/antipyretics, antibiotics, possible decongestants, possible drainage with myringotomy or ventilation tube

Front 699

Besides middle ear atelectasis, what other problem can be caused by ETD?

Back 699

Cholesteatoma – skin/keratin debris trapped behind the ear drum; usually arise at the top of the eardrum (pars flaccida)

Front 700

What is the problem with middle ear atelectasis?

Back 700

Collapse of the middle ear (severely retracted) – end-result of chronic and severe Eustachian tube dysfunction (ETD)

Front 701

What treatment can be given for the treatment of otitis media with effusion?

Back 701

Antibiotics, possible decongestants, possibly steroids, tincture of time (most important), myringotomy, ventilation tubes

Front 702

What can be seen in otitis media with effusion?

Back 702

A retracted TM, air-fluid levels (bubbles), discoloration, impaired mobility, hearing loss, not painful

Front 703

What are the complications of AOM?

Back 703

TM perforation (usually heal spontaneously), meningitis, brain abscess, facial nerve paralysis, labyrinthitis (otitis interna --> can predispose to meningitis and permanent hearing loss), otitis media with effusion

Front 704

What antibiotics are used for AOM?

Back 704

β-lactams (penicillins/cephalosporins), macrolides, sulfonamides, quinolones (in adults)

Front 705

What are the two biggest clues to the condition of the middle ear?

Back 705

Translucency and color of the TM

Front 706

What are the most common bacteria seen in AOM?

Back 706

Strep. pneumo.; H. flu.; M. cat.

Front 707

What are the symptoms of acute otitis media (AOM)?

Back 707

Fever, otalgia, hearing loss (!), systemic symptoms

Front 708

What treatment is used with otitis externa?

Back 708

Gentle debridement, ototopical medications (ear drops), wick placement if swelling prevents proper delivery of ear drops, occasionally oral antibiotics (ciprofloxacin)

Front 709

What is the treatment of ABS?

Back 709

Antibiotics (for Strep pneumo./H. flu./M. cat); decongestants, warm soaks to face, analgesics, rarely surgery (when ABS becomes complicated)

Front 710

How does bacterial sinusitis compare to viral sinusitis?

Back 710

The duration differs (viral lasts about 7-10 days, whereas bacterial lasts longer); there is more intense nasal obstruction with bacterial sinusitis as well as purulent discharge (in the nose)

Front 711

What symptoms are associated with ABS?

Back 711

Common symptoms: nasal obstruction, rhinorrhea (usually purulent), HA, facial pain;
Variable symptoms: odontalgia, fever, sore throat

Front 712

What is the challenge in diagnosing acute bacterial sinusitis (ABS)?
It is very hard to distinguish

Back 712

from allergic rhinitis, viral URI, or nasal masses

Front 713

What is the treatment of malignant otitis externa?

Back 713

Treat aggressively with systemic antibiotics against pseudomonas and possible surgical debridement

Front 714

What is characteristic of malignant otitis externa?

Back 714

Usually seen in diabetics; most commonly caused by pseudomonas; can lead to necrotizing osteitis of skull base and paralysis of cranial nerves (e.g. VII, XI); often fatal

Front 715

What microbes are associated with otitis externa?

Back 715

Staph, pseudomonas, fungi

Front 716

What characterizes otitis externa?

Back 716

Infection/inflammation of external auditory canal causing severe pain (especially on manipulation of pinna), drainage, swelling, and hearing loss (if canal is completely occluded)

Front 717

What symptoms are seen with cholesteatoma?

Back 717

Pain, hearing loss (due to the production of osteolytic enzymes), recurring otorrhea

Front 718

What differentiates the early phase from the late phase reaction in allergic rhinitis?

Back 718

Early: pruritus, urticaria, vasodilation/leakage, bronchoconstriction, mucous secretion;
Late: infiltration with eosinophils, fibrin deposition, infiltration with monocytes, tissue destruction

Front 719

What hormonal imbalances can cause rhinitis?

Back 719

Pregnancy, hypothyroidism

Front 720

What is the problem with the use of nasal decongestant sprays?

Back 720

Although they provide immediate relief to patients with nasal congestion (by causing vasoconstriction), once the effects wear off, they are followed by a rebound nasal vasodilation that will be worse than their initial problem (thus causing continuous use of the nasal spray)

Front 721

What characterizes allergic shiners and Dennie lines?

Back 721

Allergic shiners: dark discoloration under the eyes; Dennie lines: folds below the lower eyelids;
these signs are due to chronic obstruction of nasal venous return and hypoxia leading to spasm of striated muscles of Mueller

Front 722

What characterizes the nasal salute?

Back 722

Maneuver of scratching the nose by lifting the tip (temporarily improves congestion); leads to a nasal crease developing right above the nasal tip

Front 723

What are the characteristics of an adenoid face?

Back 723

Chronic mouth breathing which results in hypognathic jaw, open-mouthed facies, arched palate

Front 724

What characterizes nasal polyps?

Back 724

Benign growths arising from nasal or sinus mucosa; unclear etiology; treat underlying factors; if symptomatic, surgical extirpation may be necessary (send to pathologist)

Front 725

What factors are important in diagnosing allergic rhinitis?

Back 725

Symptoms: hypersecretion (rhinorrhea), itching, irritation (sneezing/burning), congestion;
Seasons/circumstances: spring (grasses/trees/molds), summer (grasses), fall (weeds/molds), winter (dust mite, animal dander) – molds can be year-round antigens;
Family history: there is a genetic predisposition (ask about allergies/asthma) --> 1 parent allergic: 1/3 chance for child; 2 parents allergic: 2/3 chance for child

Front 726

What type of immunological reactions is associated with allergic rhinitis?

Back 726

Type I (Gell and Coombs)

Front 727

What is an antrochoanal polyp?

Back 727

A polyp originating in the maxillary sinus protruding in the middle nasal meatus (may be visible behind the soft palate if very large)

Front 728

What distinguishes acute tonsillitis from infectious mononucleosis?

Back 728

In mono, the lymph nodes affected are mostly posterior whereas with Strep pyogenes they are mostly anterior

Front 729

What causes biphasic stridor?

Back 729

Usually a more severe obstruction at the level of the larynx or below (sign of impending airway obstruction)

Front 730

What differentiates inspiratory vs. expiratory stridor?

Back 730

Inspiratory stridor is caused by extrathoracic obstruction (vocal cords and above);
Expiratory stridor is caused by intrathoracic obstruction (in the lungs, upper trachea, subglottis)

Front 731

What are some examples of laryngeal dysfunction?

Back 731

Aspiration, hoarseness (usually first symptoms to present), cough, dyspnea/stridor

Front 732

What is the main function of the larynx?

Back 732

Airway protection (keep food/fluids out of the lungs); also important are respiration and speech

Front 733

How is tonsil size graded?

Back 733

Grade 1+: totally contained within the tonsillar fossa; Grade 2+: barely protruding out of the tonsillar fossa; Grade 3+: protrude to touch the uvula; Grade 4+: tonsils touch in midline

Front 734

What are the indications for tonsillectomy?

Back 734

Obstructive hypertrophy (interferes with breathing or swallowing); Recurrent infection (6 episodes in one year, or 3-4 per year for 2+ years)

Front 735

What is the management of allergy?

Back 735

Environmental control (most effective and difficult); Pharmacotherapy; Immunotherapy (when other options fail) – avoidance --> antihistamines --> corticosteroids --> immunotherapy

Front 736

What symptoms are associated with acute tonsillitis?

Back 736

Fever, sore throat, odynophagia – symptoms are frequently caused by Strep pyogenes

Front 737

What is the usual treatment of acute tonsillitis and what complication can occur?

