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Internal Med > firecrack feb 1 > Flashcards

firecrack feb 1 Flashcards

1
Q

goal FiO2

A

less than 60% (need to minimze oxygen radicals)

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2
Q

tidal volume =

A

8-10ml/kg of ideal body wt

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3
Q

how to change patient’s arterial pco2

A

by modifying TV or RR

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4
Q

high resp rates use to

A

blow off excess pco2

ex severe metabolic acidosis

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5
Q

low resp rates use to

A

increase pco2

resp alkalosis

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6
Q

how to change pts arterial po2

A

modify fio2 or peep

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7
Q

most common complication of mechanical ventilation

A

barotrauma

risk increase with PEEP

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8
Q

PEEP

A

alveolar pressure above atomspheric pressure found in lung at end of expiration
keeps alveoli from collpasing on expiration

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9
Q

complications of peep

A

increased intracranial pressure
inrecased risk of barotrauma
hypotension from diminished venous return

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10
Q

classic presentation of pheo

A

htn, tachycardia

diaphoresis, headaches, palpitations

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11
Q

long standing undiganosed pheo causes

A

catecholamine cardiomyopathy

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12
Q

radiology for pheo

A

CT scans - adrenal adenoma

MIBG scans, pheo not on adrenal gland

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13
Q

pheo crisis

A

adrenergic hypertensive crisis leads to multiple system organ faliure

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14
Q

conditions that can induce pheo crisis

A

anesthesia induction agents
emotional stress
iv urographic contrast
drugs

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15
Q

pheo treatment - first choice

A

surgical resection

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16
Q

pheo medical management

A

alpha blocker: phenoxybenzamine

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17
Q

CML mutation

A

constiutively active tyrosine kinase
t9:22
bcr-ab1

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18
Q

median age of onset for CML

A

50

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19
Q

CML presents with

A

nonspecific - fatigue, fever, wt loss
early satiety (enlarged spleen)
LUQ pain - spleen infarction or spleenomegaly

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20
Q

CML & LAP

A

low leukocyte alkaline phosphatase

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21
Q

CML DOC

A

tyrosine kinase inhibitors - imatinib

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22
Q

CML with blast crisis

A

need hematopoietic stem cell transplant

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23
Q

CML can conver to

A

ALL or AML in a blast crisis
myeloid/lymphoid blasts proliferate
usually fatal

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24
Q

How is genetic sideroblastic anemia treated?

A

iron levels managed by transfusions, chelation, phlebotomy

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25
Q

What metabolic defect causes sideroblastic anemia?

A

defective heme synthesis
iron can’t combine with heme
unused iron accumulates in mitochondria and around nucleus

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26
Q

hat is a potential long-term complication of acquired, irreversible sideroblastic anemia?

A

myelodysplastic syndrome

acute leukemia

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27
Q

What vitamin can treat sideroblastic anemia?

A

vit b6 (pyridoxine)

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28
Q

What stain is used to diagnose sideroblastic anemia?

A

Prussian Blue of bone marrow

basophilic inclusions

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29
Q

what is a ringed sideroblast?

A

unused iron encircling nucleus

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30
Q

How is molluscum contagiosum diagnosed?

A

clinical

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31
Q

What histological findings are associated with molluscum contagiosum?

A

giemsa or wright stains - inclusion bodies

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32
Q

What treatment options are available for patients with molluscum contagiosum?

A

cryotherapy
curettage
cantharidin
topical trichloroacetic acid

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33
Q

What are five reversible causes of sideroblastic anemia?

A 
lead, zinc, alcohol tox
copper def
isonizaid
chloramphenicol
hypothermia
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34
Q

diagnosis of CMV infection

A

urinarylsis
culture buffy coat WBC
PCR or serology

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35
Q

What effect can CMV infection have on the adrenal glands?

A

addison’s dz (primary adrenal insuff)

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36
Q

What is the classic description of microscopy findings in CMV infection?

A

large intranuclear basophilic inclusion surrounded by a halo and small intracytoplasmic basophilic inclusion

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37
Q

What are the most significant adverse effects of ganciclovir?

