Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Exam 6 MHD/THER > MHD > Flashcards

MHD Flashcards

1
Q

What is the relationship between Calveolin and Idiopathic Pulmonary Fibrosis?

A

Epithelial activation/injury leads to the release of TGF-B1 and this goes to block Caveolin in the fibroblasts. Caveolin normally functions to block deposition of collagen and extracellular matrix. W/o Caveolin, pulmonary fibrosis has a clearer path to development.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Anthracosis

A

Deposition of coal dust in the lungs

One form of Pneumoconioses (other examples include silicosis and asbestosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the key characteristic of sarcoidosis?

A

Non-caseating granulomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are Schaumann bodies and Asteroid Bodies, and what disease process are they associated with?

A

Schaumann: Concretions (hard masses) of calcium and protein

Asteroid: Star like stellate inclusions

Both found in SARCOIDOSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What changes in FEV1 w/ a bronchodilator defines reversibility?

A

12% and 200cc’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

99% of obstructions are _________ (upper/lower) airway.

A

Lower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Equation for Diffusion Capacity

A

DLCO = [CO]inhaled - [CO]exhaled

This is the difference between the CO inhaled and the CO exhaled, which tells you how much ended up diffusing into the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

If DLCO is low, but spirometry and lung volumes are normal, what lung issue might you suspect?

A

Pulmonary HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the (3) main components to a PFT and what do they each tell you?

A
  1. Spirometry (used to ID obstruction)
  2. Long Volume Determination (used to ID restriction)
  3. Diffusion Capcity Measurement (used to ID diffusion defect)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the (4) Categories for Asthma and what values define each (based on each criteria below):

*daytime symptoms/wk, nighttime symptoms/mo, FEV1 or PEFR, PEFR variability

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

RADS

A

Reactive Airway Dysfunction Syndrome

No prior asthma, then a “big-bang” exposure (ex. 9/11) leads to asthma which normally resolves in 6 months or so.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Samter’s Triad

A

A triad of symptoms which point to aspirin sensitivity:

  1. Asthma
  2. Nasal polyposis
  3. NSAID sensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Allergic Bronchopulmonary Aspergillous

A

Asthma + Allergic response (+ skin test, IgE, eosinophils, etc.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Stages of Sarcoidosis based on CXR

A

LAD = lymphadenopathy

ILD = Interstitial lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are your (3) main differentials when a pt presents w/ a cough?

A
  1. Postnasal drip
  2. Acid reflux
  3. Asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Fleischner Guidlines

What is it used for, and what are the guidlines?

A

Used for determining course of action after nodules found on low dose CT scan.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Identify the type of lung cancers being shown in each section

A
  1. Squamous cell
  2. Adenocarcinoma
  3. Small cell carcinoma
  4. Large cell undifferentiated carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which bug is the most common cause for Community Acquired Pneumonia?

What are the clinical presentations associated with this bug (5)?

What does this bug look like?

A

Strep Pneumo

Acute onset fever, shaking chill, rusty sputum, shortness of breath, pleuritic chest pain

Lancet shaped diplococcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ALL

Name the cytogenic markers which correlate with a good prognosis.

Name the cytogenic markers which correlate with a poor prognosis.

A

Good sign:

  1. t(12;21) [TEL1-AML1]
  2. Hyperdiploidy

Poor signs:

  1. t(9;22) [BCR-ABL] - Philidelphia chromosome
  2. t(4;11) [AF4-MLL]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Name the 4 WHO classifications of AML

What are the affliated cytogenic markers and what do they indicate?

A
  1. AML w/ recurrent genetic abnormalities
    • t(15;17)PML/RARA good prognosis
    • t(11q23;v)MLL poor prognosis
  2. AML arising from Myelodysplastic Syndrome (MDS) poor prognosis
  3. Therapy Related poor prognosis
    • post chemo/radiation
  4. NOS intermediate prognosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is Myelodysplastic syndrome? What can it progress to?

A

It is also known as “preleukemia”

Hypercellular bone marrow which leads to a peripheral cytopenia and many morphological abnormalities. Often progresses to AML.

Poor prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Acute Promyelocytic Anemia

What is it a type of? What is the genetic change? What does it increase risk of? How is it treated? What is the prognosis?

A

It is one of the classifications of AML

t(15;17)PML/RARA

There is fusion between the PML/Retinoic Acid Receptor genes creating an abnormal RAR.

Greatly increased risk of DIC due to the presence of MPO based auer rods.