Back 737

Antibiotics – if an abscess forms underneath the tonsil, it may have to be removed – peritonsillar abscess will cause the tonsil to become displaced and the patient will present with pain on opening the mouth (trismus)

Front 738

What can a wart-like growth on the vocal cords indicate?

Back 738

Laryngeal papilloma

Front 739

What aspects are included in a neck mass evaluation?

Back 739

History (duration, mode of onset, symptoms); Complete head and neck exam (size, location, tenderness, mobility, consistency); Fine needle aspiration biopsy (most important test);
CT, ultrasound, other radiological evaluations

Front 740

What are the etiologies associated with a neck mass?

Back 740

Infectious/inflammatory, neoplastic, congenital (cysts) – neck masses should be assumed to be malignant until proven otherwise (especially when asymptomatic and not present from birth)

Front 741

What characterizes laryngeal cancer?

Back 741

Classic symptom triad: hoarseness, sore throat, otalgia (!); 95% are squamous cell carcinomas; risk factors include tobacco and alcohol (if taken both, synergisms will occur); if the vocal cord loses mobility, the cancer will be more progressed – treatment with surgery, chemotherapy, radiation (with metastasis)

Front 742

What is the treatment for an oropharyngeal papilloma?

Back 742

Cut it off (no anesthesia necessary)

Front 743

What causes recurrent respiratory papilloma?

Back 743

HPV 6 and 11; more common in children (transmitted in birth canal), may require multiple surgical procedures; if they migrate into the trachea, treatment will be complicated

Front 744

What are causes of hoarseness?

Back 744

Vocal cord paralysis, vocal cord mass, functional deficits (muscle tension dysphonia/spastic dysphonia)

Front 745

What characterizes vocal cord nodules (screamers/singers nodules)?

Back 745

Slight elevations on the vocal cords

Front 746

What characterizes blastomycosis?

Back 746

Marked epithelial hyperplasia; Non-specific symptoms; CXR: lobar consolidation, multilobar/ perihilar infiltrates, multiple nodules; Organisms undergo broad-based budding (!)

Front 747

What distinguishes Mycobacterium tuberculosis from Mycobacterium avium-intracellular complex (MAC)?

Back 747

TB: pathogen, immunocompromised patients (not severely), florid granulomatous inflammation with caseation, few bacilli noted in tissue and stains;
MAC: opportunistic infection, severely immunocompromised patients, no florid granulomas/ caseation, numerous bacilli noted in tissues and stains

Front 748

How can a person acquire intestinal TB?

Back 748

Either by a disseminated form of TB or by drinking contaminated milk

Front 749

Where in the lungs does TB usually reside?

Back 749

Distal airways of upper lobes (subpleural)

Front 750

What are common opportunistic lung infections?

Back 750

Diffuse: Pneumocystis, CMV; Focal: Gram-negative rods, S. aureus, Aspergillus, Candida

Front 751

What characterizes coccidioidomycosis?

Back 751

Ubiquitous in SW US, most asymptomatic; Patient can have lung lesions, fever, cough, pleuritic pain, erythema nodosum/multiforme; Rarely a disseminated form can develop; C. immitis consists of thick-walled, non-budding spherules filled with small endospores within macrophages/giant cells; Can affect lungs, meninges, skin, bones, adrenals, lymph nodes, spleen, liver

Front 752

What geographical locations are associated with fungal infections responsible for causing chronic pneumonia?

Back 752

Histoplasma: Ohio, Mississippi, Caribbean; Blastomyces: Central/SE US;
Coccidioides: SW US, Mexico

Front 753

What characterizes histoplasmosis?

Back 753

Caused by inhalation of bird/bat droppings; Intracellular parasite of macrophages; Resembles TB (coin lesions, apex, night sweats), but mostly asymptomatic; Patient can have epithelioid granulomas, coagulative necrosis, concentric fibrosis (“tree-barking”)

Front 754

Which lung cancers are considered central/hilar?

Back 754

Squamous cell carcinoma, small cell carcinoma – they are more easily diagnosed on sputum

Front 755

How does squamous cell carcinoma appear on sputum cytology?

Back 755

Orange-pink cytoplasm with dark, pyknotic nucleus

Front 756

How does squamous cell carcinoma appear on H&E?

Back 756

Large, pink cells

Front 757

How does squamous cell carcinoma appear radiologically?

Back 757

As cavitary lesions

Front 758

What genetic changes are seen with squamous cell carcinoma?

Back 758

p53 overexpression (highest frequency); also Rb loss, p16INK4a mutation, EGFR and Her-2/Neu overexpression

Front 759

What characterizes the spread of squamous cell carcinomas?

Back 759

Spread locally, metastasize later; rapid rate of growth; may see associated pre-malignant lesion (i.e. squamous metaplasia, dysplasia)

Front 760

In what age group does lung cancer occur mostly and what is the 5-year survival rate?

Back 760

Ages 50-60; 5-year survival: 15%

Front 761

What is the classification of lung cancers?

Back 761

Non-small cell carcinomas: squamous cell carcinoma (current smokers), adenocarcinoma (past smokers), large cell carcinoma; Small cell carcinoma (non-surgical disease)

Front 762

What molecular genetics are associated with lung cancers?

Back 762

Small/non-small cell carcinoma: p53; Small cell only: c-myc, Rb; Non-small cell: ras, p16INK4a; also, EGFR, Her-2/Neu

Front 763

What industrial hazards are associated with smoking?

Back 763

Radon progeny, asbestos

Front 764

What characterizes neuroendocrine carcinomas (small cell carcinomas)?

Back 764

Strong association with smoking; Central/hilar location; Aggressive, metastasize early and often (sites of metastases frequently diagnosed before small cell carcinoma in lung);
Associated with paraneoplastic syndromes: ACTH, ADH

Front 765

What characterizes a small cell carcinoma on H&E?

Back 765

Small blue cells, round-oval, little cytoplasm, salt&pepper chromatin pattern, high mitotic grade, cells tend to mold against each other; used to be called oat cell carcinomas

Front 766

What is meant by the Azzopardi effect?

Back 766

Deposition of DNA around vessels, seen with small cell carcinoma

Front 767

What is the prognosis for small cell carcinoma?

Back 767

Untreated: 6-17 weeks; very radio-sensitive; potential cure rates 15-25% for limited disease

Front 768

What genetic changes are seen in small cell carcinoma?

Back 768

p53, Rb mutations; Bcl-2 expression

Front 769

Where do small cell carcinomas originate from?

Back 769

Argentaffin (Kulchitsky) cells in bronchial epithelium

Front 770

What characterizes adenocarcinoma?

Back 770

Incidence is increasing since more common in ex-smokers; They are peripheral in origin and slow growing; k-ras mutations are most common

Front 771

What characterizes bronchioloalveolar carcinoma?

Back 771

Subtype of adenocarcinoma; Peripheral location: multiple lesions with diffuse consolidation;
Growth along septae (mucinous spreads aerogenously vs. non-mucinous rarely aerogenously)

Front 772

How does adenocarcinoma appear on sputum culture?

Back 772

Contains ample cytoplasm and vacuoles

Front 773

How does adenocarcinoma appear on H&E?

Back 773

Glandular, spherical

Front 774

What secondary pathology is associated with lung cancers?

Back 774

Partial obstruction (marked focal emphysema), total obstruction (atelectasis), impaired airway drainage, pulmonary abscess, SVC syndrome, pericarditis/pleuritis

Front 775

What is seen in carcinoid syndrome?

Back 775

Diarrhea, flushing, cyanosis – due to the secretion of vasoactive amines

Front 776

How are carcinoids classified?

Back 776

Typical: <2 mitoses/10hpf; Atypical: 2-10 mitoses/10hpf and/or necrosis

Front 777

What are tumorlets?

