Week 3 Buzzwords Flashcards
AAAAAAHHHHHHHHHHH (148 cards)
1
Q
DVT:
A
Can propagate and manifest as a pulmonary embolism
2
Q
DVT First line imaging:
A
Duplex Doppler ultrasound
3
Q
Great Saphenous vein:
A
not a deep vein but clot within 1.5 cm of junction gets DVT treatment
4
Q
Whole Body Low Dose CT:
A
Good for monitoring Multiple Myeloma treatment response
5
Q
Extraosseous Myeloma:
A
most commonly seen in lymph nodes
6
Q
Diagnostic for Multiple Myeloma:
A
> 5mm lytic lesion, axial skeleton most common (ie. vertebrae)
7
Q
Osteonecrosis:
A
sickle cell anemia associated disease
8
Q
Asplenia, gallstones, CNS infarcts:
A
Sickle Cell radiologic manifestations
9
Q
Best diagnostic imaging for lymphoma:
A
CT is workhorse
10
Q
Pathologic node for lymphoma:
A
> 1 cm on short axis
11
Q
4 T’s of Anterior Mediastinal Mass Differential:
A
Teratoma, thymoma, thyroid, “Terrible” lymphoma
12
Q
Dengue Fever:
A
flavivirus, 4 serotypes, aedes mosquito, no person/person transmission, “bone break fever”, secondary infection due to different serotype
42% Mosquitos Prefer Bone Flavor
13
Q
Arenaviruses:
A
“sandy” or “string of beads” appearance under EM, rodent host, fever / headache / fatigue / hemorrhagic fever, South America / West Africa
14
Q
Lassa Fever virus:
A
arenavirus, alpha-dystroglycan, rat, west africa
15
Q
Filovirus:
A
Ebola and Marburg - can be transmitted through sexual contact
16
Q
Ebola:
A
Zaire strain is most deadly
17
Q
Bunyaviridae:
A
zoonotic, phlebovirus is Rift Valley Fever while Nairovirus is Crimean-Congo hemorrhagic Fever
18
Q
Colorado Tick Fever:
A
coltivirus, reoviridae family with double layered capsid, elevation >4,000 ft, dermacentor andersoni, prolonged viremia
Colts rear double when Anderson takes them past 4k ft for too long.
19
Q
Malaria:
A
Plasmodium falciparum, ovale, malariae, knowlesi, female anopheles mosquitoes
20
Q
Fever Types Malaria:
A
P. Falciparum - malignant tertian, p. Vivax - benign tertian (liver stage), P. Ovale - benign tertian (liver stage), P. malariae - quartan, P. knowlesi - quotidian (every day)
21
Q
Malaria Stages:
A
sporozoite injected into blood, merozoite is multiplication in liver and invade RBC, form ring and become schizont, burst and release new merozoites, cycle continues causing fever, some merozoites develop into gametocytes which are taken up when mosquito bites again
22
Q
Babesia:
A
intracellular sporozoan with ixodes tick, maltese cross (tetrads), severe in immunocompromised
23
Q
Wuchereria bancrofti and Brugia malayi:
A
sheathed microfilariae, filarial worms, mosquito, endosymbionts, nocturnal circulation
SF MEN
24
Q
Loa loa:
A
calabar Swellings, worms migrate under Eye, Eosinophilia, move during Day, Sheathed
SEE SD
25
Mansonella:
blackflies, non sheathed, no lymph involved
26
Schistosoma mansoni, Schistosoma japonicum:
blood fluke in guts and mesenteric, move out through fecal
27
Schistosoma haematobium:
veins urinary bladder, out through urine
28
Components of Hemostasis:
vessels, platelets, soluble coagulation factors, blood flow
29
Blood contents are:
constantly under low rate activation
30
Protective systems in blood:
dilute and inactivate factors
31
Flow should be:
brisk and laminar
32
Clotting due to poor hemodynamics:
atrial fibrillation, varicose veins
33
Initial response to vascular injury:
vasoconstriction, slowing blood loss
34
Primary hemostasis:
endothelium activated and secreting vWF to which platelets Adhere, Activate, Aggregate
35
Secondary hemostasis define:
Fibrin clot forms to enmesh platelet aggregation