A

hematologic - neutropenia, etc

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38
Q

What are the signs/symptoms of congenital CMV?

A 
microcephaly
MR
Deafness
Intracranial Califications
Seizures
(MRDICS)
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39
Q

What s/sx of CMV may be present at birth, but resolve within the first few weeks of life?

A

thrombocytopenia purpura - blueberry muffin rash (also in rubella)
HSM, jaundice

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40
Q

What medication is used to treat ganciclovir-resistant CMV?

A

foscarnet

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41
Q

Why is congenital CMV important?

A
  • # 1 congenital infection in the developed world
  • # 1 viral cause of mental retardation in the U.S.
  • # 1 cause of sensorineural hearing loss
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42
Q

How does CMV infection manifest in immunocompetent vs immunocompromised hosts?

A

asymptomatic, mono vs

GI,pulm,renal,adrenal dz

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43
Q

What are the GI sequelae of CMV infection?

A

esophagitis (AIDs, painful swallowing)
hepatitis (granulmatous0
colitis

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44
Q

What infection does CMV cause in the lung?

A

interstitial/atypical pneumonia

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45
Q

How does CMV affect the kidneys?

A

progressive renal failure

will see intranuclear inclusions

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46
Q

Why does presence of HbS result in vaso-occlusive phenomena?

A

HbS - poorly soluble when deoxygenated

polymerize within RBCs, impaired RBC deformability - vaso occlusions

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47
Q

Sickle Cell Disease Lab Findings

A

elevated reticulocyte index 3-15%
indirect hyperbilirubenimia
elevated LDH, decrease haptoglobin
sickle cells, polychormasis, howell-jolly bodies

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48
Q

Why do children with sickle cell disease experience delayed growth and development?

A

primary hypogonadism, hypopituitarism, hypothalamic insuff

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49
Q

sickle cell bacteremia

A

s pneumo

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50
Q

sickle cell meningitis

A

s pneumo

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51
Q

sickle cell pneumonia

A

mycoplasma, chlamydia, legionella

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52
Q

What screening test regimens should sickle cell patients begin?

A

Transcranial Doppler ultrasound for evaluation of cerebral blood flow, starting at age 2 and repeated every 1-2 years until age 16
Retinal evaluation should start at age 10 and repeated routinely

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53
Q

How is sickle cell disease diagnosed in the prenatal period? How is it diagnosed after birth?

A

prenatal: dna pcr testing
newborn: electrophoresis (HbF, HbS but no HbA)

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54
Q

What antimicrobial prophylaxis is recommended for sickle cell patients?

A

vaccianations: s pneumo/h flu/mengitis
hep b
3 months - 5 years: penicillin or erythromycin

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55
Q

What medication & supplements can be provided for patients with symptomatic sickle cell disease?

A

hydroxyurea

folic acid supplementation

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56
Q

What are 6 common neurological complications of sickle cell disease?

A 
TIA, ischemic stroke
intracerebral hemorrhage
vestibular dysfxn
sensory hearing loss
retinopathy
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57
Q

What are 3 common skeletal complications of sickle cell disease?

A

osteonecrosis
pancytopenia
osteoporosis

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58
Q

What cardiac complication are sickle cell patients at risk for?

A

increased cardiac output to compensate for anemia

MI

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59
Q

What type of gallstones are typically seen in patients with sickle cell disease?

A

pigmented

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60
Q

acute chest syndrome

A

appearance of new infiltrate on CXR along with pulm symptoms

can be due to infarction or infection

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61
Q

What are the most common causes of malignant solitary pulmonary nodules?

A

primary lung cancer
metastasis
carcinoid tumor

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62
Q

Following an episode of pharyngitis, a 7-year-old child develops periorbital edema and hematuria. Explain the pathophysiology of this patient’s condition.

A

type III hypersensitivity

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63
Q

Infections of what organ systems can result in PSGN (post streptococcal glomerulonephritis)?

A

skin or URI

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64
Q

What is the confirmatory test for PSGN?

A

kidney biopsy

igg and c3 positive bumpy deposits on renal basement membrane

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65
Q

What are symptoms of PSGN (post streptococcal glomerulonephritis) aside from the classic triad?