Back 777

Small, inconsequential hyperplastic neuroendocrine cells

Front 778

What paraneoplastic syndromes are seen with lung cancer?

Back 778

ADH (hyponatremia), ACTH (Cushing’s), PTH (hypercalcemia), Calcitonin (hypocalcemia), Gonadotropins (gynecomastia), Serotonin/bradykinin (carcinoid syndrome)

Front 779

What characterizes the clinical presentation of lung cancers?

Back 779

Cough > Weigh loss = Chest pain > Dyspnea; may present as metastasis

Front 780

How does a patient with SVC syndrome often present?

Back 780

Swollen, edematous neck

Front 781

Why are small cell carcinomas associated with paraneoplastic syndromes?

Back 781

They contain secretory granules (seen on EM) that contain neuroendocrine hormones (e.g. ACTH)

Front 782

What characterizes large cell carcinomas?

Back 782

Undifferentiated with large, atypical cells

Front 783

Between what two structures are the palatine tonsils located?

Back 783

Anterior tonsillar pillar (palatoglossal fold) and posterior tonsillar pillar (palatopharyngeal fold)

Front 784

How do bacteria cause breakdown of the enamel/cementum?

Back 784

The bacteria metabolize sugars and in the process liberate acids that lead to decalcification

Front 785

What characterizes dental caries?

Back 785

An infectious disease that begins as chalky white decalcification of enamel/cementum, becomes more discolored (yellow, brown, black) eventually leading to brittle enamel/cementum; when the pulp becomes involved, pain and abscess develop

Front 786

What is the ligament called that goes from the tooth to the alveolar bone in which it sits?

Back 786

Periodontal ligament

Front 787

What causes a tooth abscess?

Back 787

Infection of the pulp of the tooth

Front 788

What are the layers of the tooth from the outside in?

Back 788

Enamel, dentin, cementum

Front 789

How many deciduous teeth and how many permanent teeth do humans normally have?

Back 789

Deciduous (20 total): 4 incisors, 2 canines, 4 molars (each half --> 2-1-2)
Permanent (32 total): 4 incisors, 2 canines, 4 bicuspids, 6 molars (each half --> 2-1-2-3)

Front 790

What ducts are associated with the salivary glands, and where do they drain, respectively?

Back 790

Stenson’s duct: parotid gland, drains out in the buccal mucosa opposite the 2nd maxillary molar;
Wharton’s duct: submandibular gland, drains in the floor of mouth adjacent to lingual frenulum;
The sublingual gland has multiple unnamed/invisible openings in the floor of the mouth

Front 791

What is the relationship between size of the salivary gland and malignancy of an associated tumor?

Back 791

The larger the gland (e.g. parotid) the more commonly it will have benign tumors associated with it, whereas minor salivary glands will almost always have malignant tumors associated with it

Front 792

What is the problem with sialolithiasis and sialadenitis?

Back 792

Sialolithiasis: stones in the salivary ducts leading to obstruction;
Sialadenitis: infection/inflammation of ducts due to obstruction (pain worse with eating)

Front 793

What is benign migratory glossitis (geographic tongue)?

Back 793

Areas of discoloration of the tongue that appear in different locations at different times

Front 794

What is the treatment associated with aphthous ulcers?

Back 794

Usually none required; there is no treatment that is beneficial to all patients, but silver nitrate cautery, topical steroids, pasty salves, tetracycline rinse, and other treatments have been used

Front 795

What characterizes aphthous ulcers?

Back 795

Small, painful ulcers found on unattached gingiva (alveolar mucosa); disease of unknown cause

Front 796

What is acute necrotizing ulcerative gingivostomatitis also known as and what characterizes it?

Back 796

Trench mouth – comes on rapidly and can be very painful and severe; patient gets punched-out-papilla; completely reversible if caught early (use same treatment as for gingivitis)

Front 797

What is the treatment for gingivitis and periodontitis?

Back 797

Removal of plaque and calculus; meticulous oral hygiene, surgical debridement of diseased gingiva and bone; antibiotics

Front 798

What characterizes gingivitis?

Back 798

An infectious disease of plaque that causes the gingiva to become red, swollen, friable, tender or painful; untreated it will lead to a loss of alveolar bone (i.e. periodontitis), but in its early stages is completely reversible

Front 799

What are the systemic consequences associated with periodontal disease?

Back 799

The inflammatory mediators released with periodontal disease can affect multiple organ systems and increase a patient’s risk for conditions such as heart disease, stroke, diabetes

Front 800

What is the purpose of fluoride in preventing dental caries?

Back 800

It makes enamel more resistant to decalcification

Front 801

What are Fordyce spots (granules)?

Back 801

Yellow-white spots found in the buccal mucosa; they represent ectopic sebaceous glands

Front 802

What is torus palatinus and torus mandibularis?

Back 802

Torus palatinus: bony lump (osteoma–benign excrescence of bone) in the palate (usually midline);
Torus mandibularis: osteomas found along the lingual surface of the mandible in the vicinity of the canine and bicuspid teeth (usually symmetric)

Front 803

What is major aphthous stomatitis also known as and what characterizes it?

Back 803

Sutton’s disease: large deep ulcers with sharp borders that can last for several months; patients often have several ulcers at a time; etiology is unknown but thought to be autoimmune

Front 804

In what people is oral candidiasis seen?

Back 804

Infants and people taking antibiotics or inhaled steroids

Front 805

What are some triggers associated with secondary HSV infections and what characterizes them?

Back 805

UV light, menstruation, stress, trauma – most commonly occur as a single lip lesion; lesions are sometimes announced by an initial tingling (at which time treatment should be applied); if lesions occur intraorally, they would most likely be found on keratinized mucosa (as opposed to aphthous ulcers appearing on nonkeratinized mucosa)

Front 806

What is the treatment associated with a primary HSV infection?

Back 806

Usually no treatment is needed and symptoms will resolve in 1-2 weeks (however, virus will remain dormant in trigeminal ganglion) – acyclovir, valacyclovir, and famciclovir can help reduce severity of disease (but not eradicate it)

Front 807

How does a primary HSV infection usually present?

Back 807

Most common in children/young adults; seen as multiple discrete vesicles on the mucosa of the mouth/lips/face(occasionally) which quickly rupture causing severe pain and surrounding erythema/edema; patients can have a seven day prodrome with slight fever, malaise, and cervical lymphadenopathy

Front 808

What effect do benzodiazepines have?

Back 808

Potentiation of the effects of GABA (as opposed to barbiturates, which can act without the presence of GABA)

Front 809

What are the BZ1-selective (α1) benzodiazepines (associated with sedation)?

Back 809

Zolpidem, Zaleplon, Zopiclone, Eszopiclone

Front 810

What is the α2 subunit of the GABAA receptor critical for?

Back 810

Anxiolytic effects

Front 811

What is the α1 subunit of the GABAA receptor critical for?

Back 811

Sedative effects

Front 812

What effects, besides anxiolytic, are associated with Diazepam?

Back 812

Sedative, anticonvulsant, cognitive impairing, muscle relaxant, potentiation of alcohol

Front 813

For which GABAA subunits does Diazepam have a high affinity?

Back 813

α1, 2, 3, 5 – they share a conserved histidine-101 required for Diazepam binding

Front 814

What is the difference between BZ1 and BZ2 receptors?

Back 814

Both are involved in anxiolytic effects; BZ1: associated with sleep, Zaleplon/Zolpidem exhibit selectivity; BZ2: muscle relaxation

Front 815

What brain areas are associated with anxiety?