36
Tertiary hemostasis:
clot limitation and dissolution
37
Patients with Vasoconstriction (aka intrinsic vascular) disorders:
palpable purpura and ecchymoses
38
Patients with plug formation (aka platelet) defects or deficiency:
Mucosal bleeding, small cutaneous bleeds, VERY low platelet counts
39
Patients with fibrin clot (aka coagulation) defects:
soft tissue bleeds, join bleeds (hemarthrosis)
40
Patients with clot dissolution (aka hypercoagulability) problems:
venous (plt/coag/flow) thrombosis and arterial (endothelial) thrombosis
41
Platelet Adhesion:
GPIb (receptor on platelet) → vWF (on endothelium)
42
Ristocetin:
exogenous activation of vWF
43
vWF multimer binds:
GPIb
44
Platelet Activation:
ADP → shape change and surface molecule change (sticky feet with GP IIB/IIIA) which bind to fibrinogen
45
Serotonin and ADP released:
recruitment more platelets and stimulation aggregation
46
Platelet Aggregation:
shape change increases surface area and binding to fibrinogen
47
Ristocetin enhances in vitro:
GPIb binding to vWF
48
Physiologic ADP / Collagen /Epinephrine enhances:
Platelet aggregation
(via GPIIb/IIIA receptor)
49
Factor VIII activity decreased:
vWD type 3
50
Primary Hemostasis Disorders:
vWD, Bernard-Soulier, Glanzmann Thrombasthenia, Immune Thrombocytopenic Purpura
51
Platelet bleeding symptoms:
mucosal bleeding, petechiae/purpura, menorrhagia, GI bleeding
52
vWD Type 1:
most common, mild, AD, normal activity, RIPA low if severe, PTT normal usually, multimers normal, quantitative
53
vWD Type 2:
rare subtypes, qualitative, Antigen>Activity, prolonged RIPA, abnormal multimeric assays, AR
54
vWD Type 3:
AR, absence of wWF, ristocetin prolonged, PTT prolonged, hybrid Hemophilia-vWD phenotype
55
vWD treatment:
ddAVP producing release of vWF multimers, vWF products, antifibrinolytics
56
Bernard Soulier Syndrome:
AR GPIb deficiency, large platelets, thrombocytopenia, decreased RIPA
57
Bernard-Soulier treatment:
ddAVP (desmopressin) or antifibrinolytics ; platelet transfusion if severe
58
Glanzmann Thrombasthenia:
AR defective GPIIb/IIIA, decreased binding fibrinogen, normal platelet morph/number, severe bleeding time, treat with transfusion if severe
59
Glanzmann Thrombasthenia ristocetin reaction:
partial preservation
60
Immune Thrombocytopenic Purpura:
acquired autoimmune destruction of platelets, antibodies against GPIIb/IIIa
61
Childhood ITP:
acute, following viral infection, self limiting
62
Adult ITP:
chronic, low platelet count, normal RBC, normal WBC morph, treat with steroids, splenectomy, IVIG, Rituximab
63
Heparin Induced Thrombocytopenia:
antibody induced platelet activation and aggregation, thrombosis with low platelet count post heparin exposure
64
HIT criteria:
5-10 days post exposure, >50% decrease in platelet count, thrombosis evidence, no other cause
65
Heparin forms complexes with:
PF4 of alpha granules (which antibodies form against this complex)
66
HIT measure:
serotonin release assay with susceptible donor platelets to measure antibody activity
67
Secondary Homeostasis:
formation of fibrin clot, cascade of serine proteases
68
Activated Protein C inhibits:
Factor Va
69
Intrinsic Pathway:
collagen activates F12 -11, 9, 8-> activates 10, cleaves fibrinogen, fibrin polymer forms enmesh platelets
70
Extrinsic Pathway:
activated by Tissue Factor release → 7 → activates 10
71
Common Pathway:
10a activates prothrombin to thrombin (2) with help of Va, cleaves fibrinogen to fibrin (1), F13 crosslinks fibrin polymers