A

brown urine, renal failure

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66
Q

What lab findings are common in PSGN (post streptococcal glomerulonephritis) other than hematuria and proteinuria

A

aso titer
increase bun,cr
postivie anti-dnase b titer

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67
Q

What is the classical clinical presentation of post-strep glomerulonephritis?

A

edema, esp periorbital
hematuria
hypertension

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68
Q

What levels of hematuria and proteinuria are found in PSGN (post streptococcal glomerulonephritis)?

A

4+ blood on urine dipstick

<3.5g protein/day

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69
Q

treatment for psgn

A

self limited

only for complications (diuretics, acei)

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70
Q

What is the most common anatomic location for a carcinoid tumor?

A

appendix
bronchopulm tree
ileum
rectum

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71
Q

In addition to octreotide, what therapies are indicated for the treatment of metastatic carcinoid disease?

A

IFN-alpha

chemoembolization of hepatic artery

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72
Q

What is a carcinoid tumor?

A

neuroendocrine origin

derived from primitive stem cells in gut wall

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73
Q

What are some potential complications of a carcinoid tumor?

A

carcinoid syndrome and carcinoid crisis
bowel obstruction
carcinoid heart disease
metastasis, recurrence

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74
Q

Describe the constellation of symptoms seen in a patient with carcinoid syndrome.

A

flushing
diarrhea
bronchoonstriction
tricuspid/pulm valvular dz

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75
Q

What is the best screening method for carcinoid tumor?

A

urine 5 HIAA

serum serotonin

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76
Q

What parameters are associated with a poor prognosis in a patient with a carcinoid tumor?

A

mets
tumors greater than 2 cm in size
positive lymph nodes

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77
Q

What substance secreted by carcinoid tumors is responsible for the symptoms seen in carcinoid syndrome?

A

serotonin

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78
Q

Carcinoid tumors are most likely to be found in what patient population?

A

adults

rare in kids

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79
Q

Under what conditions can a carcinoid tumor cause carcinoid syndrome?

A

GI tumor metastasizes to liver
or
primary tumor outside of GI system

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80
Q

In a patient with carcinoid syndrome, what abnormalities may be present on cardiopulmonary exam?

A

wheezing

rs heart murmur

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81
Q

What is the standard treatment for a localized carcinoid tumor?

A

resection

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82
Q

What pharmacologic agent may be administered for symptomatic relief in a patient with carcinoid syndrome?

A

octreotide

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83
Q

kidney biopsy for iga nephropathy

A

increased prolif of mesangial cells

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84
Q

iga nephropathy classic presentation

A

hematuria
flank pain
low grade fever

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85
Q

What is the basic pathophysiology of IgA nephropathy?

A

igA immune complexes deposit in mesangial cells of kidneys, cause damage to glomeruli

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86
Q

diseases iga nephropathy is associated with

A

HSP
cirrhosis
celiac disease
inflamm disorders - sarcoidosis, IBD

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87
Q

What is the most common cause of glomerular hematuria world-wide?

A

iga nephropathy

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88
Q

What will the urine dipstick show for IgA nephropathy?

A

pos for blood and protein

RBC and RBC casts can be present

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89
Q

What is seen on light microscopy in IgA nephropathy?

A

normal-appearing glomeruli or mesangial widening due to mesangial proliferation

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90
Q

What are the medical treatment options for IgA nephropathy?

A

acei/arb with statins

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91
Q

When are steroids indicated for treating IgA nephropathy?

A

nephrotic range proteinuria

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92
Q

What are some features that distinguish IgA nephropathy from Post-Streptococcal Glomerulonephritis?