Back 815

Amygdala: activated in fear/anxiety responses, GABA inhibits neuronal activity;
Hippocampus: storage of emotional memories;
Raphe nucleus: serotonergic cell bodies, widespread projections to forebrain

Front 816

What are the clinical uses of benzodiazepines?

Back 816

Situational anxiety, generalized anxiety disorder, panic disorder, combined treatment (for early actions)

Front 817

What are the classes of anxiolytic drugs?

Back 817

Benzodiazepines, Azapirones, Beta blockers, SSRIs, others

Front 818

What are contraindications of benzodiazepines?

Back 818

Acute alcohol intoxication, abrupt discontinuation – Cautions: pregnancy, lactation, children/elderly (increased sensitivity)

Front 819

What are beta blockers (Propranolol, Nadolol) used for regarding their anxiolytic function?

Back 819

Situational anxiety: reduced physiological symptoms of anxiety (i.e. sympathetic effects, feedback mechanism to CNS)

Front 820

What contraindications are associated with Buspirone?

Back 820

Lacks those of benzodiazepines; Contraindicated with MAOIs, CYP interactions

Front 821

What are the pharmacological effects of Buspirone?

Back 821

Decreased motor tension (not a muscle relaxant), decreased autonomic hyperactivity, decreased vigilance and scanning – Lacks may effects of benzodiazepines: not an anticonvulsant, not a muscle relaxant, does not impair psychomotor function, minimal sedation, no physical dependence

Front 822

What is the mechanism of action of Buspirone?

Back 822

Partial 5-HT1A agonist; D2 antagonist

Front 823

What is the only drug in the Azapirones class available for commercial use?

Back 823

Buspirone: used for generalized anxiety disorder; slow onset of action (3-6 weeks), not used for other anxiety disorders

Front 824

What drug interactions are seen with benzodiazepines?

Back 824

CNS depressants: synergistic CNS, cardiovascular, respiratory depression; CYP interactions

Front 825

What are the BZ2-selective (α2, 3, 5) benzodiazepines (associated with the anti-anxiety/anti-convulsant effects)?

Back 825

Alprazolam (high potency, short duration), Chlordiazepoxide (low, long),
Clonazepam (high, long), Diazepam (low, long), Lorazepam (high, short), Oxazepam (low, short)

Front 826

What adverse effects are associated with benzodiazepines used as anxiolytics?

Back 826

Sedation, impaired cognition and motor function; Cardiovascular and respiratory depression with overdose, Teratogenicity; Paradoxical CNS stimulation; Physiological dependence (especially with short half-life drugs)

Front 827

What are the pharmacological effects of benzodiazepines?

Back 827

Sedation, hypnosis, anesthesia, anticonvulsant, anxiolytic, muscle relaxant – effects are rapid

Front 828

What characterizes the use of SSRIs regarding their anxiolytic function?

Back 828

Used for most types of anxiety disorders (not for situational anxiety); slow onset of action (weeks) – Fluvoxamine is used for OCD

Front 829

What characterizes the use of antihistamines regarding their anxiolytic function?

Back 829

Cause short-term sedation – used in patients who cannot take other anxiolytics

Front 830

What characterizes Chloral Hydrate?

Back 830

Occasionally used for situational anxiety, narrow therapeutic window

Front 831

What characterizes the use of SSRIs regarding their anxiolytic function?

Back 831

Used for most types of anxiety disorders (not for situational anxiety); slow onset of action (weeks) – Fluvoxamine is used for OCD

Front 832

What characterizes the use of antihistamines regarding their anxiolytic function?

Back 832

Cause short-term sedation – used in patients who cannot take other anxiolytics

Front 833

What characterizes Chloral Hydrate?

Back 833

Occasionally used for situational anxiety, narrow therapeutic window

Front 834

What characterizes Group A Streptococci (GAS)?

Back 834

Spherical cells that grow in chains; they are non-motile and spore-forming; they have fastidious growth (complex nutrient requirements), are facultatively anaerobic, and produce a capsule

Front 835

What secreted factors are produced by GAS?

Back 835

Streptolysin O, hyaluronidase, pyrogenic exotoxins, NADase

Front 836

What are examples of other infections caused by GAS?

Back 836

Pneumonia, meningitis, sinusitis, otitis

Front 837

What diseases are caused by GAS exotoxins released into the bloodstream?

Back 837

Scarlet fever, toxic shock syndrome

Front 838

What are examples of non-suppurative GAS infections?

Back 838

Acute rheumatic fever, acute post-streptococcal glomerulonephritis

Front 839

What are examples of suppurative (pus forming) GAS infections?

Back 839

Pharyngitis, tonsillitis, impetigo, erysipelas, cellulitis, necrotizing fasciitis, myositis

Front 840

What diagnostic criteria are associated with GAS?

Back 840

Gram+ cocci, catalase-negative, β-hemolytic on blood agar; can use Rapid Antigen Detecting Tests (RADT)

Front 841

What are the classes of Streptococci based on hemolytic patterns?

Back 841

α (greenish), β (clear), γ (none, non-hemolytic)

Front 842

What is the classification for Streptococcus pyogenes?

Back 842

Group A, β-hemolytic

Front 843

What is the Lancefield classification of Streptococci based on?

Back 843

Group-specific antigens (A-U)

Front 844

What is currently used for epidemiological GAS typing?

Back 844

emm-types: sequencing of 5` end of emm gene (codes for M protein)

Front 845

What is the purpose of Hyaluronidase?

Back 845

It hydrolyzes hyaluronic acid thus helping GAS invade deeper tissues

Front 846

What is the purpose of Streptolysin O?

Back 846

It is responsible for the characteristic β-hemolysis and it is toxic to a variety of human cells

Front 847

What is the purpose of Streptolysin S, produced by GAS?

Back 847

It attacks eukaryotic cell membranes and makes pores

Front 848

How does GAS cause the breaking up of blood clots?

Back 848

It produces streptokinase (converts plasminogen to plasmin which degrades the fibrin clot)

Front 849

What anti-phagocytic proteins are made by GAS?

Back 849

M-like protein which binds plasma inhibitors and IgGs; C5a peptidase which cleaves the chemoattractant C5a (thus inhibiting the influx of PMNs to the site of infection)

Front 850

What is the purpose of Fn-binding proteins?

Back 850

They bind fibronectin and thereby enhance host colonization

Front 851

What is a purpose of lipoteichoic acid?

Back 851

It has adhesive properties to mucous membranes

Front 852

What characterizes M protein of GAS?

Back 852

Virulence factor; dimeric protein that coils around itself; carboxy-terminal inserts in GAS cell membrane, whereas the amino-terminal contains a hypervariable region (elicits antibody response); M protein has sites that bind factor H, fibrinogen, and IgG, which inhibits opsonization and phagocytosis

Front 853

What is the most important virulence factor of GAS?

Back 853

Hyaluronic acid capsule – chemically identical to connective tissue components, so it functions as camouflage; it also has antiphagocytic properties

Front 854

What is the most common cause of heart disease in children in developing countries?

Back 854

Acute rheumatic fever

Front 855

What is the therapy for strep throat?

Back 855

No licensed vaccine available; single IM injection of penicillin G, or can give penicillin V orally (all strain are susceptible) – erythromycin is used in patients with a penicillin allergy (some strains are resistant)

Front 856

What is the gold standard for strep throat diagnosis?

Back 856

Throat culture (presence of GAP colonies confirms diagnosis, but about 10% of culture-negative patients have strep throat); if the condition are severe a rapid antigen-detecting test should be performed (while waiting on blood agar test)

Front 857

What other agents can cause pharyngitis besides GAS?

Back 857

Viral, other bacterial infections, mycoplasma, chlamydia

Front 858

What epidemiology is associated with GAP pharyngitis?

