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3/26 - UW 25 Flashcards

1
Q

What is the posterior neck mass in Turner’s syndrome composed of? What is it called?

A

Cystic hygroma, consisting of cystic spaces separated by connective tissue rich in lymphoid aggregates

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2
Q

Infants with Turner’s syndrome usually have what two manifestations due to abnormalities in lymphatic outflow?

A

Cystic hygromas

Lymphedema in the hands and feet

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3
Q

Another word for reliable is?

A

Precise

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4
Q

On what type of cells would one find P antigen (globoside)?

A

Mostly on mature erythrocytes and erythroid progenitors

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5
Q

Why does parvovirus B19 target the bone marrow?

A

Due to the high concentration of P antigen (B19 receptor) on erythrocytes and erythroblasts

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6
Q

What is the acute, flu-like, self-limiting disease of Legionella called?

A

Pontiac fever

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7
Q

What are some common exposure sources for Legionnaire’s disease?

A

Cruise ships, spas, hospitals, hotels

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8
Q

What is suggested by patchy lung infiltrates, high fever, relative bradycardia, neuro sx, GI sx, with no organisms shown on gram stain?

A

Legionnaire’s disease

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9
Q

What type of medium does Legionella grow on?

A

BCYE

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10
Q

What is the most common lab abnormality in Legionnaire’s disease?

A

HypoNa

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11
Q

What is the first line tx for myoclonic sz?

A

Valproic acid

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12
Q

What treatment is recommended for Tourette syndrome?

A

Typical and atypical neuroleptics (Haloperidol)

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13
Q

How to differentiate between a myoclonic sz and Tourette syndrome?

A

Myoclonic: brief, symmetric contractions with loss of body tone causing fall or slumping. Precipitated by stress and sleep deprivation, esp in the morning.

Tourette: Nonrhythmic, suppressible motor tics preceded by prodromal sensation.

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14
Q

What is the first line treatment for partial sz?

A

Carbamazepine

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15
Q

Prophylactic medication given to traveler to Africa causing anemia, hematuria, and Heinz bodies is indicative of what disease?

A

G6PD deficiency unmasked by anti-malarial drugs

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16
Q

Inheritance of G6PD deficiency?

A

X linked recessive

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17
Q

What class of drugs will mask the sx of hypoglycemia?

A

Non selective beta blockers (propranolol, timolol, nadolol)

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18
Q

Vascular intimal thickening in response to injury is mediated by what process?

A

Migration of medial Smooth Muscle Cells (SMC) across internal elastic lamina and into the intima

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19
Q

What are the positive waves in a JVP?

A

A wave: atrial contraction (late diastole)
C wave: tricuspid bulging into atrium (early systole)
V wave: atrial filling (late systole, early diastole)

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20
Q

What are the negative waves in a JVP?

A

X descent: relaxation of the R atrium (mid systole)

Y descent: tricuspid opens and passive filling of R ventricle (early diastole)

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21
Q

What is a normal A-a gradient?

A

10-15 mmHg

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22
Q

What is the dequence of events in base excision repair?

A

Glycosylase, endonuclease/lyase, polymerase, ligase

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23
Q

In what cases of atherosclorotic disease would ACE-I be contraindicated?

A

Renal artery stenosis

24
Q

Mallory-Weiss tears are associated with what anatomic abnormality?

A

Hiatal hernias

25
Q

Thick rope-like cords of mycobacteria indicate presence of what factor? What is its significance?

A

Cord factor, which increases virulence by inactivating neutrophiles, damaging mitochondria, and increasing release of TNF

26
Q

What is the most common cause of death, post-MI?

A

Ventricular arrhythmia

27
Q

What antiarrhythmic do you administer for post-MI ventricular arrhythmias?

A

Lidocaine

28
Q

What is the preferred treatment for ventricular tachycardia?

A

Amiodarone

29
Q

What are the short acting benzodiazepines (<10 hours)? Pros/Cons?