Great prognosis if treated with all-trans retinoic acid (ATRA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is SIRS and what qualifications must be present for something to count as SIRS? (4 total options)

A

Systemic Inflammatory Response Syndrome

Massive inflammatory reaction from systemic cytokine release

At least 2 of the following must be present:

  1. Temperature >38° C or
  2. Heart rate >90
  3. Respiratory rate >20 or PaCO2
  4. WBC >12,000 or 10% immature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the (2) key cytokines in Sepsis Syndrome?

What 3rd cytokine has a key role?

A

TNFa and IL-1

IL-6 also plays a key role

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

List the (3) components of clinical shock

A
  1. Systemic arterial Hypotension
  2. Clinical signs of hypoperfusion
    • Skin (cold, clammy, etc.)
    • Renal (oliguria)
    • Neurologic (AMS)
  3. Hyperlactemia (due to decreased muscle perfusion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What should be completed in first (3) hours of Sepsis Bundle? (4)

A

First (3) Hours:

  1. Measure lactate level
  2. Obtain blood cultures prior to administration of antibiotics
  3. Administer broad spectrum antibiotics
  4. Adminster 30 mL/kg crystalloid for hypotension or lactate > or equal to 4mmol/L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What should be completed within (6) hours of the Sepsis Bundle? (3)

A
  1. Apply vasopressor if it doesn’t respond to fluid resuscitation (to maintain MAP over 65 mmHg)
  2. Measure CVP and CV O2 sats if hypotension persists or initial lactate was high
  3. Remeasure lactate if initial lactate was elevated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

When markers/factors correlate with a better prognosis for CLL/SLL? Worse?

A

Better: Mutations of the IGH gene

Worse: Richter syndrome/transformation to a higher process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Cytochemical staining for Hairy Cell Leukemia

A

Tartrate resistant acid phosphate (TRAP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the cause for Adult T-cell Leukemia/Lymphoma? What kind of cells does it lead to and what is the prognosis?

A

HTLV-1

Usually fatal and leads to floret-like CD-4 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the key genetic change which leads to Follicular Lymphoma?

A

A t(14;18) BCL2/IGH fusion which leads to BCL2 over-amplification and an inability for apoptosis to occur as a result.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Key B cell markers?

T cell markers?

Myeloid markers?

A

B: CD19, CD20

T: CD3

Myeloid: Myeloperoxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Key genetic change in Mantle Cell Lymphoma

A

t (11;14) [Cyclin D1-IGH fusion] leading to cyclin D1 over-amplification and increased proliferation as a result.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Key translocations for Burkitt lymphoma

A

t(8;14) [MYC/IGH fusion]

Leads to MYC over-amplification and increased proliferation as a result

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the 2 distinct subtypes of Diffuse Large B-cell lymphoma? What are the potential cytogenic features associated with diffuse large B-cell lymphoma?

A

Subtypes:

  1. Germinal Center B-cell (GCB): better prognosis
  2. Activated B-cell (ABC)

Cytogenic features:

  • t(14;18)
  • BCL6
  • double hit: t(14; 18) + BCL6 (very poor prognosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the cytological change associated with CML? What does this lead to? What does the BM look like? How are the progentitors affected?

A

BCR-ABL fusion (philadelphia)

Early transformation leads to B and T cell involvement. This leads to a marked increase in neoplastic granulocytic precursors in the marrow.

Close to 100% BM cellularity

More megakaryocytes, fewer erythroid progenitors, and High basophil count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the mutation which leads to polycythemia vera?

A

JAK2 mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the mutations which lead to primary myelofibrosis (chronic idiopathic myelofibrosis)? What is the pathogenesis of this disease?

A

JAK2, CALR, and MPL point mutations

This disease is an early progression to obliterating marrow fibrosis. There are excessive collagen deposits in bone marrow due to secretion of PDGF and TGF-B by neoplastic megakaryocytes.

Normal marrow elements are displaced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the mutations which cause essential thrombocytosis? What happens and what is the treatment.

A

Activating JAK2/MPL mutations. These lead to proliferation of the megakaryocytic lineage . Treated with aspirin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Name the (3) Phases of ARDS

A
  1. Acute- early exudative phase
  2. Organizing- subacute proliferative phase
  3. Late- Fibrotic phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Acute interstitial pneumonia

A

A catch-all term for a disease which presents like ARDS w/o any known etiology (thus ruling out ARDS). All declared after everything else has been ruled out.

Average time until patient dies = 2 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What (2) diseases fall under the umbrella of COPD?

A

Emphysema and Chronic Bronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Atopic vs Non-atopic Asthma

A

Atopic: Immune-mediated. Involves IgE and mast cells. Triggered by environmental allergens. + skin test.