A

iga within one week of URI, psgn several weeks latera
normal complement in iga nephropathy
positive throat culture in PSGN

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93
Q

cell that accumulates in CLL

A

functionally incompetent, but mature appearing lymphocytes

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94
Q

Rai staging system

A

stage 0 - lymphocytosis
I, II, LAD, organomegaly
III, IV: anemia, thrombocytopenia

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95
Q

median survival for CLL pts

A

10 years

very variable

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96
Q

scabies

A

mite sarcoptes scabiei

pruritic lesions

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97
Q

populations affected by CLL

A

caucasions, male, elderly (70)

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98
Q

next step in treatment of localized CLL

A

radiation

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99
Q

two staging systems for CLL

A

Rai and Binet

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100
Q

most common PE findings for CLL

A

LAD, HSM

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101
Q

CLL complications

A

infection, anemia, thrombocytopenia

tumor lysis syndrome

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102
Q

Binet staging system

A

a: fewer than 3 LN
b: 3 or more LN
c: anemia or thrombocytopenia

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103
Q

CLL pts that should receive chemo

A

advanced, symptomatic

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104
Q

scabies presents with

A

itching

worse at night and after a hot bath

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105
Q

presenting symptoms of CLL

A

asympatomtic

b symptoms

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106
Q

leukemia cutis

A

plum-colored purpur

manifestaton of leukemia

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107
Q

scabies treatment

A

topical permethrin cream or oral ivermectin

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108
Q

graves dz highest risk

A

women, age 20-40

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109
Q

RA spares

A

DIP joints

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110
Q

Graves disease cellular infiltrate

A

lymphocytic infiltrate, germinal centers

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111
Q

RA first line DMARDS

A

MTX
sulfasalazine
hydroxychloroquine
leflunomide

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112
Q

NSAIDS/glucticorticoids in RA

A

adjuntive antiinflamm agents

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113
Q

RA clinical diagnosis, next step

A

x ray imaging:
joint erosion
joint space narrowing
subluxation

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114
Q

drugs for prinzmetals

A

dihydropyridine CCB

amlodipine, nifedipine

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115
Q

joint space aspiration in RA

A

decreased complement

increased leukocyte count

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116
Q

RA lab findings

A

increase ESR, CRP
+ RF
+ ANA
Anti=CCP

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117
Q

prinzmetal complication that occurs with coronary relaxation

A

severe life threatening arrhythmias (v fib, vtach, etc)

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118
Q

prinzmetal contraindicated drug

A

aspirin

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119
Q

RA - systemic manifestations

A 
pericarditis
scleritis
felty's syndrome
still's disease
sjogren's syndrome
120
Q

management of hyperthyroidism during pregnancy

A

PTU in first trimester
methimazole after that
meth - teratogenic, PTU - liver injury

121
Q

gold standard test for prinzmetal’s angina

A

coronary angiography with provocative test for vasospasm (acetylcholine infusion directly into the vessel)

122
Q

RA - classic hand deformitites

A

ulnar deviation
swan-neck deform, boutonnier deform
z-thumb
mcp joint hypertrophy

123
Q

graves dz antibodies

A

TSH receptor

can have anti-TPO and anti-thyroglobulin

124
Q

RA - joints affected first

A

hands and feet

125
Q

rheumatoid factor is..

A

IgM against the constant region of patient’s own IgG antibodies

126
Q

diverticulitis complications

A

obstruction
perforation
abscess formation

127
Q

diverticulitis symptoms

A

LLQ or diffuse abd pain
fever
leukocytosis

128
Q

diverticulitis with abscess greater than 4cm

A

CT guided percutaneous drainage

fecal materal or perforation –> surgery

129
Q

diverticulitis imaging

A

CT with oral and IV contrast

130
Q

treatment of diverticulitis

A

NPO
BS atb
IV fluids
pain control

131
Q

exposure to lead in children, adults

A

lead paint in kids

occupational in adults

132
Q

bone lead level indicative of

A

total lifetime lead exposure

133
Q

lead poisoning treatment

A

dimercaprol, EDTA, succimer

134
Q

use of x-ray in children with lead poisoning

A

looking for foreign body containing lead

dense metaphyses

135
Q

hemochromatosis - HLA ?

