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Clinical Medicine I > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

viral infection

A

lymphocytes > neutrophils

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2
Q

acute bacterial infection

A

leukocytosis (elevated WBC) and elevated neutrophils

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3
Q

parasitic infection

A

elevated eosinophils

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4
Q

Basophils

A

least common
allergic and helminth responses
release histamine and heparin (decreased clotting and increased blood flow from vasodilation)

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5
Q

Eosinophils

A

particularly found in GI and respiratory tracts
asthma and allergic reactions
release leukotrienes (airway smooth muscle contraction)

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6
Q

Neutrophils

A 
most abundant
"first responders"
strongly phagocytic
respond to and subsequently release cytokines to amplify immune response
release anti-microbial proteins
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7
Q

Mast Cells

A

basophils that mature in the tissues
release histamine and heparin
massive release of histamine = anaphylaxis and body-wide vasodilation

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8
Q

Monocytes

A

differentiate into dendritic cells and macrophages when stimulated by pathogens
50% migrate to spleen

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9
Q

Dendritic cells

A

antigen-presenting cells (APC)
migrate to nearest lymph node once antigen is captured and presents to T and B cells
Langerhans cells = specialized dendritic cell in the skin

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10
Q

Macrophages

A

APC
large phagocytes
skin, lungs and GI tract
resting, primed and hyper-activated stages

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11
Q

Kupffer cells

A

specialized macrophages of the liver
destroy bacteria and old RBCs

*chronic activation via EtOH causes overproduction of inflammatory cytokines and chronic inflammation (cirrhosis and CA)

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12
Q

Natural Killer Cells (NK cells)

A

cytotoxic lymphocytes that do NOT need to recognize pathogen to kill it
killing activity enhanced by cytokines released from macrophages
kill via releasing perforins and proteases that cause cell membrane lysis or trigger apoptosis

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13
Q

opsonization

A

enhancing phagocytosis of antigens by “marking” them for destruction

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14
Q

membrane attack complex (MAC)

A

complement cascade resulting in cell lysis via puncturing cell membrane

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15
Q

humoral immunity

A

type of adaptive immunity
B cells and antibodies
defense against extracellular pathogens (ie. S. pneumonia, M. catarrhalis)

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16
Q

cell-mediated immunity

A

type of adaptive immunity
T cells and APCs (dendritic cells and macrophages)
defense against intracellular pathogens (ie. virus, fungi, protozoans)

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17
Q

secondary lymphatic organs

A

spleen
lymph nodes
tonsils
MALT (mucosal associated lymphoid tissue)

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18
Q

MHCII

A

B cells
dendritic cells
activated macrophages
thymic epithelial cells

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19
Q

T helper cells

A

T cell receptors and CD4 co-receptors
MHCII molecule presents antigen and has binding site for CD4
activated cells release cytokines to direct immune response

different subtypes activate different cells

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20
Q

T memory cells

A

recognize antigens from previous exposure

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21
Q

T regulatory (suppressor) cells

A

prevent immune reactions from getting out of hand

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22
Q

T killer cells (cytotoxic)

A

activated by T helper cells
CD8 co-receptor
MHCI molecules present antigens
secrete perforin and cytotoxins to cause cell death

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23
Q

primary response

A

IgM “iMmediate” produced first
IgG follows
B memory cells persist

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24
Q

secondary response

A

subsequent encounter with same antigen
previously generated B memory cells activated rapidly
IgM formed, but IgG most involved

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25
Q

IgG

A

75-85% of antibodies in the blood
major immunoglobin in the extravascular tissues and longest half life
*only one to cross placenta = fetal protection
secondary response
neutralize, opsonize, mediate complement and MAC

type II hypersensitivity reactions (ie. Rh factor, Graves’ disease)

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26
Q

IgM

A

acute infection - primary response
5-10% antibodies in the blood
neutralize, complement, agglutinate
good against carbs on bacterial cell walls

type II hypersensitivity reactions (ie. Rh factor, Graves’ disease)

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27
Q

IgA

A

10% antibodies in serum
monomer or dimer with J chain
mucosal areas and secreted in bodily fluids
found in breast milk = protects infant GI tract
blocks attachment and agglutinizes

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28
Q

IgD

A

required for B cell activation (found on mature B cell membranes)

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29
Q

IgE

A

binding on mast cell or basophil results in release of histamine
defense of parasites

type I hypersensitivity reactions (allergy/asthma, hives, food/drug)

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30
Q

symptoms of anemia

A

fatigue, weakness
lightheadedness/syncope
dyspnea
palpitations

often occur when Hb

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31
Q

signs of anemia

A 
pallor
tachycardia
bounding pulses
orthostatic bP
heme in stool (GI blood loss)
cardiac failure and shock (severe)
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32
Q

microcytic, hypochromic

A

Fe deficiency
thalassemia
sideroblastic

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33
Q

normocytic, normochromic

A

hypothyroidism
liver disease
chronic disease

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34
Q

macrocytic (megaloblastic)

A

folate deficiency

vitamin B12 deficiency

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35
Q 
microcytic, hypochromic
increased RDW (body tries to compensate)
decreased ferritin
decreased serum Fe
increased TIBC

glossitis, chelitis, koilonychia
pica
dysphagia
restless leg syndrome

Tx: underlying cause
oral ferrous sulfate 325mg BID-TID x3-6mo
blood transfusions for select pts

A

Iron deficiency anemia (IDA)
most common cause of anemia worldwide

decreased ferritin because depletion of Fe stores occurs first

36
Q

microcytic, hypochromic
normal RDW
normal to increased ferritin and serum Fe
poikilocytosis (abnormal shapes)

*Dx: Hb electrophoresis

Tx: tailored to severity of disease
folic acid supplement
AVOID iron supplement (overload)
regular transfusions and splenectomy if severe

A

Thalassemia

inherited disorder

37
Q

Alpha Thalassemia

A

deletion of 1+ of the 4 alpha-globing chains

1 = silent carrier
2 = alpha trait, mild microcytic anemia (often asymptomatic)
3 = hemolytic anemia
4 = hydrops fetalis (incompatible with life)
38
Q

Beta Thalassemia

A

reduced or absent beta-globing chains

minor (trait) = dysfunction of 1 chain (asymptomatic)
major = severe dysfunction of both chains –> most patients die before 30yo

39
Q

normocytic, normochromic
normal to increased ferritin
variable serum Fe and TIBC

Tx: underlying disease
EPO may benefit

common: inflammation, organ failure, elderly

A

Anemia of Chronic Disease

40
Q

MCV can be low, normal or slightly elevated
poikilocytosis and anisocytosis
anemia usually moderate
systemic iron overload

BM biopsy = ringed sideroblasts (nucleated RBC precursors)

Tx: underlying cause (ie. alcoholism, meds, lead poison)
refer if transfusion support needed

A

Sideroblastic Anemia
type of Myelodysplastic Syndrome (MDS)
hereditary or acquired

41
Q

megaloblastic (elevated MCV)
peripheral smear = hypersegmented neutrophils
low serum B12
+ Schilling test or antibodies to IF (intrinsic factor)
*elevated serum methylmalonic acid and homocysteine levels

*neuro problems:
dec. vibratory and position sense
ataxia
paresthesia
confusion/dementia

Tx: parenteral B12 (can’t absorb oral)
daily IM 1000ug x1wk
then weekly x1mo, then monthly for life

A

Pernicious Anemia
1-2 ug/day B12 req

deficiency of IF causes B12 malabsorption
autoantibodies against gastric parietal cells impair IF secretion

42
Q

megaloblastic
anemia sxs
low serum folate
*elevated homocysteine levels ONLY (not methylmalonic acid)

Tx: underlying cause (if known)
replacement therapy –> 1mg PO daily, 5mg PO if malabsorption

occurs in:
alcoholism
end of pregnancy
malabsorption syndromes
*hemolytic anemias (ie. sickle cell)
A

Folic Acid Deficiency Anemia
200 ug/day req.
4-5 mo. deprivation = anemia

43
Q

anemia sxs
jaundice (increased unconjugated bilirubin)
gallstones
increased risk of infection from salmonella and pneumococcus

elevated retic count (polychromasia)
peripheral smear = nucleated RBCs and possible schistocytes (fragmented RBC)

destruction of RBCs

A

Hemolytic Anemias

44
Q

Intravascular hemolysis

A 
fragmented syndromes (ie. trauma from prosthetic heart valve)
red cell enzyme defects (ie. G6PD deficiency = Heinz bodies)

serum haptoglobin is low
–> mucoprotein produced in liver which binds Hb released from lysed RBCs

45
Q

Extravascular hemolysis

A 
hereditary spherocytosis
sickle cell anemia
autoimmune hemolytic anemia
incompatible blood transfusion
drug-induced
46
Q

normocytic but decreased SA (dense, globular w/o central pallor)
often asymptomatic
mild jaundice
splenomegaly
chronic hemolysis creates need for increased folate

+ osmotic fragility (RBC show increased hemolysis in hypotonic fluid due to membrane defect)

Tx: splenectomy - delay until adulthood if possible
give pneumococcal vaccine early

A

Hereditary Spherocytosis

autosomal dominant

47
Q

normocytic, normochromic
usually develop in childhood as HbF –> HbA
delayed growth and development
increased susceptibility to infections

*vaso-occlusive ischemic tissue injury ==> pain crises

A

Sickle Cell Anemia (SSA)

autosomal recessive
RBCs become “sickle shaped” when deoxygenated causing painful sxs

48
Q

Sickle Cell Anemia Labs and Tx

A 
elevated relic (10-20%)
*Hb electrophoresis reveals HbS
peripheral smear = sickled, nucleated RBCs, Howell Jolly bodies, thrombocytosis

Tx: avoid precipitating factors
RBC transfusions PRN
analgesics, fluids and O2 during pain crises
hydroxyurea to decrease incidence of pain crises
bone marrow transplant may help

49
Q

clinical features variable
caused by antibodies that adhere to surface of RBCs and induce hemolysis by fixing complement and damaging cell membrane

elevated retic and spherocytes formed

ex: incompatible blood transfusion, hemolytic disease of newborn
+ Coombs test can detect antibodies of the patient

Tx: identify and treat underlying cause
corticosteroids helpful (inflammatory process)
splenectomy
folic acid supplementation

A

Autoimmune Hemolytic Anemia

50
Q

pancytopenia (anemia, leukopenia, thrombocytopenia)
bone marrow shows absence of precursors of these cells

Tx: bone marrow transplant
hematology referral

50% idiopathic
drug/chem exposure, viral illnesss, ionizing radiation

A

Aplastic Anemia

acquired abnormality of bone marrow stem cells (total or selective)

51
Q

bruits are predictive of CAD/future MI and CV death
– area where carotid vessel bifurcate = disturbance
low sensitivity but high specificity

symptomatic pt:
contralateral weakness
contralateral sensory deficits
amaurosis fugax - shade coming down over eye (retinal branch is first off internal carotid)
hollenhorst plaque - cholesterol deposits get stuck in vessels

*generally >75% occlusion of a vessel needed for sxs

Carotid endarterectomy (CEA) - open surgery preferred

A

Carotid Artery Disease (CAD)

52
Q

Ascending
compression, pain, hoarseness (RLN), valve regurgitation
Arch and descending
wheezing/coughing/SOB, hemoptysis, hoarseness,
dysphagia, chest/back pain