A 
Pro: less daytime drowsiness
Con: more addictive
- Alprazolam
- Triazolam
- Oxazepam
"AlTO is addicting and reduces daytime drowsiness"
30
Q

What are the medium duration benzodiazepines (10-20 hrs)?

A

Estazolam
Lorazepam
Temazepam

31
Q

What are the long acting benzodiazepines (days)? Pros/cons?

A 
Pro: less addictive
Con: severe daytime drowsiness
- Chlordiazepoxide
- Clorazepate
- Diazepam
- Flurazepam
"Chloe Feels like Dying"
32
Q

What hormone level should be monitored in patients on long term Lithium therapy?

A

TSH (hypothyroidism is common)

33
Q

What are some side effects of Lithium treatment?

A

Hypothyroidism, nephropathy, nephrogenic DI, fetal cardiac malformations (Ebstein’s anomaly of the tricuspid: “atrialization of the R ventricle”)

34
Q

What pathology shows on radiography as diffuse gallbladder calcifications? Is it bad?

A

“Porcelain gallbladder”: bluish, brittle, calcified gallbladder wall.
Yes! 11-33% progress to gallbladder carcinoma

35
Q

What type of capsule does S. pneumo have?

A

Polysaccharide capsule (preventing phagocytosis)

36
Q

What toxicity is a risk from nitroprusside administration?

A

Cyanide!

37
Q

What two coumpounds is nitroprusside metabolized into?

A

CN and NO

38
Q

What to give for CN toxicity?

A

Sodium thioSULFATE (which donates sulfur to liver rhodanase, detoxifying CN to thiocyanate)

39
Q

What liver enzyme detoxifies CN?

A

Rhodanase

40
Q

What are sx of CN toxicity?

A

AMS and lactic acidosis

41
Q

What are the “fatty streaks” on the inner surface of aortas in children after age 10?

A

Intimal lipid-filled foam cells, derived from macrophages and smooth muscle cells that engulf LDL and enter the intima through the endothelium

42
Q

What is another name for epithelioid macrophages without central necrosis?

A

Noncaseating granuloma

43
Q

Which IBD is indicated by presence of noncaseating granulomas?

A

Crohn’s disease

44
Q

Cobblestone appearance of the colon with skip lesions indicate what disease?

A

Crohn’s disease

45
Q

Where do very long chain and some branched chain fatty acids get metabolized?

A

In peroxisomes (not mitochondria, like other fatty acids)

46
Q

What is a branched chain fatty acid that cannot undergo mitochondrial beta-oxidation?

A

Phytanic acid (defect in its peroxisomal alpha oxidation = Refsum disease)

47
Q

How do you treat Refsum disease?

A

Strict avoidance of chlorophyll in the diet

48
Q

Cushing syndrome in SLE patient is caused by what?

A

Iatrogenic, from exogenous glucocorticoids. This can lead to HPA suppression and bilateral adrenal atrophy

49
Q

In what pathology would you see unilateral adrenal atrophy? Bilateral?

A

Unilateral atrophy: Adrenocortical adenoma suppressing contralateral adrenal

Bilateral atrophy: Exogenous or extra-adrenal glucocorticoids

50
Q

What liver pathology would be seen on acetaminophen toxicity?

A

Centrilobular hepatic necrosis and liver failure (treat with NAC)

51
Q

When would you see HIGH Leukocyte Alkaline Phosphatase?

A

Polycythemia vera
Essential thrombocytosis
Primary myelofibrosis
Leukomoid reaction

52
Q

When would you see LOW Leukocyte Alkaline Phosphatase?

A

CML, AML, paroxysysmal nocturnal hemoglobinuria

53
Q

What differentiates CML from Leukemoid reaction?

A

Leukocyte (neutrophil) alkaline phosphatase:
CML: Low
LR: High

Similarities: Leukocytosis, few blasts

54
Q

What differentiates AML from CML?

A

AML has increased blasts (>20% of total nucleated cells)

Both have low neutrophil alk phos

55
Q

What is CREST syndrome?

A 
Calcinosis
Raynaud
Esophageal dysmotility
Sclerodactyly
Telangiectasias

Syndrome of systemic sclerosis

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