Non-atopic: Non-immune triggering mechanisms (Hyperirritable bronchial tree; virus induced inflammation of the respiratory mucosa, etc.). - skin test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Name (2) of the key genes involved in asthma

A
  1. Chromosome 5q (has several susceptibility genes)
  2. ADAM 33-20q
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

(3) key histological findings associated with asthma

A
  1. Curshmann spirals (mucous plugs + whirls of shed epithelium)
  2. Eosinophils
  3. Charcot-leyden Crystals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Describe the pathophyiology of Chronic Bronchitis

What is the reid index and how does it factor in?

A

Hypertrophy of mucus secreting glands (goblet cell metaplasia). Leads to inflammation and fibrosis. Could result in cor pulmonale, infections, or carcinoma.

Reid index: gland:wall ratio. It is increased in CB.

Blue Bloater

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Centriacinar emphysema

Where is it in the lung? What is the usual patient demographic? What other disease is it oft associated with?

A

C.R.U.M.

Coal workers/ Chronic Bronchitis

Respiratory Bronchioles

Upper lobes

Male Smokers

48
Q

Panacinar emphysema

What parts of the lung are affected? What genetic disorder is oft associated?

A

Lower lobes/ whole acinus

Alpha-1-antitrypsin deficiency

49
Q

Distal acinar emphysema

What part of the lung is affected? What does the tissue look like as a result?

A

Distal acinus (alveolar ducts/alveoli)

Adacent to areas of fibrosis, scarring or atelectasis. Can form huge cyst (bullae)

50
Q

Irregular emphysema

What tissues are involved and what do they look like? Describe the clinical manifestations.

A

Acini are irregularly involved and have scarring/healed inflammatory lesions.

Mostly asymptomatic

51
Q

What is the normal phenotype for the alpha 1 antitrypsin proteinase inhibitor? What is the common phenotype in deficiency?

A

Normal: PiMM

Deficiency: PiZZ

52
Q

What conditions are predisposing for Bronchiectasis? Describe the basic pathogenesis.

A

O.H.I.O.

Obstruction

Hereditary (CF, Kartagener’s syndrome, Immunodeficiency)

Infection

Other (RA, SLE, GvHD)

Pooling of nasty stuff due to impaired cleaning mechanisms, which leads to inflammation, necrosis, fibrosis and eventual dilatation with foul-smelling/purulent sputum

53
Q

What chromosome is defected in Cystic Fibrosis?

A

Chromosome 7 (CFTR gene)

54
Q

Kartagenor Syndrome

A

Malformed, non-functional cilia due to absence or shortening of dynein arms. Leads to:

  1. sinusitis
  2. bronchiectasis
  3. situs inversus
  4. infertility
55
Q

Describe the pathogenesis of Idiopathic Pulmonary Fibrosis

A
  1. Repeated cycles of epithelial activation/injury by some unidentified agent
  2. Abnormal epithelial repair
  3. Fibroblastic proliferation
  4. Release of TGF-B due to destruction also blocks Caveolin which is normally responsible for blocking collagen and extracellular matrix deposits.
56
Q

What do the lungs look like, for patients with Idiopathic Pulmonary Fibrosis?

A
  • Cobblestone lung due to irregular scarring
  • Rubbery surface
  • Can be honeycombing
57
Q

What is the name for inhaled carbon pigment? How does this lead to fibrosous?

A

Anthracosis

This and other deposited entities in pneumoconioss are eaten by macrophages, leading to the release of inflammatory mediators and subsequent fibrogenesis and collagen deposits.

58
Q

Caplan Syndrome

A

Rheumatoid Pneumoconiosis

Coal deposits (anthrocosis) + RA

Nodules may cavitate in radiology

59
Q

What is characteristic about the nodules in silicosis? How does the lung look when silicosis is advanced?

A

Nodules w/ concentric hyalinized collagen. Nodules often coalescence, leading to progresive massive fibrosis.

You get a carred, contracted upper lobe in advanced silicosis.

60
Q

What is another name for an asbestos body?

A

Ferruginous body

61
Q

Smoking adds how much of a risk of lung cancer to someone who also has asbestos exposure? How much of an increased risk of malignant mesothelioma is there for a smoker?

A

55x

62
Q

How is sarcoidosis dx?

A

Dx based on a transbronchial biopsy. It is a diagnosis of exclusion, characterized by non-caseating granulomas.

63
Q

What FEV1 percent values correlate with…

  1. Mild severity?
  2. Moderate severity?
  3. Severe severity?
A
  1. Mild: 80-60%
  2. Moderate: 60-40%
  3. Severe:
64
Q

Tram tracking and the signet ring sign are associated with which disease process?