A

HLA-A3

136
Q

hemochromatosis when i s surgery indicated

A 
end stage liver dz (transplant)
severe arthropathy (arthroplasty)
137
Q

presentation of acute lead poisoning

A

abdominal and neurological symptoms

138
Q

secondary hemochromatosis

A

ineffective erythropoiesis (thalassemia, sideroblastic anemia)
multiple transfusions
chronic liver disease

139
Q

lead toxicity pts peripheral smear

A

basophilic stippling

microcytic, sideroblastic, hypochromic anemia

140
Q

triad of adult onset hemochromatosis

A

micronodular cirrhosis
diabetes mellitus
bronze skin pigmentation

141
Q

hemochromatosis other symptoms

A

arthropathy/chondrocalcinosis
dilated cm
amenorrhea, impotence, hypogonadism

142
Q

lead toxicity effects on fetus

A

miscarriages, stillbirths, low birth wt

143
Q

HFE

A

chromosome 6

AR

144
Q

liver biopsy in hemochromatosis

A

high iron content seen with prussian blue staining

145
Q

most accurate test for lead toxicity

A

blood lead level

146
Q

hemochromatosis treatment

A

phlebotomy

deferoxamine

147
Q

chronic lead exposure symptoms

A

nonspecific GI
behavorial
peripheral neuropathies

148
Q

lead-induced peripheral neuropathy

A

wrist or foot drop in adults

hand-eye coordination in children

149
Q

hemochromatosis labs

A

serum iron increased
transferrin sat increase
increased ferritin
decreased TIBC

150
Q

screening text for hemochromatosis

A

transferrin sat

151
Q

lead poisoning anemia - age group

A

children

under 6, BBB not fully formed

152
Q

areas of intrinsic weakness inside colon –

A

vasa recta enters muscularis externa

153
Q

treatment of trichinella

A

self limiting

severe -bendazoles

154
Q

how do humans acuqire trichinellosis

A

undercooked infected meat

155
Q

antibiotic for cellulitis

A

clindamycin, linezolid

156
Q

acne vulgaris is inflamm of

A

hair follicules, sebaceous glands

157
Q

common preseentation of trichinellosis

A

muscle pain, tenderness, swelling, weakness

158
Q

cutaneous structures affected by cellulitis

A

deeper dermis

subc fat

159
Q

acne complications

A

permanent scarring

vit a - birth defects, hepatotoxicity

160
Q

where does trichinella encyst

A

brain
heart
skeletal muscle

161
Q

antibiotic for cellulitis, febrile pts

A

IV ceftriaxone or cefazolin

162
Q

trichinella diagnosis

A

clinical, confirm with serology

163
Q

severe acne treatment

A

oral isotretinoin

164
Q

trichinella neuro symptom

A

ha worse with movement

165
Q

erysipelas affects what cutaneous structures

A

upper dermis

superficial lymphatics

166
Q

trichenella - cardiac

A

eosinophilic myocarditis

167
Q

erysipelas specific symptoms

A

acute onset

systemic - fever and chills

168
Q

cellulitis with systemic toxicity, suspect

A

necrotizing fasciitis
toxic shock syndrome
gas gangrene

169
Q

AML - pt population

A

elderly (65), female

170
Q

AML complications

A

anemia infection, bleeding
leukostasis, metabolic abn, CNS involvement
neutropenic enterocolitis
DIC

171
Q

pathophysiology of AML

A

failure of bone marrow stem cells to mature
suppression of all cell lines
rapid prolif of immature myeloid cells

172
Q

cholangiocarcinoma age group

A

elderly

173
Q

AML presenting symptoms

A

pancytopenia

infections, fatigue, pallor, bone pain, bleeding

174
Q

AML bone marrow biopsy

A

greater than 20% blasts

175
Q

symptoms of cholangiocarcinoma

A

jaundice, pruritis, wt loss

176
Q

cholangiocarcinoma =

A

cancer of bile ducts

adenocarcinoma

177
Q

AML lab tests

A

myeloperoxidase
auer rods
myeloid markers

178
Q

risk factor for cholangiocarcinoma

A

PSC

179
Q

auer rods - what subtype

A

M1, M3

180
Q

cholangiocarcinoma most common location

A

proximal common bile duct

181
Q

aeur rods =

A

AML
myeloblasts
peroxidase positive

182
Q

AML treatment

A

chemotherapy

183
Q

treatmetn for M3 subtype of AML or APL

A

all trans retinoic acid (vit A)