Back 858

5-15yo children; occurs mostly in late winter/early spring, often in military personnel; it spreads by person-to-person contact and there are many asymptomatic carriers (15-20%)

Front 859

What causes scarlet fever?

Back 859

GAP strains that produce erythrogenic exotoxins; associated with pharyngotonsillitis; present with scarlatinal rash (starts on trunk --> extremities), and “strawberry tongue”; in severe forms, septic and toxic scarlet fever can occur (very rare)

Front 860

What characterizes GAS pharyngitis?

Back 860

Sudden onset of sore throat, fever, HA, abdominal pain, n/v; Physical findings include pharyngeal erythema/edema, enlarged tonsil with white exudate, uvulitis

Front 861

What is Streptozyme?

Back 861

An screening test that looks for GAS antibodies

Front 862

What can be caused by GAS pyrogenic exotoxins?

Back 862

They can function as superantigens thus non-specifically activating T cells, inducing a massive inflammatory response – they are the hallmark for toxic shock syndrome

Front 863

What are the three GAS pyrogenic exotoxins?

Back 863

SPE A and SPE C: phage encoded; SPE B: cysteine protease that degrades connective tissue

Front 864

What clinical signs are associated with acute glomerulonephritis?

Back 864

Glomerular lesions, edema, HTN, hematuria, proteinuria; also immune complexes of IgG and C3 deposited in the glomerular basement membrane – treated with penicillin/erythromycin

Front 865

What is the treatment of necrotizing fasciitis?

Back 865

Debridement of fasciotomy, amputation of 1-4 extremities; also penicillin/clindamycin

Front 866

What characterizes necrotizing fasciitis?

Back 866

Infection of deeper tissues/fascia with extensive and rapid spreading necrosis and gangrene; mortality can reach 70% within 2-3 days; signs include fever, severe pain, portal of entry not always obvious – diagnosis is made by surgical exploration with Gram-stain and biopsy

Front 867

What is Erysipelas?

Back 867

A form of cellulitis which often involves the face (butterfly distribution)

Front 868

What characterizes streptococcal cellulitis?

Back 868

Acute, spreading inflammation of the skin, usually as a result from infections of burns/wounds/ surgery; systemic signs include fever, chills, bacteremia – treated with penicillin or vancomycin (when staph cannot be excluded)

Front 869

What are the signs associated with streptococcus pyoderma?

Back 869

Crusty lesions (amber crust, honey-yellow crust), GAS culture, anti-strep antibodies

Front 870

What is streptococcal pyoderma also known as and what is the epidemiology?

Back 870

Impetigo: found mostly in young children in tropical climates; usually associated with poor hygiene; the GAS skin strains are genetically different from those causing pharyngitis

Front 871

What are the Jones criteria for acute rheumatic fever (ARF)?

Back 871

Major: carditis, migratory polyarthritis (most commonly), Sydenham’s chorea (unique to ARF), erythema marginatum (skin rash on trunk, unique to ARF), subcutaneous nodules;
Minor: less specific symptoms – need 2 major or 1 major/2 minor for diagnosis

Front 872

What are the three requirements for an autoimmune disease to occur?

Back 872

Significant antigen sharing; Abnormal immune response (humoral/cellular); Genetic predisposition to abnormal reaction

Front 873

Why does GAS cause autoimmune symptoms in ARF?

Back 873

Molecular mimicry (antigen sharing)

Front 874

What is the pathogenesis of C. diphtheria?

Back 874

Colonizes pharynx after inhalation --> 2-4 days later the patient will have a mild sore throat and a low grade fever --> 12-24 hours later a local lesion in the tonsil area will appear creating white exudate and fibrin network (due to local toxin) known as a pseudomembrane --> patient may develop localized edema (bull neck) --> bacteria do not invade beyond the throat lesion, but the toxin they produce disseminates systemically (heart, muscles, nerves, kidneys, liver, spleen)

Front 875

What characterizes diphtheria toxin?

Back 875

One diphtheria toxin can kill an entire cell

Front 876

How does diphtheria toxin get into the cell and what happens subsequently?

Back 876

The HB-EGF/CD9 receptor binding domain binds to the DTR and is taken up by endocytosis --> the AB-toxin is cleaved by Furin --> the vessel fuses with a lysosome which acidifies it --> this causes a deformation in the translocation fragment which forms a pore --> the A-fragment is released through this pore --> the A-fragment contains a signal sequence that translocates it to the ER where it is able to transfer ADP-ribose from NAD to EF2 causing protein synthesis to halt

Front 877

What is the receptor that the B-fragment of diphtheria toxin binds?

Back 877

Diphtheria toxin receptor (DTR): heparin-binding epidermal growth factor precursor protein/CD9

Front 878

What is the mechanism of diphtheria toxin?

Back 878

It transfers an ADP-ribose from NAD to EF2, thus inactivating EF2 --> since EF2 is an elongation factor used in protein synthesis, the cell can no longer make proteins and dies

Front 879

What are the components of the diphtheria toxin?

Back 879

AB-toxin --> A-fragment: ADP-ribosyltransferase (EF2); B-fragment: internalization domain (contains many α-helices), HB-EGF/CD9 receptor binding domain

Front 880

What is the clinical presentation associated with diphtheria?

Back 880

Sore throat/fever, severe distress, pseudomembrane, lack of immunization, travel to diphtheria endemic region, high WBC count; also, punched-out non-healing ulcers (more rare)

Front 881

What is the hallmark of diphtheria?

Back 881

Formation of a pseudomembrane in the mouth

Front 882

How does diphtheria spread?

Back 882

By droplets and direct contact

Front 883

What are the two diseases caused by Corynebacterium diphtheriae?

Back 883

Localized respiratory tract infection; Localized skin infection – both localized infections produce a systemic toxin

Front 884

What laboratory tests aid in the diagnosis of C. diphtheria infection?

Back 884

Gram stain showing Gram+ rods, aerobic, non-motile; Bacteria are club or V-shaped, resembling Chinese letters; Culture from mucosa or skin on selective tellurite medium (exclude normal flora); Non-hemolytic on blood agar; Test for diphtheria toxin via PCR/immunological/cytotoxicity

Front 885

What A-fragment is used in current immunotoxins and why?

Back 885

A pseudomonas exotoxin (PE38), since humans are not immunized against it

Front 886

What is an important function of immunotoxins?

Back 886

They can selectively localize cytotoxic drugs to tumor cells – can be made by altering the receptor binding domain of AB-toxins

Front 887

What part of the AB-toxin should be targeted with vaccines?

Back 887

The receptor binding domain (on the B-fragment)

Front 888

What is done when a toxoid vaccine made by formaldehyde treatment is ineffective?

Back 888

Recombinant toxin vaccines are used (mutant, enzymatically inactive forms of toxin)

Front 889

What therapy is ineffective with diphtheria?

Back 889

Antibiotics, innate immune response (since treatment has to be antibody-mediated)

Front 890

What is the treatment for diphtheria?

Back 890

Treat with antitoxin as soon as possible; Antibiotics (penicillin/erythromycin); Supportive (ventilation); Immunize at discharge (toxoid vaccine); Give booster/antibiotics to patient contacts

Front 891

How is release of diphtheria toxin regulated by C. diphtheria?

Back 891

Under normal circumstances, iron is bound to a diphtheria toxin repressor protein which is bound to the promoter sequence associated with diphtheria toxin --> when iron levels drop, this repressor protein will release, allowing the bacterial machinery to produce the diphtheria toxin –
the toxin is encoded on a phage

Front 892

What is the normal immunization schedule for diphtheria?

Back 892

5 doses of DTaP (diphtheria, tetanus, acellular pertussis) at 2, 4, 6, 12-15 months, and 4-6 years;
then again at age 11-16 years and subsequently every 10 years

Front 893

What does the diphtheria vaccine consist of?