A

Bronchiectasis

65
Q

Key tennets for COPD treatment (5)

A
  1. STOP SMOKING
  2. Medications
  3. Long-term Oxygen Therapy
  4. Cardiopulmonary Rehab
  5. Other (transplant)
66
Q

Idiopathic Pulmonary FIbrosis Rx

A
  1. Pirfenidone
  2. Nintedanib
67
Q

2 main causes for central sleep apnea

A

CNS disease or heart failure

68
Q

Mallampti Classification is based on…

A

Space between the tongue and the Uvula.

Used for determination of obstructive sleep apnea

69
Q

What are Loculations? And what do they imply?

A

One sign associated with pleural effusion.

Thick walled off lung area housing fluids. Implies adhesions and indicates infections. Antibiotics + surgery.

70
Q

What is the max fluid amount that can be removed from a P. Effusion at a time? What is this process called?

A

Thoracentesis- max of 1.5L removal

71
Q

Define the (4) Light’s Criteria for Exudates

A

TPpl/TPserum >0.5

LDHpl/LDHserum >0.6

LDHpl >200

Cholesterolpl >45

If any one of these is present, the fluid is exudate. Otherwise it is transudate.

72
Q

Empyema

A

Infection of plural space

73
Q

Pleurodesis

A

Removal of pleural space via chemical or mechanical irritiation

74
Q

1% change in body weight will give you a ___% change inthe apnea-hypopnea index (AHI)

A

3%

75
Q

In addition to hypersomnolence and hypoxia, what is another major consequence of sleep apnea?

A

Pulmonary HTN

76
Q

Lead-time bias vs Length-time bias

A

Lead: Pt knows they have cancer earlier but die at same point anyway

Length: More cancers are found and cured but that increase is due to slow growing cancers that weren’t going to kill the patient anyway

77
Q

FInding of a non-calcified nodule in the lung is a ________ (good/bad) sign

A

Bad

78
Q

USPSTF guidlines for lung cancer screening

A

annual screening for adults 55-80 w/ 30 pack-year history and who smoked in last 15 years

79
Q

Keritization and intracellular bridges are associated with which cancer type?

A

Squamous cell carcinoma

80
Q

What type of immuno-reactivity does SCC how? What kind of mutations are often present in SCC?

A
  • Shows p63/p40 immuno-reactivity
  • p53 mutations are most common.
81
Q

What criteria must be present for a dx of adenocarcinoma?

A
  1. Gland forming, or
  2. Mucin forming, or
    • TTF-1
82
Q

Describe the progression of the adenocarcinoma precursors

A

AAH [AIS/BAC] in MIA, now I have [ADC]

AAH- well demarcated; less than 5mm; cuboidal/low columnar; mild atypia

AIS/BAC- less than 3cm; preservation of alveolar architecture; no invasion

MIA- 3cm or less and invasive focus (less than 5mm); no pleura invasion, lymphatics, blood vessels

83
Q

What are the (3) activating mutations for ADC? Describe key features for each

A
  1. EGFR- always active tyrosine kinase; asian women; Erlotinib treatment
  2. ALK- younger patients; non-smokers; Crizotinib treatment
  3. KRAS- 30% caucasion; worse outcomes; no specific targeted therapy
84
Q

Inactivation of what (2) genes is present in 100% of small cell carcinoma (oat cell carcinoma)?

A

p53 inactivation

RB inactivation

85
Q

Bronchial Carcinoid

Tumor type? Invasion/Metastatis? Prognosis?

A
  • Low grade malignant neuroendocrine tumor
  • Locally invasive/ rarely metastatic
  • Good prognosis
86
Q

Chylothorax

A

Lymphatic fluid in the pleural space

87
Q

What are the key complications of lung cancer?

A

SPHERE

  • Superior vena cava syndrome
  • Pancoast tumor
  • Horner syndrome
  • Endocrine (paraneoplastic)
  • Recurrent laryngeal nerve compression
  • Effusions (pleural or pericardial)
88
Q

Kerly B-lines on X-ray are indicative of what disorder?

A

High Pressure Pulmonary Edema

89
Q

What is the gold standard of PE dx?

A

Pulmonary angiogram

90
Q

What vasodilator is given for Pulmonary HTN?

A

CCBs, and NO OTHER VASODILATORS

91
Q

What are the common bugs for CAP? What are the atypical CAP bugs?