Tx:
beta blockers - decrease force of ejection
angiotensin II receptor blockers
statins (decrease cholesterol b/c atherosclerotic)
smoking cessation
control HTN

5-6cm SURGERY
4.5-5cm or rapid growth for Marfans = SURGERY

A

Thoracic Aortic Aneurysm

53
Q

acute onset “tearing” pain in chest/abdomen/back
HTN - check both arms and legs

*spiral CT scan with contrast is GOLD STD

Tx:
beta blockers, pain control and HTN control initially
Arch/Ascending = emergency surgery
Descending = med therapy if no rupture, surgery if rupture (use a stent)

A

Aortic Dissections

54
Q

abdominal pain
pulsatile abdominal mass
tenderness
hypotension

U/S for Dx and follow size
>5.5cm, symptomatic, or rapid expansion (>0.5cm 6-12mo)
–> endovascular stent graft, often bifurcated

A

Abdominal Aortic Aneurysm (AAA)

55
Q

Chronic
younger, typically female
work up with angiogram or MRI
Tx: angioplasty +/- stenting

Acute
*neuro deficit including paralysis
*ABSENT femoral pulses
saddle embolism at bifurcation
vascular emergency
Tx: quick imaging --> OPERATE
A

Aorta-Iliac Occlusive Disease

56
Q

rare –> >2cm is risk factor
thrombosis or embolization with limb ischemia
DDx: Baker’s cyst or varicose veins

Tx: surgery or endovascular therapy

A

Popliteal Aneurysm

57
Q

Signs of Peripheral Vascular Disease (PVD)

A
  1. Claudication - mild (more than 2 blocks walking)
    moderate (1 block)
    severe (less than 1 block)
  2. rest pain (toes and dorsum of foot)
  3. Leriche syndrome (decreased femoral pulse, impotence and butt/thigh claudication)
58
Q

hair loss on leg/foot (poor perfusion)
atrophic skin and nail changes
pallor with raised extremity
delayed capillary refill

Ankle-Brachial index (ABI)
ankle systolic P/brachial systolic P --> normal 1.0-1.1
>0.8 = no claudication
0.5-0.8 = claudication
0.2-0.5 = rest pain
less than 0.2 = limb threat
A

Arterial Insufficiency

59
Q 
Pain
Pallor
Paresthesia
Paralysis
Pulselessness

Tx: emergency surgical consultation to remove thrombus/embolus
anticoagulation via heparin keeps clot from getting worse

A

Acute Arterial Obstruction

60
Q 
Pain out of proportion to findings
Passive stretch pain
Paresthesias
Paralysis
Pulselessness
Poikliothermia (inability to regulate core body temp)

commonly seen after repercussion of ischemic limb

Tx: fasciotomy with delayed closure often with skin grafts

A

Compartment Syndrome

61
Q

may be asymptomatic
aching/burning sensation
“tired” or “heavy” feeling in the extremities
worse with standing or sitting with legs bent
relieved by elevation

dilated, tortuous superficial veins
start distally and move upward
can rupture, bleed and erode
ulcerations near ankle

Tx: compression stockings and short frequent walks
sclerotherapy, laser therapy, vein stripping

A

Varicose Veins

62
Q

due to valvular incompetence or as a result of DVT with residual damage to the vein
veins rigid and thick-walled
high pressure develop and distend the walls creating further valve incompetence

Tx: limb elevation
compression stockings
wound care (dry/wet non-adherent)
diuretics for edema or abs for secondary infection
surgery
A

Chronic Venous Insufficiency

63
Q 
often asymptomatic
swelling of LE
pain
warmth and redness
palpable cord (thrombosed vein)
A

Deep Vein Thrombosis (DVT)

64
Q

Virchow’s Triad

A

stasis - alterations in blood flow
hyper-coagulability - alterations in constituents of blood
–> acquired or hereditary
vessel wall injury (vascular endothelium)