184
Q

AML supportive therapy

A

platelet, RBC transfusions
antibiotics
uric acid lowering agents

185
Q

AML genetics

A

t 15 17 translocation

186
Q

ITP associated with what conditions

A

HIV
Hep C
SLE
CLL

187
Q

ITP =

A

acquire thrombocytopenia mediated by antibodies

188
Q

ITP diagnosed by

A

exclusion

189
Q

ITP: when to transfuse platelets

A

severe bleeding (GI or intracranial)

190
Q

ITP treatment guided by

A

platelet counts

presence of bleeding

191
Q

mild ITP vs severe ITP

A

mild - clinically silent/mild drop in platelets

severe - bleeding

192
Q

ITP First line treatment

A

corticosteroids and/or IVIG

193
Q

ITP level above to not treat

A

30,000

194
Q

ITP second line treatment

A

splenectomy

rituximab

195
Q

polymyalgia rheumatica common in what populations

A

elderly
women
african americans

196
Q

what is polymyalgia rheumatica

A

autoimmune dz with several sites of muscle and joint pain

associated with temporal arteritis

197
Q

5 PE findings in polymyalgia rheumatica

A
  • fatigue
  • edema of extremities
  • tenderness to palpitation
  • movement limited by pain
  • normal muscle strength
198
Q

polymyalgia rheumatica MRI

A

increased signal at tendon sheaths and tissue outside of joints

199
Q

polymyalgia rheumatica lab findings

A

decreased hct

increased ESR

200
Q

clinical presentation of polymyalgia rheumatica

A

morning muscle stiffness

pain in neck, shoulders, hips

201
Q

treatment for polymyalgia rheumatica

A

low dose corticosteroids

202
Q

alport’s underlying defect

A

type IV collagen

203
Q

alport’s triad

A

hematuria
sensorineural hearing loss
ocural abnormalities

204
Q

alports urinalysis

A

hematuria, proteinuria,
RBC casts
pyuria

205
Q

alports treatment

A

ACEI/ARBs

206
Q

alports electron microscopy

A

basketweave apperance

thickeninning/thinning of GBM

207
Q

alports mode of inheritance

A

x-linked

208
Q

who is most commonly affected by polymyositis and dermatomyositis?

A

poly - adults
derm - children
women

209
Q

Raynaud + myositisi

A

1/3 will develop it

210
Q

myosititis immune cells

A

poly - CD8 T cells

derm - B and T cells

211
Q

how do polymyositis and dermatomyositis present?

A

symmetrical proximal limb and neck weakness over 3 to 6 months

212
Q

life threatening complications associated with myositis

A

resp failure
myoglobinuric renal failure
cardiomyopathy

213
Q

myositis - HLA subtypes

A

BA
DR3
DRW52

214
Q

non-pharmacologic treatment may be required if there is severe inflammation associated with polymyositis and dermatomyositis?

A

bed rest with PT to prevent contractures

215
Q

What are the first line treatments for polymyositis and dermatomyositis?

A

oral glucocorticoids

topical steroids for derm

216
Q

What is the age distribution of patients commonly affected by polymyositis and dermatomyositis?

A

bimodal
10-15
45-60

217
Q

What is the second line therapy for polymyositis and dermatomyositis?

A

MTX,aza, other immunosuppressants

218
Q

In addition to symmetrical proximal limb weakness, what symptoms are associated with polymyositis and dermatomyositis?

A

myalgia
dysphagia/arthralgia
raynaud

219
Q

What limitations associated with polymyositis and dermatomyositis may cause patients to first visit a physicians office?

A

trouble combing hair or climbing stairs

220
Q

How are polymyositis and dermatomysitis diagnosed?