Back 893

Formalin treated purified toxin (made in horses)

Front 894

What is the most important virulence factor associated with H. flu?

Back 894

Its capsule: polyribosyl ribitol phosphate (PRP) – there are 7 capsule types (PRP is type B)

Front 895

How do the non-typeable H. flu strains differ from the capsulated forms?

Back 895

They are less invasive; they induce inflammatory disease and can be opportunistic; they are associated with otitis media, conjunctivitis, sinusitis, and pneumonia

Front 896

Besides meningitis, what other complications can be seen with an H. flu infection?

Back 896

Acute epiglottitis (can result in airway obstruction/suffocation); Childhood septic arthritis, cellulitis

Front 897

What does the H. flu vaccine consist of?

Back 897

It is protein conjugated to PRP-polysaccharide (the added protein is important since children <18mo do not have a T-cell independent antigen response to the polysaccharide component only)

Front 898

What is the treatment for H. flu?

Back 898

Nafcillin, Cephalosporin (for meningitis), Tetracycline/Sulfa drugs (for non-typeable H. flu), Corticosteroids (for brain inflammation)

Front 899

What is the diagnosis of H. flu based on?

Back 899

Presumptive diagnosis is based on H&P; Established diagnosis is based on positive cultures for H. flu (should be serotyped to identify PRP capsule – type B)

Front 900

What characterizes the transmission of H. flu?

Back 900

Person-to-person contact (via secretions/aerosol); humans are the only reservoir; peak incidence if unvaccinated is 6-11 months

Front 901

What is the differential diagnosis associated with acute exacerbation of chronic bronchitis?

Back 901

Non-typeable Hemophilus influenza; Streptococcus pneumoniae/Moraxella catarrhalis (more likely to see pneumonia), viruses (adeno, influenza, parainfluenza – would not see sputum)

Front 902

What are the signs/symptoms associated with H. flu?

Back 902

Initially: runny nose, low-grade fever, HA (1-3 days); invasive organism: enters the circulation, crosses BBB, rapidly progresses to meningitis (stiff neck), convulsions, coma, death (almost 100% fatal without treatment; with treatment 5-10% mortality)

Front 903

What characterizes Hemophilus influenza?

Back 903

Blood loving: requires factors V (NAD) and X(hematin); grows on chocolate agar (lysed RBCs); grows better in CO2 enriched atmosphere; small Gram– coccobacillus, non-motile, facultative anaerobe; grows rapidly; nutritionally fastidious; does not grow on blood agar

Front 904

What complications are associated with Pertussis?

Back 904

Bronchopneumonia (linked to superinfection); Neurological damage (edema/hemorrhage due to coughing)

Front 905

How is the diagnosis of Bordetella pertussis made?

Back 905

Cough lasting > 2weeks, lymphocytosis; definitive diagnosis is made by recovery of organism from nasopharyngeal mucus (fragile organism, must be cultured on Bordet-Gengou agar); PCR

Front 906

What are the key differences between the AB-toxin of Pertussis and that of Cholera?

Back 906

The Cholera AB-toxin also have 5 B-fragments, but they are all the same (whereas Pertussis have 4 different fragments) – Cholera toxin binds to the GM1 ganglioside and causes an increase in cAMP by ribosylating Gs (prevents Gs inactivation) whereas Pertussis toxin binds to S2-5 and causes an increase in cAMP by ribosylating Gi, Gt, and Go (causes Gi inactivation)

Front 907

What kind of toxin in Pertussis toxin?

Back 907

AB5-toxin: A-fragment contains the ADP-ribosyl transferase that targets trimeric G-proteins, whereas the B fragment consists of 5 segments that bind to different receptors – it is secreted by a type IV secretion mechanism, targets macrophages and lymphocytes and is internalized by receptor-mediated endocytosis

Front 908

What other virulence factors are associated with Pertussis?

Back 908

Adenylate cyclase; Tracheal cytotoxin (leads to characteristic cough); Dermonecrotic toxin (causes tracheal tissue death); Pertussis toxin (causes cell death)

Front 909

What virulence factors are associated with Pertussis?

Back 909

Fimbriae (pili that bind to β1 integrins); Filamentous hemagglutinin (FHA – target for antibodies); Pertussis toxin (complex) – virulence factors are associated with improving the ability to colonize and destroy ciliated respiratory epithelium

Front 910

What symptoms are associated with Pertussis?

Back 910

Local symptoms: acute inflammation, hypoxia, cough; Systemic symptoms: fever, peripheral lymphocytosis

Front 911

What characterizes H. ducreyi, H. aegypticus, and H. parainfluenza?

Back 911

H. ducreyi: causes genital ulcers (chancroid), requires only factor X; H. aegypticus: pink eye;
H. parainfluenza: requires only factor V

Front 912

What characterizes the morphology of Bordetella pertussis?

Back 912

Tiny, Gram– coccobacillus; strict aerobe, nutritionally fastidious, slow growing

Front 913

What are the stages associated with Pertussis?

Back 913

Organism colonizes URT (transmitter through air-droplets, highly contagious) --> 7-10 days later, patient enters catarrhal stage (profuse URT disease that mimics the common cold) --> 7-10 days after that, patient enter the paroxysmal stage (severe, repetitive paroxysmal cough followed by a prolonged inspiratory gasp – whoop) --> 2-4 weeks later patient will recover

Front 914

What characterizes the Pertussis vaccine?

Back 914

Inactivated pertussis toxin + FHA; part of DTaP vaccine

Front 915

What is the treatment for Psittacosis?

Back 915

Tetracyclines (e.g. Doxycycline)

Front 916

How is the diagnosis of Psittacosis made?

Back 916

Clinical history (illness, pet parrot), positive chlamydial Ab titer; for a definitive diagnosis, need serological tests

Front 917

What is the disease process associated with Psittacosis?

Back 917

5-14 day incubation period --> fever, chills, HA, malaise, myalgia, respiratory infection (cough, breathing difficulty, chest tightness) – in pregnant women it can cause severe illness, respiratory failure, thrombocytopenia, hepatitis, and fetal death

Front 918

What disease does Chlamydia psittaci cause?

Back 918

Psittacosis/Parrot fever: zoonosis (mainly from companion birds via inhalation of the aerosolized organism)

Front 919

What characterizes Chlamydia psittaci?

Back 919

Obligate intracellular parasite with a Gram– outer membrane, but no peptidoglycan; it depends on host ATP synthesis (energy parasite); it exists in two forms: elementary body (infectious phage, metabolically inactive), reticulate body (intracellular, non-infectious)

Front 920

What are the key differences between H. flu and B. pertussis?

Back 920

H. flu is an invasive organism that causes meningitis/otitis media in children and pneumonia in all age group; B. pertussis is a toxigenic disease that in non-invasive and causes whooping cough

Front 921

What is the treatment of Pertussis?

Back 921

Stage 1: erythromycin; Stage 2: provide supportive care; erythromycin can also be used prophylactically

Front 922

What other diseases, besides pneumonia, can be caused by pneumococcal infections?

Back 922

Meningitis, sinusitis, otitis media, bacteremia; also, less frequently: endocarditis, septic carditis, peritonitis

Front 923

What molecules of Strep pneumo aid in its spread?

Back 923

Autolysin: lyses cells and activates complement; Pneumolysin: inhibits beating of cilia, activity of PMNs, and is pro-inflammatory…

Front 924

What molecules of Strep pneumo aid in its attachment to host cells?

Back 924

Teichoic acid, choline-binding proteins, protein A, surface adhesin A, neuraminidase, hyaluronidase

Front 925

What parts of Strep pneumo do cause activation of the immune system?