65
Q

DVT diagnostics

A

Homan’s sign (sensitive but not specific)
*Wells criteria
*compression US test of choice
D-Dimer - detectable at >500ng/mL in ALL pts with VTE (venous thromboembolism) = sensitive but not specific
impedance plethysmography
contrast venography (invasive)

66
Q

DVT treatment

A

prevent PE
decrease risk of recurrent VTE

*anticoagulation therapy (admit to hospital)
–> initial administration 5-10 days during high risk period SQ LMWH
–> long term administration for minimum 3 months (extended to 6-12mo in some pts) WARFARIN
early ambulation
compression stockings

67
Q 
dyspnea (and tachypnea)
tachycardia
pleuritic pain
DVT sxs
may vary from no sxs to shock and sudden death
A

Pulmonary Embolism (PE)

68
Q

PE classification criteria

A 
hemodynamic stability
--> instability means systolic BP under 90mmHg
temporal pattern
anatomic location
presence/absence of sxs
69
Q

PE diagnostics

A

if hemodynamically unstable - imaging unsafe, so bedside US works better

if hemodynamically stable - Wells criteria, CTPA of chest and d-dimer
pulmonary angiography was once gold std
*now CT pulmonary angiography (CTPA) test of choice
–> less accurate for detection of smaller PE
–> exclude use if IV contract allergy or renal dysfunction
V/Q scan (sensitive but not specific)
EFG (nonspecific) - S1Q3T3 pattern
CXR - not specific or sensitive
–> Hampton’s hump (opacity = infarct of tissue)
–>Westermark sign (oligemia = decreased Bf)

70
Q

PE treatment

A
  • anticoagulation therapy (admit to hospital)
  • -> initial administration 5-10 days during high risk period SQ LMWH most often
  • -> long term administration for minimum 3 months (extended to 6-12mo in some pts) WARFARIN most often

IVC filter if anticoagulation is contraindicated, high risk of bleeding or recurrent PE (use acutely)

thrombolytics = good for unstable patients with PE
thrombectomy/embolectomy
prophylactic measures = sequential compression devices, TED hoes and low dose SG UFH/LMWH for hospitalized pts

71
Q 
anemia
--> angina
--> dyspnea on exertion
--> fatigue and pallor
neutropenia - increased risk of infection
thrombocytopenia = problems clotting

AUER RODS on peripheral smear
bone marrow biopsy - blasts more than 20% of sample

*most common acute leukemia in adults
accumulation of leukemic blasts (immature cells)
65yo at dx

A

Acute Myelogenous Leukemia (AML)

72
Q

cytopenias
ineffective hematopoiesis
may progress to AML (unfavorable)
typically asymptomatic

Tx: immunosuppressive, hematopoietic growth factors

A

Myelodysplastic Syndrome (MDS)

73
Q 
increased K+ (arrhythmia risk)
increased phosphate
nucleic acids
hypocalcemia (tetany)
hyperuricemia

EMERGENCY –> high mortality
associated with ALL and CML

A

Tumor Lysis Syndrome (TLS)

74
Q

Tumor Lysis Syndrome (TLS) treatment

A 
prevention, fluids
frequent monitoring
allopurinol
seizure precautions
dialysis
treat hyperkalemia and hyperphosphatemia
75
Q

fatigue, malaise
splenomegaly
B sxs: fever, weight loss, night sweats

*more than 90% due to Ph chromosome translocation

A

Chronic Myelogenous Leukemia (CML)

76
Q

Chronic Myelogenous Leukemia (CML) phases and complications

A

Chronic = 80% pts, asymptomatic, WBC >100,000 (high chance of remission)
Accelerated = 10-19% blasts, symptomatic
Blast (crisis) = more than 20% blasts, more serious sxs including splenomegaly

TLS
hyperleukocytosis (tx with leukapheresis or else hyperviscosity syndrome)
--> spontaneous bleeding
--> visual disturbances (retinopathy)
--> neuro = HA/vertigo, seizures, coma
77
Q