A
  • symmetric proximal muscle weakness
  • elevated skeletal muscle enzymes
  • myopathic changes on EMG
  • inflamm on muscle biopsy
221
Q

Gottron sign

A

lacy purple rash around MCP or PIP joints

222
Q

pathophysiology of polycythemia vera

A

JAK 2 mutation

stimulation of EPO receptor

223
Q

polycythemia vera imaging

A

look for tumor that produce EPO (pheo, RCC, hemangioblastoma, HCC)

224
Q

what is polycythemia vera

A

myeloproliferative disorder
increased RBC volume
hyperviscosity syndrome

225
Q

What are some complications of polycythemia vera NOT related to hyperviscosity syndrome?

A

post-PV myelofibrosis

AML

226
Q

What lab findings are required to make the diagnosis of polycythemia vera?

A

elevated hgb, hct

jak2 mutation

227
Q

What are some complications of polycythemia vera related to hyperviscosity syndrome?

A

MI
ischemic stroke
budd-chiarir syndrome

228
Q

What is the life expectancy of treated & untreated polycythemia vera patients?

A

10 or more years vs 6-18 months

229
Q

What are the 5 aspects of medical treatment of polycythemia vera?

A 
phlebotomy
myelosuppresive agents - hydroxyurea
aspirin
antihistaminies
uric acid lowering agents
230
Q

What are the 5 chief presenting symptoms of polycythemia vera?

A 
aquagenic pururitis
burning pain in hands & feet
fatigue
easy bleeding and bruising
headache
231
Q

most common causes of death in polycythemia vera?

A

thrombosis
hematologic malginancies
hemorrhage
post pv-myelofibrosis

232
Q

polycytehmia vera oxygen sat

A

> 92%

otherwise hypoxia-induced erythrocytosis

233
Q

EPO in polycythemia vera

A

should eb low (negative feedback)

234
Q

polycythemia vera bone marrow biopsy

A

generalized hypercellularity

235
Q

polycythemia vera PE

A

HSM

236
Q

TdT & CD10

A

ALL

237
Q

ALL symptoms

A

nonspecific

238
Q

ALL treatment

A

chemotherapy

prophylatic intrathecal chemo with MTX

239
Q

T cell ALL symptoms

A

SOB due to mediastinal mass

240
Q

effect of ALL on other cell lines

A

decreases other cell lines

thrombocytopenia, anemia, neutropenia

241
Q

ALL peripheral smear

A

lymphoblasts

242
Q

ALL prognosis

A

cured in children

worse in adults

243
Q

ALL cell of origin

A

immature lymphoblasts

B cells > T cells

244
Q

ALL population

A

children age 2-5

boys, caucasians

245
Q

aplastic anemia - 2 broad mechanisms

A

injury to pluripotent stem cells

hereditary

246
Q

aplastic anemia =

A

diminshed or abscent hematopoietic precursors in bone marrow

247
Q

aplastic anemia drugs/toxins

A

radiation
anti-epilpetics
nsaids
sulfonamides

248
Q

aplastic anemia symptoms

A

anemia – fatigue
leukopenia - recurrent infections
thrombocytopneia - mucosal hemorrhage

249
Q

aplastic anemia caused by what viruses

A

parvovirus b19
hepatitis
HIV

250
Q

aplastic anemia hereditary cause

A

fanconi anemia (impaired dna repair mechanisms)

251
Q

aplastic anemia bone marrow biopsy

A

hypocellulairty
no fibrotic infiltration or malignant cells
morphologically normal

252
Q

aplastic anemia treatment

A

removal of offending agent
supportive care
transplant or immunosuppressive thearpy

253
Q

hodgkin lymphoma cell type

A

B cell

254
Q

hodgkin lymphoma histo findings

A

Reed-Sternberg cells in inflamm background

255
Q

4 types of hodgkin lymphoma

A

lymphocytic predom
nodular sclerosis
mixed cellularity
lymphocyte depleted

256
Q

hodgkin lymphoma pt risk factors

A

age 20 & 65
EBV virus
family hx

257
Q

stages I-IV of hodgkin lymphoma

A

1 - single LN or site
2 - 2 or more LN, site on same side of diaphargm
3 - both sides of diaphragm
4 - outside of LN

258
Q

Reed-sternberg cells

A

CD 15 and CD 30

259
Q

presenting symptoms of hodgkin lymphoma

A

cervical LAD

nonspecific b symptoms

260
Q

early vs late hodgkin lymphoma

A

early - cure (chemo + rad)

late - prognosis by IPS (chemo only)