Back 925

Peptidoglycan and teichoic acid --> stimulate cytokine production --> complement activation and infiltration of PMNs

Front 926

How does Strep pneumo evade the immune system?

Back 926

Phagocytic cells lack receptors for the capsule; Capsule masks surface antigens, which prevents complement fixation and subsequent ingestion

Front 927

How is Strep pneumo diagnosed in the lab (4 criteria)?

Back 927

Catalase negative, α-hemolysis on blood agar (green discoloration – seen with many oral bacteria), susceptible to optochin, soluble in bile salts

Front 928

What characterizes Strep pneumo?

Back 928

Gram+ cocci, α-hemolytic, replicate in pairs or chains

Front 929

In what four categories can pneumonia be divided based on clinical manifestations, what are the major causative agents of each?

Back 929

Lobar pneumonia (lobe/part): Pneumococci, H. influenza, Legionella;
Bronchopneumonia (patchy): Mycoplasma pneumoniae, respiratory viruses;
Interstitial pneumonia in immunosuppressed: viral etiology (influenza, CMV);
Lung abscess (severe): polymicrobial (normal mouth flora/nosocomial: K. pneumonia, S. aureus)

Front 930

What is a common cause of the acute form of pneumonia?

Back 930

Streptococcus pneumoniae

Front 931

What are the classifications of pneumonia based on the progression of symptoms?

Back 931

Acute: community-acquired, hospital-acquired (nosocomial); Subacute/chronic: tuberculosis, fungal, lung abscess; Pneumonia in the immunocompromised host

Front 932

What are the classical symptoms associated with pneumococcal pneumonia?

Back 932

Sudden onset of chills/sweats; high-grade fever; chest pain; cough with production of mucopurulent sputum; fatigue; grayish, anxious appearance (differentiates it from a mycoplasmal or viral etiology)

Front 933

What antibiotics have very little/no resistance associated with Strep pneumo infections?

Back 933

Quinolones; Vancomycin

Front 934

What specifically has been responsible for Strep pneumo resistance to Erythromycin in the US and Europe, respectively?

Back 934

US: M-phenotype (changes in cell wall, efflux pump); Europe: ermB-gene polymorphism

Front 935

What has been responsible for penicillin resistance to Strep pneumo?

Back 935

Mutations in PBPs – cross-resistance with Cephalosporins

Front 936

What are predisposing conditions for pneumococcal pneumonia?

Back 936

Defective antibody formation: agammaglobulinemia (primary reason), lymphoma, HIV infection;
Defective complement; Insufficient/poorly functioning PMNs; Splenectomized patients; Prior respiratory infections; Multifactorial causes (aging, diabetes)

Front 937

What is the natural niche of Strep pneumo in humans?

Back 937

Nasopharynx; 5-10% of adults/20-40% of children are carriers – transmission is via direct contact

Front 938

What lab findings are associated with pneumococcal pneumonia?

Back 938

Low hemoglobin (25% of cases); Leukocytosis (although normal WBC counts are common too, and even low WBC counts are possible) – can also do Gram stain on sputum (25% positive)

Front 939

935. What is produced by all clinical strains of Strep pneumo?

Back 939

Polymerized oligosaccharide capsule – important in human antibody response

Front 940

What are the radiological findings associated with a pneumococcal pneumonia?

Back 940

Fluid accumulation seen as a non-lucent area; typically, a single lobe is involved; there is a lack of lung abscess

Front 941

What is the pathogenesis of Strep pneumo?

Back 941

Infection of alveoli --> complement activation --> exudate and WBC activation --> severe inflammation --> pneumonia

Front 942

What characterizes Legionella pneumophila?

Back 942

Gram– bacillus, fastidious, thermophilic, found in ponds (inside unicellular protozoa), acquired by inhalation following exposure to water systems (hotels/nursing homes)

Front 943

What is the most common reason for nosocomial pneumonias?

Back 943

Use of ventilators in the ICU (ventilator-associated pneumonia – VAP)

Front 944

What are the most common causes of early- and late-

Back 944

onset nosocomial pneumonia?
Early-onset (<48 hours after admission): Pneumococci, H. influenza;
Late-onset (~6 days after admission): Gram– bacilli, S. aureus

Front 945

What is the treatment of Legionaire’s disease?

Back 945

Erythromycin or Quinolones

Front 946

How does the chest x-ray of a patient with L. pneumophila infection appear?

Back 946

Initially it appears similar to that of a Mycoplasma pneumoniae infection, but there is a rapid progression to multi-lobe stage with pleural effusion

Front 947

What lab tests are useful in the diagnosis of L. pneumophila?

Back 947

DFA, DNA hybridization, ELISA; culture is most specific but takes 3-5 days

Front 948

What is the pathology of Legionella pneumophila?

Back 948

Bacteria are inhaled from contaminated water --> invade and survive in alveolar macrophages causing Legionnaire’s disease (severe pneumonia); there is no person-to-person transmission – predisposing factors include old age, smoking, immunosuppression

Front 949

What characterizes Mycoplasma pneumoniae?

Back 949

Small, fastidious, slow growing, lack of cell wall, “fried-egg appearance”, milder than acute pneumonia causing sore throat/fever/cough

Front 950

What is the treatment for a Mycoplasma pneumonia infection?

Back 950

Erythromycin, Quinolones; (not β-lactams!)

Front 951

What may be helpful in making the diagnosis of Mycoplasma pneumonia infection?

Back 951

The presence of cold hemagglutinins: cause clumping of RBCs on ice; unilateral/bilateral patchy distribution in the lower lobes

Front 952

What is the pathogenesis of nosocomial pneumonia?

Back 952

Microaspiration (most common): aspiration of secretions of upper airway colonized with Gram– bacteria and S. aureus; Marcoaspiration (less common): infection with esophageal/gastric material (associated with ventilator tubing); Hematogenous spread of bacteria (rare)

Front 953

What are the signs associated with nosocomial pneumonia?

Back 953

Fever, leukocytosis, production of purulent sputum, presence of new lobar infiltrate – diagnosed by sputum inspection, radiograph, Gram-stain, blood/sputum cultures

Front 954

Why does intubation lead to nosocomial pneumonia?

Back 954

Biofilm development on the tube paves the way for infection

Front 955

How are the M2 ion pores created by orthomyxovirus?

Back 955

By alternative splicing of the gene encoding for the M1 matrix protein

Front 956

What distinguishes between the human and the avian flu?

Back 956

Human: H1-4; Avian: H5+

Front 957

What is meant by the term antigenic shift?

Back 957

Swapping of genes between two different viruses (especially when combining a human virus and a virus from another animal)

Front 958

What causes the antigenic drift of certain viruses?

Back 958

Mistakes made by the RNA-dependent RNA polymerase leading to mutations in the virus that enable it to bypass human immune defense mechanisms in a future infection

Front 959

By what mechanism does assembly and budding of orthomyxoviruses occur?

Back 959

HA, NA, and M proteins are delivered to the host cell membrane --> the 8 strands of –RNA contact these structural proteins --> budding occurs passively (some host membrane proteins may be acquired in this process) --> neuraminidases cleave off sialic acid from the virion to prevent other viruses from clumping to it

Front 960

How are the 10 strands of +RNA created from the original 8 segments of viral –RNA?

Back 960

The –RNA travels to the nucleus along with the RNA-dependent RNA polymerases where it uses small primers from the nucleus as well as host alternative splicing machinery to create the 10 strands of +RNA needed for its replication (it also makes copies of the –RNA for new virions)

Front 961

How is influenza virus released from the endocytic vesicle in has gained entry to by the receptor mediated endocytosis?