Chronic Myelogenous Leukemia (CML) diagnostics and treatment

A

bone marrow biopsy = Ph chromosome

depends on stage:
tyrosine kinase inhibitor (Imatinib/Gleevec)
monoclonal antibodies
stem cell transplant in later phases (cure but not many can tolerate)

78
Q

*testicular mass
cytopenias
*most common CA in children and teens
associated with Down Syndrome and NF-1

more favorable if:
B cell rather than T cell (hyperleukocytosis and older age)
under 35yo @ dx
favorable cytogenetics
absence of CNS disease
A

Acute Lymphocytic Leukemia (ALL)

79
Q

Acute Lymphocytic Leukemia (ALL) diagnostics and treatment

A

lymphoblasts on peripheral smear

chemotherapy - induction, consolidation, maintenance
monoclonal antibodies
oral tyrosine kinase inhibitors

80
Q 
cytopenias --> can be asymptomatic/indolent
advanced disease:
organomegaly
B sxs
atypical infections
death due to infection/bleeding

accumulation of incompetent lymphocytes
*highest inheritability of any malignancy
*most prevalent chronic leukemia in adults in Western countries
72yo at dx

A

Chronic Lymphocytic Leukemia (CLL)

81
Q

Chronic Lymphocytic Leukemia (CLL) diagnostic and treatment

A

bone marrow biopsy
lymph node biopsy

chemotherapy/radiation
immunotherapy with Rituximab (CD20) and other monoclonal antibodies
splenectomy

82
Q

painless LAD (often cervical, but also supraclavicular and mediastinal)
pruritic
EtOH-induced pain of affected lymph nodes
enlargement of:
lymph nodes
spleen
liver

REED-STERNBERG cells = multinucleated B cells (arrested development)

etiology: Epstein-Barr virus in 40-50% cases
most common 15-34yo

A

Hodgkin Lymphoma

83
Q

Hodgkin Lymphoma diagnostics and treatment

A

Reed-Sternberg cells in biopsy of lymph node tissue

combo chemo often with radiation
stem cell transplant

worse prognosis:
B sxs (fever, weight loss, night sweats)
bulky
distant spread
affects lymph nodes on both sides of diaphragm
84
Q 
*painless, persistent LAD
B sxs (more common) = fever, night sweats, weight loss

associated with HIV, EBV, Hep B/C, H. pylori, etc.
66yo at dx
aggressive = rapidly growing, B sxs, elevated LDH and uric acid

*someone with CLL can develop this

A

Non-Hodgkin Lymphoma (NHL)

85
Q

Non-Hodgkin Lymphoma (NHL) diagnostics and treatment

A

biopsy enlarged lymph nodes
CT- staging
bone marrow biopsy (cytopenias)
lumbar puncture

based on stage and clinical status
indolent = radiation alone
aggressive = chemo, immunotherapy, autologous HCT (hematopoietic cell transplant)

86
Q

back pain
bone pain - low back and ribs - osteoporosis
bleeding (from thrombocytopenia)
hypercalcemia (all malignancies)
pathologic fractures
hyperviscosity syndrome = spontaneous bleeding, visual disturbances and neuro sxs)

65yo at dx
instead of making Ig, plasma cells secrete paraproteins
–> replace bone marrow
–> destroy bone
–> forms tumors (spinal cord compression)

A

Multiple Myeloma

87
Q

Multiple Myeloma diagnostics and treatment

A

protein electrophoresis on blood and urine (SPEP & UPEP)
*M spike (monoclonal)
*Bence-Jones proteins in urine
CRAB: calcium >10.5, renal insufficiency (Cre >2), anemia (Hb less than 10), bone lesions

refer to oncology
*bone marrow transplant
combo chemo
IV bisphosphate

Clinical Medicine I (4 decks)

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