72
Intrinsic Test:
PTT, Factors VIII, IX, XI, XII
73
Extrinsic Test:
PT, VII
74
Common Test:
PTT and PT, II, V, X
75
Fibrinogen Test:
Thrombin Time
76
Mixing Study shows:
PTT long due to inhibitor or factor deficiency – mixing fixes factor deficiency, not inhibitor
77
Urea clot Stability:
aged clot incubated in urea solution, cross-linked will remain clotted, otherwise will dissolve (tests for F13a)
78
Secondary Coagulation Bleeding Symptoms:
deep hematomas, hemarthrosis, delayed bleeding, rebleeding after injury
79
Bleeding Secondary Disorders:
Factor 8,9,13, Factor inhibitors
80
Clotting Secondary Disorders:
Factor 5, Antithrombin, Prothrombin, Antiphospholipid, Protein C/S, Dysfibrinogenemia
PAPA 5D (50)
81
Factor VIII deficiency:
X linked recessive, Hemophilia A, newborn bleeding, spontaneous bleeds at high impact sites, PTT prolonged, normal PT, mixing studies correct
82
Factor VIII deficiency complications:
degenerative joint disease and alloantibodies
83
Factor IX deficiency:
X linked recessive, Hemophilia B, PTT prolonged, PT norma, mixing studies to correct, reduced in Vit K deficiency, neonatal period can be physiologic
84
Factor 8 vs Factor 9:
need factor antigen and activity levels
85
Acquired Factor VIII Inhibitor:
autoantibody against Factor VIII, usually elderly, same as deficiency EXCEPT mixing study does not correct
86
Factor XIII deficiency:
AR with defective fibrin crosslinking, hx delayed umbilical cord stump bleeding, delayed wound healing, F13 assay to diagnose
87
Acquired Dysfibrinogenemia laboratory test result:
prolonged thrombin time
88
Protein C degrades:
Factor Va via cleavage
89
Antithrombin inactivates:
thrombin by binding IXa and Xa
90
Heparin potentiates:
antithrombin activity
91
Factor V Leiden:
activated protein C resistance causing increase risk of thrombosis
92
Factor V Leiden results in:
increased FV activity
93
Special Test for Factor V Leiden:
aPTT with and without APC for ratio; PTT fails to prolong after APC addition
94
Protein C/S Deficiency:
AD, C degrades FV adn VIII, S is cofactor, both vit K dependent
95
Prothrombin G20210A:
genetic factor II causing increased prothrombin
96
Antiphospholipid syndrome:
aka lupus anticoagulant, produces prolonged PTT and clinical thrombophilia, autoantibodies against phospholipid bound proteins causing coagulation, BUT will see prolonged PTT
97
Clinical and Lab Antiphospholipid Syndrome:
Clin - thrombosis and pregnancy ; Lab - anti-cardiolipin antibody or anti-beta2 GPI or Lupus anticoagulant (dRVVT)
98
Hyperhomocysteinemia:
increase leads to accelerated atherosclerosis and thrombosis risk, cystathionine Beta synthetase deficiency for inherited and acquired is dietary or vitamin B6/12/9 deficiency
99
Dysfibrinogenemia:
abnormal fibrinogen which may cause increased (thrombosis) or decreased (bleeding) activity – PROLONGED THROMBIN TIME
100
Lab for Extrinsic/Intrinsic/Common/Fibrinogen:
E-PT, I-PTT, C-PT/PTT, F-Thrombin Time
101
Vit K deficiency or Warfarin causes low:
2,7,9,10 and C/S
102
Liver disease causes low:
5 with normal 8
103
Bleeding umbilicus see low:
13
104
Hemophilia A or inhibitor low:
8
105
Hemophilia B low:
9
106
Tertiary hemostasis labs:
d-Dimers, Fibrin Degradation Product
107
DIC:
acquired with intravascular coagulation with loss of localization; tissue injury causing uncontrolled thrombin formation, Tissue Factor released and creates clots via activation VII; when factors all used up and platelets used up, start to bleed
108
DIC labs:
High PT (more than PTT) decrease in F7, low PLT, low fibrinogen, high FDP and high D-Dimers, schistocyte if severe
109
DIC treat:
TREAT UNDERLYING CONDITION
110
Thrombotic Thrombocytopenic Purpura:
due to ADAMTS13 deficiency, chronic relapsing, failure to cleave vWF, thrombocytopenia, renal failure (mild), NEUROLOGIC SYMPTOMS, petechiae, treat with plasmapheresis
111
Hemolytic Uremic Syndrome:
children, preceding infection, bloody diarrhea, ACUTE RENAL FAILURE, endothelial injury, shiga toxin
112
Liver disease will not affect:
F8 or vWF
113
Cirrhosis vs DIC:
FV (decrease DIC), FVIII (decrease DIC) - FV (decrease Cirrhosis), FVIII (increase Cirrhosis)
114
Venous Thrombosis arise:
hypercoagulable states with DVT or PE
115
Arterial Thrombosis arise:
vascular damage / plt coagulation see ischemic bowel, CVA
116
Heparin released:
from mast cells – abundant in liver, lungs, intestines
117
Heparin promotes:
inactivation of FXa and FIIa
118
Heparin and Pregnancy:
does not cross placental, can be used
119
LMWH has greater capacity:
increase FXa inhibition
120
Heparin thrombin inhibition:
simultaneous bind to antithrombin and thrombin
121
Heparin does not:
dissolve clots
122
Activity of heparin is:
immediate activity
123
Heparin dosage for thrombosis:
low dose for prevention and high does for events
124
Heparin contraindications:
active bleeding, brain/eye/spinal cord surgery, liver/kidney disease, hypertension, co-use with other anticoags
125
AE of Heparin:
Thromboembolism, MI, stroke, osteoporosis
MOST
126
Heparin Antidote:
protamine sulfate - forms inactive complex, less effective against LMWH, fondaparinux poor response, no antidote
127
HIT 4 T’s:
Thrombocytopenia, Timing (5-10 days), New thrombosis or sequelae, threat (likelihood) of other causes
128
Warfarin MOA:
inhibit vitamin K epoxide reductase
129
Warfarin A/E:
Bleeding, Skin necrosis, teratogenicity
130
Warfarin and drug interaction:
CYP metabolism
131
Warfarin Contraindications:
ulcer hx, blood disorders, hepatic/renal disease, recent surgery, pregnancy
Here Be RPU
132
Warfarin does not:
directly alter clotting factors
133
Warfarin can be reversed with:
Vitamin K, FFP, and Kcentra
134
Kcentra:
F4 prothrombin complex concentrate with risk of thromboembolic events
135
Aminocaproic acid:
acute fibrinolytic hemorrhage management
136
Tranexamic acid:
severe menstrual bleeding prevention
137
Desmopressin (DDAVP):
release vWF for vWD and Hem A
138
Monitoring Heparin vs Warfarin:
Hep PTT and Warfarin PT
139
Heparin major points:
VI, rapid, acute duration, protamine sulfate, safe for pregnancy
140
Warfarin major points:
oral, slow, long duration, Vit K or FFP, Teratogenic
141
Dabigatran etexilate:
oral direct competitive inhibitor of thrombin, used for a fib therapy that does not have valve problem - no regular monitoring, pregnancy OK, avoid abrupt discontinuation
142
Dabigatran antidote:
idarucizumab
143
Rivaroxaban, Apixaban, Edoxaban:
direct inhibitor FXa
144
Aspirin:
irreversible COX-1 blocker, fast, lasts lifetime of platelet with A/E of GI problems, increased bleed time, and neurologic issues
145
Clopidogrel MOA:
blocks ADP binding P2Y12 inhibiting GPIIb/IIIa activation, transformed to active form (IS PRODRUG)
146
Ticlopidine relation to:
TTP
147
Epitfibatide:
GP IIb/IIIa inhibitor with effect persisting roughly 10 hours (Tirofiban only lasts the duration of infusion)
148
Herbals for bleeding:
ginger, garlic, fish oil, ginseng, feverfew increasing bleeding risk when used with anticoagulants or platelet aggregation inhibitors