Back 961

As the pH is pumped down in the endocytic vesicle, HA undergoes a conformational change that reveals a fusion sequences, thus allowing the content to be released into the host cell cytoplasm – the lowered pH also creates an influx in hydrogen ions through the M2 ion pore, thus breaking up the interactions between the various viral proteins

Front 962

What are the key differences between the influenza types?

Back 962

Type A: most severe, infects humans/birds/other mammals; Type B: intermediate severity, only affects humans; Type C: common cold, only affects humans

Front 963

What happens when hydrogen ions flow into the M2 ion pore?

Back 963

The interactions between hemagglutinin, matrix protein (M1), RNA-dependent RNA polymerase (PB1/PB2), and the RNA are destabilized

Front 964

What characterizes orthomyxoviruses?

Back 964

Enveloped, helical, 8 segment, –RNA, contains neuraminidase (cuts through mucus) and hemagglutinin (HA - for host cell entry), has a hydrogen ion pore in membrane (M2 ion pore)

Front 965

What is the mechanism of action of Ribavirin?

Back 965

It is a purine analog that gets incorporated into viral RNA and terminates chain elongation – it is not specific for Influenza virus

Front 966

What is the most contagious human virus known and what characterizes it?

Back 966

Measles (rubeola): typified by fever, rash, and encephalitis, as well as Koplik’s spots (small, white spots on inside of mouth, multinucleated giant cells/syncytia) – transmission is through respiratory droplets/aerosol; outbreaks are highest in winter months

Front 967

Which diseases are caused by paramyxoviruses?

Back 967

Measles, mumps, parainfluenza (croup), respiratory syncytial virus

Front 968

What are the key differences between paramyxo- and orthomyxoviruses?

Back 968

Paramyxoviruses do not have a segmented genome, have an excellent RNA-dependent RNA polymerase (no antigenic drift), can cause syncytial formation (host cell fusion – multinucleated cells), and it does not enter by the endocytic route (also, replication occurs in the cytoplasm)

Front 969

What people should not receive a killed influenza vaccine?

Back 969

People allergic to eggs; people who have had severe reactions to an influenza vaccine; children less than 6 months old; people with an acute febrile illness; children on aspirin (Reyes syndrome)

Front 970

What is the killed influenza vaccine made up of?

Back 970

Two most prevalent Type A serotypes and the most prevalent Type B serotype found in the southern hemisphere during our spring/summer months

Front 971

What steps in viral replication are blocked by Zanamivir/Oseltamivir?

Back 971

Viral movement through mucus; Viral processing after release from the host cell (causes viruses to clump together)

Front 972

Why is the avian flu harder to transmit from human to human?

Back 972

It resides lower in the lung

Front 973

Why is the drug Amantadine not used much anymore?

Back 973

It binds the M2 ion pore and slows the viral life cycle down (hopefully long enough for a vaccine to take effect) – however, it has some cardiovascular side effects that make it less desirable

Front 974

What are the clinical findings associated with the flu?

Back 974

24-48 hour incubation period followed by fever, myalgia, HA, cough; resolves in 4-7 days;
in rare cases it can lead to Reyes syndrome and Guillain-Barre syndrome

Front 975

What proteins are associated with paramyxoviruses?

Back 975

HN protein (hemagglutinin), F protein (causes fusion of the virus with the host cell),
M protein (matrix proteins that cover the single –RNA strand)

Front 976

What is the treatment for severe cases of respiratory syncytial virus?

Back 976

Aerosolized Ribavirin

Front 977

What is caused by parainfluenza and respiratory syncytial virus?

Back 977

Pneumonia and bronchitis is infants, common cold in adults; they are mostly transmitted in the spring time; Parainfluenza virus can cause upper and lower respiratory tract infection with croup (hoarse cough)

Front 978

How is mumps spread?

Back 978

Coughing, sneezing, talking

Front 979

What is affected in patients with mumps and what can this lead to?

Back 979

Virus infects the upper respiratory tract, developing a viremia --> virus moves to glandular tissue (parotids, ovaries, testes, pancreas) – can lead to deafness, meningitis, encephalitis, sterility

Front 980

What characterizes the MMR vaccine?

Back 980

It is live, attenuated vaccine, which is highly effective – immunity for measles/mumps is life-long

Front 981

How does infection with rubella present?

Back 981

Mild rash and fever

Front 982

What describes the life cycle of rhinovirus?

Back 982

Attaches to host cell --> penetrates at the membrane and replicates in the cytoplasm --> makes a single polyprotein from its +RNA which then proteolytically cleaves itself into the individual viral proteins --> emerges from the cell when it dies and ruptures

Front 983

What is the difference between enterovirus and rhinovirus?

Back 983

Enterovirus grows optimally at 37 degrees C and pH 6.0 (targets intestinal tract) whereas rhinovirus grows optimally at 33 degrees C and NOT at pH 6.0 (targets respiratory tract)

Front 984

What virus is responsible for the most common form of the common cold?

Back 984

Rhinovirus – member of the picornavirus family (ss +RNA, icosahedral capsid, no envelope)

Front 985

What replication strategy is uniquely associated with the alpha/toga/rubivirus family?

Back 985

Subgenomic message strategy: replicates from 5` end first (for RNA-dependent RNA polymerase) followed by replication from the 3` end (structural proteins)

Front 986

What describes the life cycle of rubivirus?

Back 986

Attaches to host cell --> penetrates via endosome --> replicates in cytoplasm --> assembles at the membrane --> buds and takes membrane as an envelope

Front 987

What is the biggest problem associated with rubivirus?

Back 987

If a women contracts rubella during pregnancy (especially in 1st trimester), the virus will slowly kill fetal cells, resulting in a “Down syndrome”-like syndrome (MR, heart damage), cataracts, hearing impairment, and skin manifestations known as “blueberry muffin” lesions

Front 988

What terms are used to describe German measles?

Back 988

Rubella, Rubivirus (also togavirus, and it is part of the alphaviruses)

Front 989

What characterizes rubivirus?

Back 989

Grows slowly, ss +RNA with icosahedral capsid and envelope; (does not carry its RNA-dependent RNA polymerase with it inside its capsid – rather, it is encoded in its genome)

Front 990

How is rubivirus transmitted?

Back 990

Person-to-person via aerosolizes particles

Front 991

What characterizes hantavirus?

Back 991

Part of the bunyavirus family: three circular strands of ambisense (mostly –RNA) with a helical capsid (RNA-dependent RNA polymerase included) and an envelope

Front 992

What is the treatment for adenovirus infection?

Back 992

No therapy, but there is an inactivated vaccine that is given to military recruits

Front 993

What form of the common cold is DNA based?

Back 993

Adenovirus: ds DNA with pentons

Front 994

How is hantavirus prevention accomplished?

Back 994

Eliminate rodent food sources; Prevent rodents from entering buildings; Use continuous trapping methods

Front 995

How is hantavirus transmitted?

Back 995

Via aerosolized mouse urine (some rodents are chronically infected – deer mouse/cotton rat)

Front 996

What is the lifecycle of hantavirus?

Back 996

Attaches to host cell protein --> penetrates by endocytosis --> replicates in cytoplasm --> assembles and buds into vesicles (unique feature) --> vesicles transport viruses out to infect other cells

Front 997

What disease is caused by hantavirus?

Back 997

Hemorrhagic fever with renal syndrome; Hantavirus pulmonary syndrome

Front 998

How is rhinovirus transmitted?

Back 998

Aerosol or by touching an infected surface (hand to mouth or nose) – virus infects upper respiratory tract

Front 999

What describes the diagnosis and treatment of rhinovirus?

Back 999

Diagnosis is presumptive and there is no treatment (although disinfectants and hand washing work well in prevention)