261
Q

hodgkin lymphoma treatment

A

early - chemo and rad

late - chemo only

262
Q

cause of vit D def

A 
poor intake
increased loss
impared 25-hydrox
impaired 1-alpha hydroxy
target organ resistance
263
Q

treatment of osteomalacia due to poor diet

A

50,000 IU weekly for 3-12 weeks

800IU daily

264
Q

osteomalacia and rickets

A

impaired calcification of newly formed bone matrix

265
Q

treatment of osteomalacia due to increased metabolism or impaired hydroxylation

A

50,000 IU weekly

266
Q

impaired 25-hydroxylation due to

A

liver disease

isoniazid

267
Q

treatment for osteomalacia due to imapired 1alpha hydroxylation

A

give active form (1,25)oh2 vit d

268
Q

What causes of vitamin D deficiency are associated with impaired 1alpha-hydroxylation?

A

renal osteodystrophy

hypoparathyroidism

269
Q

What changes to bone structure occur in rickets?

A

changes in growth plate (hypertrophic cartilage) and bone bowing/bone cortical thinning

270
Q

What is meant when osteomalacia and rickets are called a “qualitative” defect?

A

process of bone mineralization is abnormal

271
Q

How much calcium should patients with vitamin D deficiency supplement per day?

A

1.5-2g

272
Q

How is iatrogenic osteomalacia managed?

A

withhold offending med

273
Q

What causes of vitamin D deficiency are associated with increased loss of vitamin D?

A

increased metabolism
imapired enterohepatic circulation
nephrotic syndrome

274
Q

rickets lab values

A

decreased 25 vit d
decreased ca, phosphate
increased alk phos, PTH

275
Q

rickets x ray findings

A 
Widening of physes
Bowing of long bones
Translucent lines in bones
Flattening of the skull
Enlarged costal cartilages
276
Q

What results from the hypocalcemic state seen in osteomalacia and rickets?

A

hypocalcemia tetany

277
Q

What causes of vitamin D deficiency are associated target organ resistance?

A

vit d receptor mutation

phenytoin

278
Q

internal organs affected by scleroderma

A

GI tract
lungs
MSK

279
Q

organ system most often involved with systemic sclerosis

A

skin

thick, tight, shiny skin

280
Q

populations affected by scleroderma

A

women

black

281
Q

pulmonary complications in systemic sclerosis

A

interstitial fibrosis

282
Q

how to treat esophageal conditions of scleroderma

A

PPI, H2

strictures may need surgical correction

283
Q

what causes the GI symptoms of scleroderma

A

decreased motlitly

overgrwoth of bacteria and malabsorption

284
Q

scleroderma age range

A

20-50

285
Q

CREST

A

anti-centromere Ab, skin calcification, raynaud phenomenon, esophageal dysmotility, sclerodactly, telangiectasia

286
Q

esophageal conditions associated with scleroderma

A

esophageal reflux

esophageal candida

287
Q

scleroderma - treatment of joint contractures

A

physical therapy

288
Q

what three processes contribute to scleroderma pathogenesis

A

overproduction of ECM components
microvascular dysfxn
dysfxn cell/humoarl immunity

289
Q

other diseases associated with scleroderma

A

PBC
malignacies
spontaneaous PTX

290
Q

scleroderma & the heart

A

myocardial fibrosis –> CHF, arrhythmias

291
Q

systemic sclerosis antibodiy

A

anti-topoisomerase-1 (anti-scl-70)

292
Q

scleroderma GI symptoms

A

diarrhea, constipation, esophageal disease

293
Q

GI symptoms treatment in scleroderma

A

promotility agents

metronidazole

294
Q

treatment for scleroderma renal crisis

A

ACEI

295
Q

treatment for sclerotic vessels in scleroderma

A

vasodilators

296
Q

scleroderma renal crisis

A

sudden onset of hypertension and renal insuff

297
Q

treatment of rapidly progressive scleroderma

A

cyclophophamide, steroids

Internal Med (23 decks)

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