A

Common: S. Pneumo, H. Inf., Moraxella catarhalis, Staph aureus

Atypical: Legionella, Mycoplasma, Chlamydia + viruses

92
Q

Pharyngitis usually has a ______ etiology

A

Viral

93
Q

Classic presentation for S. Pneumo

A
  1. Rusty sputum
  2. Pleuritic chest pain
  3. Fever
  4. Shaking chill
  5. SOB
94
Q

Therapy for influenza

A

-Mivir drugs

95
Q

CAP in Pediatrics

What bug is expected for a child under 2?

5-10?

10-16?

A

5-10 = mycoplasma

10-16= S. pneumo; chlamydophilia

96
Q

Therapy of CAP:

Outpatient?

Inpatient?

A

Outpatient: Macrolide/Doxycyline; Resp. fluoro if co-morbid illness/recent antibiotic

Inpatient, ICU or non-ICU: resp. Fluro (moxifloxacin); B lactam + macrolide

97
Q

Therapy of CAP + Pseudomonas

A

Anti-pseudomonal B lactam +respiratory fluoroquinolone

or

Anti-pseudomonal B lactam + macrolide + aminoglycoside

98
Q

Chronic Pneumonia Bugs

A

MEAN CAT

  1. Mycobacterium
  2. Endemic Fungi
  3. Actinomyces
  4. Nocardia
  5. Coxiella
  6. Anatomic Problem
  7. Tularemia
99
Q

CLL/SLL and transformation

A

Some patients transform to DLBL or prolymphocytic leukemia

100
Q

What kind of organisms is a patient susceptible to if they have Neutrophil dysfunction/deficiency?

A
  1. Gram negative rods
  2. Staph
  3. Aspergillus
  4. Candida
101
Q

What kind of organisms is a patient susceptible to if they have T cell dysfxn or deficiency?

A
  1. Fungi
  2. Viruses
  3. Pneumocystis
  4. Mycobacteria
  5. Listeria
102
Q

What kind of organisms is a patient susceptible to if they have B cell deficiency?

A

Encapsulated

103
Q

What characteristics of TB are not present in Nontuberculous Mycobacteria? What is the main predisposition for non-TB myco? How does it spread?

A
  • It spreads via environmental pathogens (non-cough bioaerosols; ater; soil; nosocomial)
  • Main predisposition= Structural Lung Abnormality
  • NO latent phase; NO dissemination; NO skin test/QG
104
Q

What tests are used for confirmation of TB after PPD/QG and CXR?

A
  1. Acid fast bacillus of sputum, or
  2. PCR, or
  3. Molecular tests, or
  4. Liquid media culture
105
Q

Severe sepsis vs Septic shock

A

Severe sepsis: Sepsis + Organ dysfunction*/ hypoperfusion

Septic shock: Sepsis + Refractory hypotension + hypotension abnormalities

*Organ dysfunction= H.O.L.A.

  • Hypoxemia
  • Oliguria
  • Lactic Acidosis
  • AMS
106
Q

When is hydrocortisone given for patients with sepsis?

A

Only when the hypotension is refractory

107
Q

Staining for Candidiasis

A

+ Gram stain or calcofluor

PAS

Test for germ tube presence

108
Q

Key to ID of Aspergillus fumigatus

A

ID according to color and structures

109
Q

Mucormycosis Diagnosis

A

Microscopic exam of tissues for broad, non septated hyphae

Growth is wooly white to grey

110
Q

Name the (3) genera of dermatophytes. How do you determine which is which?

A

EMT

  1. Epidermophyton
  2. Microsporum
  3. Trichophyton

To determine which is which, scrape at the leading edge and examine via KOH or Calcofluor. Can also use wood’s light. Can also id based on conidia shape.

111
Q

Where is Cryptococcus neoformans found

A

Throughout the world

112
Q

Where is blastomycosis found? What do the buds look like for this fungus?

A

Ohio river valley + great lakes + south east coast

Broad Based Buds

113
Q

Where is histoplasmosis found?

A

Ohio/mississippi river valley

114
Q

Where is Cryptococcus gotti found?

A

West coast (crips on the westside)

115
Q

Where is Coccidioidomycosis found?

A

Southwest

116
Q

What is the diagnostic method of choice for Cryptococcal infections? What are other useful techniques (4)?

A

Latex agglutination of the cryptococcal antigen is gold standard.

India pink prep, GMS, Gram stain, and mucicarmine are also very useful.

117
Q

What form does Coccidioides immitis take in the lung tissue? In culture?

A

Tissue: spherules filled with endospores

Culture: mold w/ barrel shaped anthoconidia

Exam 6 MHD/THER (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions